cholecalciferol and Kidney-Failure--Chronic

Middle East Respiratory Syndrome (MERS) is a novel respiratory illness firstly reported in Saudi Arabia in 2012. It is caused by a new corona virus, called MERS corona virus (MERS-CoV). Most people who have MERS-CoV infection developed severe acute respiratory illness.. This work is done to determine the clinical characteristics and the outcome of intensive care unit (ICU) admitted patients with confirmed MERS-CoV infection.. This study included 32 laboratory confirmed MERS corona virus infected patients who were admitted into ICU. It included 20 (62.50%) males and 12 (37.50%) females. The mean age was 43.99 ± 13.03 years. Diagnosis was done by real-time reverse transcription polymerase chain reaction (rRT-PCR) test for corona virus on throat swab, sputum, tracheal aspirate, or bronchoalveolar lavage specimens. Clinical characteristics, co-morbidities and outcome were reported for all subjects.. Most MERS corona patients present with fever, cough, dyspnea, sore throat, runny nose and sputum. The presence of abdominal symptoms may indicate bad prognosis. Prolonged duration of symptoms before patients' hospitalization, prolonged duration of mechanical ventilation and hospital stay, bilateral radiological pulmonary infiltrates, and hypoxemic respiratory failure were found to be strong predictors of mortality in such patients. Also, old age, current smoking, smoking severity, presence of associated co-morbidities like obesity, diabetes mellitus, chronic heart diseases, COPD, malignancy, renal failure, renal transplantation and liver cirrhosis are associated with a poor outcome of ICU admitted MERS corona virus infected patients.. Plasma HO-1, ferritin, p21, and NQO1 were all elevated at baseline in CKD participants. Plasma HO-1 and urine NQO1 levels each inversely correlated with eGFR (. SnPP can be safely administered and, after its injection, the resulting changes in plasma HO-1, NQO1, ferritin, and p21 concentrations can provide information as to antioxidant gene responsiveness/reserves in subjects with and without kidney disease.. A Study with RBT-1, in Healthy Volunteers and Subjects with Stage 3-4 Chronic Kidney Disease, NCT0363002 and NCT03893799.. HFNC did not significantly modify work of breathing in healthy subjects. However, a significant reduction in the minute volume was achieved, capillary [Formula: see text] remaining constant, which suggests a reduction in dead-space ventilation with flows > 20 L/min. (ClinicalTrials.gov registration NCT02495675).. 3 组患者手术时间、术中显性失血量及术后 1 周血红蛋白下降量比较差异均无统计学意义（. 对于肥胖和超重的膝关节单间室骨关节炎患者，采用 UKA 术后可获满意短中期疗效，远期疗效尚需进一步随访观察。.. Decreased muscle strength was identified at both time points in patients with hEDS/HSD. The evolution of most muscle strength parameters over time did not significantly differ between groups. Future studies should focus on the effectiveness of different types of muscle training strategies in hEDS/HSD patients.. These findings support previous adverse findings of e-cigarette exposure on neurodevelopment in a mouse model and provide substantial evidence of persistent adverse behavioral and neuroimmunological consequences to adult offspring following maternal e-cigarette exposure during pregnancy. https://doi.org/10.1289/EHP6067.. This RCT directly compares a neoadjuvant chemotherapy regimen with a standard CROSS regimen in terms of overall survival for patients with locally advanced ESCC. The results of this RCT will provide an answer for the controversy regarding the survival benefits between the two treatment strategies.. NCT04138212, date of registration: October 24, 2019.. Results of current investigation indicated that milk type and post fermentation cooling patterns had a pronounced effect on antioxidant characteristics, fatty acid profile, lipid oxidation and textural characteristics of yoghurt. Buffalo milk based yoghurt had more fat, protein, higher antioxidant capacity and vitamin content. Antioxidant and sensory characteristics of T. If milk is exposed to excessive amounts of light, Vitamins B. The two concentration of ZnO nanoparticles in the ambient air produced two different outcomes. The lower concentration resulted in significant increases in Zn content of the liver while the higher concentration significantly increased Zn in the lungs (p < 0.05). Additionally, at the lower concentration, Zn content was found to be lower in brain tissue (p < 0.05). Using TEM/EDX we detected ZnO nanoparticles inside the cells in the lungs, kidney and liver. Inhaling ZnO NP at the higher concentration increased the levels of mRNA of the following genes in the lungs: Mt2 (2.56 fold), Slc30a1 (1.52 fold) and Slc30a5 (2.34 fold). At the lower ZnO nanoparticle concentration, only Slc30a7 mRNA levels in the lungs were up (1.74 fold). Thus the two air concentrations of ZnO nanoparticles produced distinct effects on the expression of the Zn-homeostasis related genes.. Until adverse health effects of ZnO nanoparticles deposited in organs such as lungs are further investigated and/or ruled out, the exposure to ZnO nanoparticles in aerosols should be avoided or minimised.

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The magnitude of vitamin D inputs in individuals not taking supplements is unknown; however, there is a great deal of information on quantitative response to varying supplement doses. We reanalyzed individual 25-hydroxyvitamin D [25(OH)D] concentration data from 8 studies involving cholecalciferol supplementation (total sample size = 3000). We extrapolated individual study dose-response curves to zero concentration values for serum 25(OH)D by using both linear and curvilinear approaches and measured seasonal oscillation in the serum 25(OH)D concentration. The total basal input (food plus solar) was calculated to range from a low of 778 iu/d in patients with end-stage renal disease to a high of 2667 iu/d in healthy Caucasian adults. Consistent with expectations, obese individuals had lower baseline, unsupplemented 25(OH)D concentrations and a smaller response to supplements. Similarly, African Americans had both lower baseline concentrations and lower calculated basal, all-source inputs. Seasonal oscillation in 4 studies ranged from 5.20 to 11.4 nmol/L, reflecting a mean cutaneous synthesis of cholecalciferol ranging from 209 to 651 iu/d at the summer peak. We conclude that: 1) all-source, basal vitamin D inputs are approximately an order of magnitude higher than can be explained by traditional food sources; 2) cutaneous, solar input in these cohorts accounts for only 10-25% of unsupplemented input at the summer peak; and 3) the remainder must come from undocumented food sources, possibly in part as preformed 25(OH)D.

Topics: Adult; Aged; Black or African American; Cholecalciferol; Diet; Dietary Supplements; Dose-Response Relationship, Drug; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Obesity; Reference Values; Seasons; Skin; Sunlight; Vitamin D; Vitamin D Deficiency; White People

Atherosclerosis is common in patients with chronic kidney disease (CKD), and cardiovascular disease (CVD) represents a major cause of death in these patients, especially, in patients with end-stage renal disease(ESRD). The pathological features in ESRD patients are intimal atherosclerosis and medial calcific sclerosis. The important risk factors for CVD in ESRD patients are hypertension, dyslipidemia and CKD bone and mineral disorder (CKD-MBD). Atherosclerosis has been evaluated by measurements of intima-media thickness and pulse-wave velocity. Although the target blood pressure still undetermined, hypertension would be treated with renin-angiotensin system inhibitors. In addition, treatment of dyslipidemia with statins may lead to favorable CVD outcome. Finally, inhibition of vascular calcification should be important by treatment with active vitamin D and sevelamer.

Topics: Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Atherosclerosis; Bone Diseases, Metabolic; Calcinosis; Cholecalciferol; Chronic Disease; Dyslipidemias; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypertension; Kidney Failure, Chronic; Polyamines; Risk Factors; Sevelamer; Tunica Intima; Vascular Diseases

To review the data supporting combination therapy with vitamin D and vitamin D receptor activators (VDRAs) in patients with stage 5 chronic kidney disease (CKD).. Literature was searched using PubMed and EMBASE using the terms kidney disease, kidney failure-chronic, and vitamin D. Limits applied included humans, adults (19 years or older), and clinical trials (and related), with publication dates between January 1, 1980, and May 16, 2011.. All English-language publications were analyzed for relevance. Studies appropriate to the objective were evaluated, including 3 prospective observational studies, 1 prospective cohort study, and 1 retrospective study.. To our knowledge, there have been no randomized controlled trials evaluating the safety and efficacy of vitamin D supplementation in combination with VDRA therapy in patients with stage 5 CKD. Relatively small observational studies have demonstrated improvements in 25-hydroxyvitamin D (25-OHD) concentrations and markers of mineral and bone metabolism as well as reduced VDRA use in patients with stage 5 CKD. Not all patients in these studies were receiving VDRA therapy. Therapy was safe, with no patients exceeding the recommended upper limit for 25-OHD concentrations and only a small percentage experiencing transient/correctable hypercalcemia.. Vitamin D supplementation to maintain 25-OHD concentrations at 20-30 ng/mL or higher with or without VDRA therapy is inexpensive, appears safe, and may have additional health benefits in patients with stage 5 CKD. Well-designed, randomized controlled trials are needed to determine the efficacy and safety of combination vitamin D therapy in patients with stage 5 CKD.

Topics: Adult; Bone Resorption; Cholecalciferol; Drug Therapy, Combination; Ergocalciferols; Humans; Kidney Failure, Chronic; Receptors, Calcitriol; Severity of Illness Index; Vitamin D

Topics: Calcitriol; Cholecalciferol; Drug Design; Ergocalciferols; Humans; Hydroxycholecalciferols; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Vitamin D

Supplementation of vitamin D in food is available in Japan, therefore, vitamin D deficiency is not likely to occur in our country. But, in the case of nephrotic syndrome and strict dietary protein restriction, low serum 25(OH)D level might develop in chronic kidney disease (CKD)patients. Guideline issued by National Kidney Foundation as DOQI recommend the use of vitamin D2 (ergocalciferol) when serum 25(OH)D level in CKD patients become less than 30 ng/mL. In addition, for the CKD patients with stage 5, the use of active vitamin D3 is recommended because a conversion to 1,25(OH)2D3, which is the most potent vitamin D, might be impossible in these patients. However, vitamin D2 product as a supplementary medicine is not available in Japan unfortunately. In this context, I try to explain the background of the recommendation of vitamin D2 for CKD patients.

Topics: Biomarkers; Cholecalciferol; Diet, Protein-Restricted; Ergocalciferols; Humans; Kidney Failure, Chronic; Nephrotic Syndrome; Practice Guidelines as Topic; Vitamin D; Vitamin D Deficiency

Studies in rats with renal ablation indicate that anemia lessens, whereas its vigorous correction with recombinant human erythropoietin (r-HuEPO) worsens systemic and glomerular hypertension, factors known to promote progression of chronic renal failure (CRF). However, in human studies, use of r-HuEPO in predialysis patients has not been associated with worsening renal function, provided blood pressure control is achieved. Histological evidence of bone disease is common in early renal failure, and deficits in calcitriol synthesis seem to be an important factor in the pathogenesis of secondary hyperparathyroidism (HPTH) in early CRF. Reports to data, on the use of low dose active vitamin D metabolites in predialysis patients, indicate either a reversible decline or no decline in renal function. Adynamic bone disease, however, may ensure during such therapy if excessive reductions in serum intact parathyroid hormone concentrations occur. Recent data suggest that chronic metabolic acidosis decreases albumin synthesis, increases muscle proteolysis, and induces negative nitrogen balance in patients with CRF. Despite these experimental data, the clinical relevance of correction of metabolic acidosis in end-stage renal disease (ESRD) is still not defined. Even though therapy of metabolic acidosis in the adult patient with CRF remains conjectural at this time, reports indicate that its correction might lead to healing of osteomalacia and osteopenia, and possibly may decrease protein degradation and improve growth in children with CRF.

Topics: Acidosis; Adult; Anemia; Animals; Calcitriol; Calcium Compounds; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Ergocalciferols; Erythropoietin; Humans; Kidney Failure, Chronic; Rats; Recombinant Proteins; Renal Dialysis

It is well known that hyperparathyroidism begins early in renal failure and progresses, probably not linearly, throughout the natural course of renal diseases and dialysis therapy. Recent progress in basic medical science has improved our understanding of the mechanisms by which the classically known stimuli for parathyroid hormone synthesis and secretion may act, including hypocalcaemia, hyperphosphataemia and vitamin D3 metabolism disturbances. In the treatment of hyperparathyroidism, although some authors stress the benefit of treating one of these stimuli, it is probably more effective to combine the treatment of them all. There is conclusive recent work showing the efficacy of using both CaCO3 and vitamin D3, either in chronic renal failure or in dialysis patients at every stage of hyperparathyroidism. Therefore, the treatment of hyperparathyroidism should start early, long before dialysis, and it should aim to correct any of the causal factors. Both CaCO3 and vitamin D3 derivatives may be used in the prevention and treatment of renal bone disease. The limits of this association are the increasingly often reported adynamic bone disease, which in our experience has not yet given major clinical problems, and hyperphosphataemia. Uncontrolled serum phosphate levels would counterbalance the beneficial effect of vitamin D3 derivatives on hyperparathyroidism.

Topics: Administration, Oral; Animals; Bone Diseases; Calcium; Calcium Carbonate; Cholecalciferol; Humans; Hyperparathyroidism; Kidney Failure, Chronic; Phosphates; Renal Dialysis

The available data with regard to the use of calciferol, dihydrotachysterol, and calcifediol in the management of renal insufficiency are reviewed. Very limited data are available with regard to calciferol therapy; with the advent of more active metabolites, the use of calciferol is not warranted. Dihydrotachysterol seems to be effective in the treatment of renal patients with osteitis fibrosa; its low cost makes therapy with this compound a reasonable alternative, although it should not be used in the treatment of patients with liver disease. Calcifediol seems to be effective in patients with osteitis fibrosa; however, limited data on histologic characteristics of bone are available. Detailed prospective studies are necessary to establish the therapeutic benefit of calcifediol.

Topics: Absorption; Calcifediol; Cholecalciferol; Dihydrotachysterol; Ergocalciferols; Humans; Kidney Failure, Chronic; Osteitis Fibrosa Cystica; Structure-Activity Relationship

Topics: Calcitonin; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Ions; Kidney; Kidney Failure, Chronic; Magnesium; Parathyroid Hormone; Phosphates; Renal Dialysis

A rapidly growing understanding of the biochemical and physiological processes that underlie the metabolism of vitamin D has provided new insights into the pathogenesis of oestomalacia. Many of the vitamin D--resistant osteomalacia syndromes can now be explained on the basis of defects in the metabolic conversion of vitamin D to the biologically active dihydroxylated metabolite 1,25(OH)2D and perhaps, in some instances, to impairement of the actions of 1,25(OH)2D on target tissues. The availability of this new information has made possible the synthesis of 1-hydroxylated forms of the vitamin for therapeutic use in states of vitamin D resistance. Although many questions regarding the pathogenesis and most effective approaches in the management of osteomalacia remain unanswered, considerable progress has been made in this direction as a result of continued research on the subject.

Topics: Bone Neoplasms; Chemical Phenomena; Chemistry; Cholecalciferol; Dihydroxycholecalciferols; Ergocalciferols; Giant Cell Tumors; Humans; Hydroxycholecalciferols; Hypoparathyroidism; Hypophosphatemia, Familial; Kidney Failure, Chronic; Metabolism, Inborn Errors; Nephrectomy; Osteomalacia; Phosphates; Pseudohypoparathyroidism; Vitamin D; Vitamin D Deficiency

Topics: Animals; Calcium; Cholecalciferol; Humans; Intestinal Absorption; Kidney Failure, Chronic; Rats; Renal Dialysis; Vitamin D; Vitamin D Deficiency

Topics: Adolescent; Adult; Animals; Binding, Competitive; Child; Child, Preschool; Cholecalciferol; Chromatography; Female; Humans; Infant; Infant, Newborn; Kidney Failure, Chronic; Maternal-Fetal Exchange; Methods; Middle Aged; Pregnancy; Protein Binding; Rats; Rickets; Vitamin D; Vitamin D Deficiency

Topics: Anemia, Hypochromic; Arteriovenous Shunt, Surgical; Blood Flow Velocity; Cardiac Output; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Erythropoiesis; Glucose; Hemolytic-Uremic Syndrome; Humans; Hyperlipidemias; Hypertension, Renal; Infertility, Male; Kidney Failure, Chronic; Male; Parathyroid Hormone; Peripheral Nervous System Diseases; Phosphates; Renal Dialysis; Triglycerides

Topics: Aluminum Hydroxide; Animals; Calcium; Child; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Hyperparathyroidism, Secondary; Intestinal Absorption; Kidney; Kidney Failure, Chronic; Magnesium; Parathyroid Hormone; Vitamin D

The biologically active form of vitamin D3, 1,25-dihydroxycholecalciferol is produced by the kidney. The biosynthesis of 1,25-dihydroxycholecalciferol from 25-hydroxycholecalciferol is apparently controlled and important factors in this control are dietary calcium and phosphorus, and parathyroid hormone secretion. The direct effects of vitamin D and its metabolites on renal function are uncertain. Patients with chronic renal failure have defective synthesis of 1,25-dihydroxycholecalciferol. Uremic patients treated with small doses of 1,25-dihydroxycholecalciferol or 1 alpha-hydroxycholecalciferol show increased intestinal calcium absorption and bone healing.

Topics: Animals; Bone and Bones; Calcium; Cholecalciferol; Humans; Intestines; Kidney; Kidney Failure, Chronic; Parathyroid Hormone; Phosphorus; Rats; Uremia; Vitamin D

Topics: Alpha-Globulins; Animals; Biological Assay; Chickens; Cholecalciferol; Humans; Hydroxycholecalciferols; In Vitro Techniques; Kidney; Kidney Failure, Chronic; Liver; Mucous Membrane; Osteomalacia; Osteopathic Medicine; Protein Binding; Rats; Tritium; Vitamin D Deficiency

Topics: Adrenal Cortex Hormones; Animals; Anticonvulsants; Bone and Bones; Calcium; Carrier Proteins; Cholecalciferol; Dihydroxycholecalciferols; Humans; Hydroxycholecalciferols; Hypocalcemia; Hypoparathyroidism; Hypophosphatemia, Familial; Intestinal Absorption; Kidney; Kidney Failure, Chronic; Kidney Tubules; Liver; Mixed Function Oxygenases; Parathyroid Hormone; Phosphorus; Vitamin D; Vitamin D Deficiency

Topics: Animals; Calcium; Cholecalciferol; Diphosphates; Glomerular Filtration Rate; Humans; Hydroxycholecalciferols; Hypercalcemia; Kidney Failure, Chronic; Mitochondria, Liver; Parathyroid Glands; Parathyroid Hormone; Phosphates; Rats

Topics: Animals; Calcitonin; Calcium; Calcium Metabolism Disorders; Cholecalciferol; Diuretics; Extracellular Space; Glomerular Filtration Rate; Glomerulonephritis; Hypercalcemia; Kidney; Kidney Concentrating Ability; Kidney Diseases; Kidney Failure, Chronic; Metabolic Clearance Rate; Mineralocorticoids; Parathyroid Hormone; Sodium

Topics: Anticonvulsants; Bone and Bones; Bone Diseases; Calcium; Cell Membrane Permeability; Cholecalciferol; Cholesterol; Ergocalciferols; Gastrointestinal Diseases; Humans; Hypoparathyroidism; Hypophosphatemia, Familial; Intestinal Mucosa; Kidney; Kidney Failure, Chronic; Parathyroid Hormone; Sarcoidosis; Skin; Vitamin D

Topics: Biological Transport, Active; Bone and Bones; Calcium; Cell Membrane Permeability; Cholecalciferol; Endoplasmic Reticulum; Homeostasis; Humans; Hyperparathyroidism, Secondary; Intestinal Absorption; Intestinal Mucosa; Kidney; Kidney Failure, Chronic; Kidney Transplantation; Kidney Tubules; Liver; Magnesium; Muscle Contraction; Phosphates; Postoperative Complications; Sodium

Topics: Animals; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Hydroxycholecalciferols; Hyperparathyroidism, Secondary; Kidney; Kidney Failure, Chronic; Liver; Parathyroid Hormone; Rats; Uremia; Vitamin D

Topics: Bicarbonates; Bone Resorption; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Diet Therapy; Dihydroxycholecalciferols; Humans; Hyperparathyroidism, Secondary; Hypocalcemia; Kidney Failure, Chronic; Kidney Tubules; Magnesium; Parathyroid Glands; Parathyroid Hormone; Phosphorus; Renal Dialysis; Structure-Activity Relationship

Topics: Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Hyperparathyroidism, Secondary; Hypocalcemia; Intestinal Absorption; Kidney Failure, Chronic; Kidney Transplantation; Osteoporosis; Osteosclerosis; Phosphates; Transplantation, Homologous; Vitamin D

Topics: Bone and Bones; Bone Diseases; Calcium; Cholecalciferol; Dihydrotachysterol; Homeostasis; Intestinal Absorption; Kidney; Kidney Failure, Chronic; Uremia; Vitamin D

Topics: Calcitonin; Calcium; Cholecalciferol; Humans; Hyperparathyroidism; Hypocalcemia; Kidney Failure, Chronic; Osteitis Fibrosa Cystica; Osteomalacia; Parathyroid Glands; Phosphorus

Vitamin D insufficiency is common in patients suffering from end-stage renal disease (ESRD). In contrast, vitamin D supplementation could improve the status of ESRD patients (ESRDP). However, this effect's molecular mechanism is not fully understood. Therefore, this study aimed to assess vitamin D supplementation's impact on inflammation and oxidative signaling pathways in ESRDP. 104 ESRDP were divided into placebo (53) and vitamin D (51) groups. They were also categorized into four subgroups based on the severity of vitamin D deficiency. The dose of vitamin D3 (0.25-0.5mg/day) supplementation was determined based on plasma levels of calcium and parathyroid hormone (PTH). Vitamin D supplementation was performed for eight weeks. Serum levels of calcium, phosphorus, PTH, albumin, creatinine, ALP, and glomerular filtration along with antioxidant enzymes, malondialdehyde, and pro-inflammatory factors were measured. Moreover, the Nrf2 and NF-ĸB expression was evaluated in whole blood. According to the results, vitamin D supplementation improved the status of patients with ESRD significantly as compared with the placebo group (p<0.05). In addition, the expression of NF-ĸB and the serum levels of pro-inflammatory factors and malondialdehyde were significantly reduced. Finally, the expression of Nrf-2 and the serum of antioxidant enzymes were raised in the vitamin D group as compared with the placebo group (p<0.05). Vitamin D reduces clinical and metabolic symptoms in ESRDP by modulating gene expression (in oxidative stress and inflammation).

Topics: Antioxidants; Biomarkers; Calcium; Cholecalciferol; Dietary Supplements; Humans; Inflammation; Kidney Failure, Chronic; Malondialdehyde; NF-kappa B; Oxidative Stress; Parathyroid Hormone; Vitamin D; Vitamin D Deficiency; Vitamins

End-stage renal disease results in B cell lymphopenia and low levels of vitamin D. Since the link between vitamin D deficiency and B lymphocytes dysfunction are not clear in patients with end-stage renal disease, we suggest that vitamin D adequacy and factors related to the homeostasis of these cells should be investigated. B lymphocytes homeostasis is a process mainly regulated signals of grown and death as interleukin (IL)-7, B cell-activating factor (BAFF)/BAFF-receptor and CD95 expression.. As vitamin D serum levels were reduced in patients with end stage renal disease and it is associated with human B homeostasis, we evaluated the effect of cholecalciferol supplementation on dialysis.. Randomized, double blind clinical trial in dialysis patients with 25OH Vitamin D deficiency for a period of 12 weeks.. In a pilot study, we investigated the effect of cholecalciferol supplementation (100,000 UI once per week or placebo. In vitro, peripheral blood mononuclear cells isolated by Ficoll-Hypaque centrifugation from 12 healthy volunteers were incubated with healthy or uremic serum in the presence or absence of 25 (OH)DC with 5% CO.. There was an increase in the serum 25(OH)D level in the cholecalciferol group. No differences were found in BAFF and IL7 levels and CD95 and BAFF-R expression in B lymphocytes from patients on dialysis after cholecalciferol supplementation. Uremic serum induced an increase in the IL-7, BAFF, BAFF-R and CD95 expression compared with the control. However, we observed no effect of incubation of 25(OH)D3 and 1,25(OH)2D3 on the expression of IL-7, BAFF, BAFF-R and CD95 when incubated in the presence of normal or uremic serum.. Our results suggest that vitamin D is not involved in mechanisms of regulation of differentiation and survival in B lymphocytes. In conclusion, further studies are needed to explore the effects of vitamin D on B lymphocytes to better evaluate the possible impact of vitamin D on humoral response in the CKD population.

Topics: Adult; Aged; B-Cell Activating Factor; B-Lymphocytes; Cholecalciferol; Dietary Supplements; Double-Blind Method; fas Receptor; Female; Humans; Interleukin-7; Kidney Failure, Chronic; Lymphopenia; Male; Middle Aged; Pilot Projects; Renal Dialysis; Uremia; Vitamin D; Vitamin D Deficiency; Vitamins

Middle East Respiratory Syndrome (MERS) is a novel respiratory illness firstly reported in Saudi Arabia in 2012. It is caused by a new corona virus, called MERS corona virus (MERS-CoV). Most people who have MERS-CoV infection developed severe acute respiratory illness.. This work is done to determine the clinical characteristics and the outcome of intensive care unit (ICU) admitted patients with confirmed MERS-CoV infection.. This study included 32 laboratory confirmed MERS corona virus infected patients who were admitted into ICU. It included 20 (62.50%) males and 12 (37.50%) females. The mean age was 43.99 ± 13.03 years. Diagnosis was done by real-time reverse transcription polymerase chain reaction (rRT-PCR) test for corona virus on throat swab, sputum, tracheal aspirate, or bronchoalveolar lavage specimens. Clinical characteristics, co-morbidities and outcome were reported for all subjects.. Most MERS corona patients present with fever, cough, dyspnea, sore throat, runny nose and sputum. The presence of abdominal symptoms may indicate bad prognosis. Prolonged duration of symptoms before patients' hospitalization, prolonged duration of mechanical ventilation and hospital stay, bilateral radiological pulmonary infiltrates, and hypoxemic respiratory failure were found to be strong predictors of mortality in such patients. Also, old age, current smoking, smoking severity, presence of associated co-morbidities like obesity, diabetes mellitus, chronic heart diseases, COPD, malignancy, renal failure, renal transplantation and liver cirrhosis are associated with a poor outcome of ICU admitted MERS corona virus infected patients.. Plasma HO-1, ferritin, p21, and NQO1 were all elevated at baseline in CKD participants. Plasma HO-1 and urine NQO1 levels each inversely correlated with eGFR (. SnPP can be safely administered and, after its injection, the resulting changes in plasma HO-1, NQO1, ferritin, and p21 concentrations can provide information as to antioxidant gene responsiveness/reserves in subjects with and without kidney disease.. A Study with RBT-1, in Healthy Volunteers and Subjects with Stage 3-4 Chronic Kidney Disease, NCT0363002 and NCT03893799.. HFNC did not significantly modify work of breathing in healthy subjects. However, a significant reduction in the minute volume was achieved, capillary [Formula: see text] remaining constant, which suggests a reduction in dead-space ventilation with flows > 20 L/min. (ClinicalTrials.gov registration NCT02495675).. 3 组患者手术时间、术中显性失血量及术后 1 周血红蛋白下降量比较差异均无统计学意义（. 对于肥胖和超重的膝关节单间室骨关节炎患者，采用 UKA 术后可获满意短中期疗效，远期疗效尚需进一步随访观察。.. Decreased muscle strength was identified at both time points in patients with hEDS/HSD. The evolution of most muscle strength parameters over time did not significantly differ between groups. Future studies should focus on the effectiveness of different types of muscle training strategies in hEDS/HSD patients.. These findings support previous adverse findings of e-cigarette exposure on neurodevelopment in a mouse model and provide substantial evidence of persistent adverse behavioral and neuroimmunological consequences to adult offspring following maternal e-cigarette exposure during pregnancy. https://doi.org/10.1289/EHP6067.. This RCT directly compares a neoadjuvant chemotherapy regimen with a standard CROSS regimen in terms of overall survival for patients with locally advanced ESCC. The results of this RCT will provide an answer for the controversy regarding the survival benefits between the two treatment strategies.. NCT04138212, date of registration: October 24, 2019.. Results of current investigation indicated that milk type and post fermentation cooling patterns had a pronounced effect on antioxidant characteristics, fatty acid profile, lipid oxidation and textural characteristics of yoghurt. Buffalo milk based yoghurt had more fat, protein, higher antioxidant capacity and vitamin content. Antioxidant and sensory characteristics of T. If milk is exposed to excessive amounts of light, Vitamins B. The two concentration of ZnO nanoparticles in the ambient air produced two different outcomes. The lower concentration resulted in significant increases in Zn content of the liver while the higher concentration significantly increased Zn in the lungs (p < 0.05). Additionally, at the lower concentration, Zn content was found to be lower in brain tissue (p < 0.05). Using TEM/EDX we detected ZnO nanoparticles inside the cells in the lungs, kidney and liver. Inhaling ZnO NP at the higher concentration increased the levels of mRNA of the following genes in the lungs: Mt2 (2.56 fold), Slc30a1 (1.52 fold) and Slc30a5 (2.34 fold). At the lower ZnO nanoparticle concentration, only Slc30a7 mRNA levels in the lungs were up (1.74 fold). Thus the two air concentrations of ZnO nanoparticles produced distinct effects on the expression of the Zn-homeostasis related genes.. Until adverse health effects of ZnO nanoparticles deposited in organs such as lungs are further investigated and/or ruled out, the exposure to ZnO nanoparticles in aerosols should be avoided or minimised.

Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor Proteins, Signal Transducing; Adenine; Adenocarcinoma; Adipogenesis; Administration, Cutaneous; Administration, Ophthalmic; Adolescent; Adsorption; Adult; Aeromonas hydrophila; Aerosols; Aged; Aged, 80 and over; Aging; Agriculture; Air Pollutants; Air Pollution; Airway Remodeling; Alanine Transaminase; Albuminuria; Aldehyde Dehydrogenase 1 Family; Algorithms; AlkB Homolog 2, Alpha-Ketoglutarate-Dependent Dioxygenase; Alzheimer Disease; Amino Acid Sequence; Ammonia; Ammonium Compounds; Anaerobiosis; Anesthetics, Dissociative; Anesthetics, Inhalation; Animals; Anti-Bacterial Agents; Anti-HIV Agents; Anti-Infective Agents; Anti-Inflammatory Agents; Antibiotics, Antineoplastic; Antibodies, Antineutrophil Cytoplasmic; Antibodies, Monoclonal, Humanized; Antifungal Agents; Antigens, Bacterial; Antigens, CD; Antigens, Differentiation, Myelomonocytic; Antimetabolites, Antineoplastic; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Antioxidants; Antitubercular Agents; Antiviral Agents; Apolipoproteins E; Apoptosis; Arabidopsis; Arabidopsis Proteins; Arsenic; Arthritis, Rheumatoid; Asthma; Atherosclerosis; ATP-Dependent Proteases; Attitude of Health Personnel; Australia; Austria; Autophagy; Axitinib; Bacteria; Bacterial Outer Membrane Proteins; Bacterial Proteins; Bacterial Toxins; Bacterial Typing Techniques; Bariatric Surgery; Base Composition; Bayes Theorem; Benzoxazoles; Benzylamines; beta Catenin; Betacoronavirus; Betula; Binding Sites; Biological Availability; Biological Oxygen Demand Analysis; Biomarkers; Biomarkers, Tumor; Biopsy; Bioreactors; Biosensing Techniques; Birth Weight; Blindness; Blood Chemical Analysis; Blood Gas Analysis; Blood Glucose; Blood Pressure; Blood Pressure Monitoring, Ambulatory; Blood-Brain Barrier; Blotting, Western; Body Mass Index; Body Weight; Bone and Bones; Bone Density; Bone Resorption; Borates; Brain; Brain Infarction; Brain Injuries, Traumatic; Brain Neoplasms; Breakfast; Breast Milk Expression; Breast Neoplasms; Bronchi; Bronchoalveolar Lavage Fluid; Buffaloes; Cadherins; Calcification, Physiologic; Calcium Compounds; Calcium, Dietary; Cannula; Caprolactam; Carbon; Carbon Dioxide; Carboplatin; Carcinogenesis; Carcinoma, Ductal; Carcinoma, Ehrlich Tumor; Carcinoma, Hepatocellular; Carcinoma, Non-Small-Cell Lung; Carcinoma, Pancreatic Ductal; Carcinoma, Renal Cell; Cardiovascular Diseases; Carps; Carrageenan; Case-Control Studies; Catalysis; Catalytic Domain; Cattle; CD8-Positive T-Lymphocytes; Cell Adhesion; Cell Cycle Proteins; Cell Death; Cell Differentiation; Cell Line; Cell Line, Tumor; Cell Movement; Cell Nucleus; Cell Phone Use; Cell Proliferation; Cell Survival; Cell Transformation, Neoplastic; Cell Transformation, Viral; Cells, Cultured; Cellulose; Chemical Phenomena; Chemoradiotherapy; Child; Child Development; Child, Preschool; China; Chitosan; Chlorocebus aethiops; Cholecalciferol; Chromatography, Liquid; Circadian Clocks; Circadian Rhythm; Circular Dichroism; Cisplatin; Citric Acid; Clinical Competence; Clinical Laboratory Techniques; Clinical Trials, Phase I as Topic; Clinical Trials, Phase II as Topic; Clostridioides difficile; Clostridium Infections; Coculture Techniques; Cohort Studies; Cold Temperature; Colitis; Collagen Type I; Collagen Type I, alpha 1 Chain; Collagen Type XI; Color; Connective Tissue Diseases; Copper; Coronary Angiography; Coronavirus 3C Proteases; Coronavirus Infections; Cost of Illness; Counselors; COVID-19; COVID-19 Testing; Creatine Kinase; Creatinine; Cross-Over Studies; Cross-Sectional Studies; Cryoelectron Microscopy; Cryosurgery; Crystallography, X-Ray; Cues; Cultural Competency; Cultural Diversity; Curriculum; Cyclic AMP Response Element-Binding Protein; Cyclin-Dependent Kinase Inhibitor p21; Cycloparaffins; Cysteine Endopeptidases; Cytokines; Cytoplasm; Cytoprotection; Databases, Factual; Denitrification; Deoxycytidine; Diabetes Complications; Diabetes Mellitus; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Diagnosis, Differential; Diatoms; Diet; Diet, High-Fat; Dietary Exposure; Diffusion Magnetic Resonance Imaging; Diketopiperazines; Dipeptidyl Peptidase 4; Dipeptidyl-Peptidase IV Inhibitors; Disease Models, Animal; Disease Progression; Disease-Free Survival; DNA; DNA Damage; DNA Glycosylases; DNA Repair; DNA-Binding Proteins; DNA, Bacterial; DNA, Viral; Docetaxel; Dose Fractionation, Radiation; Dose-Response Relationship, Drug; Down-Regulation; Doxorubicin; Drosophila; Drosophila melanogaster; Drug Carriers; Drug Delivery Systems; Drug Liberation; Drug Repositioning; Drug Resistance, Bacterial; Drug Resistance, Multiple, Bacterial; Drug Resistance, Neoplasm; Drug Screening Assays, Antitumor; Drug Synergism; Drug Therapy, Combination; Edema; Edible Grain; Education, Graduate; Education, Medical, Graduate; Education, Pharmacy; Ehlers-Danlos Syndrome; Electron Transport Complex III; Electron Transport Complex IV; Electronic Nicotine Delivery Systems; Emergency Service, Hospital; Empathy; Emulsions; Endothelial Cells; Endurance Training; Energy Intake; Enterovirus A, Human; Environment; Environmental Monitoring; Enzyme Assays; Enzyme Inhibitors; Epithelial Cells; Epithelial-Mesenchymal Transition; Epoxide Hydrolases; Epoxy Compounds; Erythrocyte Count; Erythrocytes; Escherichia coli; Escherichia coli Infections; Escherichia coli Proteins; Esophageal Neoplasms; Esophageal Squamous Cell Carcinoma; Esophagectomy; Estrogens; Etanercept; Ethiopia; Ethnicity; Ethylenes; Exanthema; Exercise; Exercise Test; Exercise Tolerance; Extracellular Matrix; Extracorporeal Membrane Oxygenation; Eye Infections, Fungal; False Negative Reactions; Fatty Acids; Fecal Microbiota Transplantation; Feces; Female; Femur Neck; Fermentation; Ferritins; Fetal Development; Fibroblast Growth Factor-23; Fibroblast Growth Factors; Fibroblasts; Fibroins; Fish Proteins; Flavanones; Flavonoids; Focus Groups; Follow-Up Studies; Food Handling; Food Supply; Food, Formulated; Forced Expiratory Volume; Forests; Fractures, Bone; Fruit and Vegetable Juices; Fusobacteria; G1 Phase Cell Cycle Checkpoints; G2 Phase Cell Cycle Checkpoints; Gamma Rays; Gastrectomy; Gastrointestinal Microbiome; Gastrointestinal Stromal Tumors; Gefitinib; Gels; Gemcitabine; Gene Amplification; Gene Expression; Gene Expression Regulation; Gene Expression Regulation, Bacterial; Gene Expression Regulation, Neoplastic; Gene Expression Regulation, Plant; Gene Knockdown Techniques; Gene-Environment Interaction; Genotype; Germany; Glioma; Glomerular Filtration Rate; Glucagon; Glucocorticoids; Glycemic Control; Glycerol; Glycogen Synthase Kinase 3 beta; Glycolipids; Glycolysis; Goblet Cells; Gram-Negative Bacterial Infections; Granulocyte Colony-Stimulating Factor; Graphite; Greenhouse Effect; Guanidines; Haemophilus influenzae; HCT116 Cells; Health Knowledge, Attitudes, Practice; Health Personnel; Health Services Accessibility; Health Services Needs and Demand; Health Status Disparities; Healthy Volunteers; Heart Failure; Heart Rate; Heart Transplantation; Heart-Assist Devices; HEK293 Cells; Heme; Heme Oxygenase-1; Hemolysis; Hemorrhage; Hepatitis B; Hepatitis B e Antigens; Hepatitis B Surface Antigens; Hepatitis B virus; Hepatitis B, Chronic; Hepatocytes; Hexoses; High-Throughput Nucleotide Sequencing; Hippo Signaling Pathway; Histamine; Histamine Agonists; Histidine; Histone Deacetylase 2; HIV Infections; HIV Reverse Transcriptase; HIV-1; Homebound Persons; Homeodomain Proteins; Homosexuality, Male; Hospice and Palliative Care Nursing; HSP70 Heat-Shock Proteins; Humans; Hyaluronan Receptors; Hydrogen; Hydrogen Peroxide; Hydrogen-Ion Concentration; Hydrolysis; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypoglycemia; Hypoglycemic Agents; Hypoxia; Idiopathic Interstitial Pneumonias; Imaging, Three-Dimensional; Imatinib Mesylate; Immunotherapy; Implementation Science; Incidence; INDEL Mutation; Induced Pluripotent Stem Cells; Industrial Waste; Infant; Infant, Newborn; Inflammation; Inflammation Mediators; Infliximab; Infusions, Intravenous; Inhibitory Concentration 50; Injections; Insecticides; Insulin-Like Growth Factor Binding Protein 5; Insulin-Secreting Cells; Interleukin-1; Interleukin-17; Interleukin-8; Internship and Residency; Intestines; Intracellular Signaling Peptides and Proteins; Ion Transport; Iridaceae; Iridoid Glucosides; Islets of Langerhans Transplantation; Isodon; Isoflurane; Isotopes; Italy; Joint Instability; Ketamine; Kidney; Kidney Failure, Chronic; Kidney Function Tests; Kidney Neoplasms; Kinetics; Klebsiella pneumoniae; Knee Joint; Kruppel-Like Factor 4; Kruppel-Like Transcription Factors; Lactate Dehydrogenase 5; Laparoscopy; Laser Therapy; Lasers, Semiconductor; Lasers, Solid-State; Laurates; Lead; Leukocyte L1 Antigen Complex; Leukocytes, Mononuclear; Light; Lipid Peroxidation; Lipopolysaccharides; Liposomes; Liver; Liver Cirrhosis; Liver Neoplasms; Liver Transplantation; Locomotion; Longitudinal Studies; Lopinavir; Lower Urinary Tract Symptoms; Lubricants; Lung; Lung Diseases, Interstitial; Lung Neoplasms; Lymphocyte Activation; Lymphocytes, Tumor-Infiltrating; Lymphoma, Mantle-Cell; Lysosomes; Macrophages; Male; Manganese Compounds; MAP Kinase Kinase 4; Mass Screening; Maternal Health; Medicine, Chinese Traditional; Melanoma, Experimental; Memantine; Membrane Glycoproteins; Membrane Proteins; Mesenchymal Stem Cell Transplantation; Metal Nanoparticles; Metalloendopeptidases; Metalloporphyrins; Methadone; Methane; Methicillin-Resistant Staphylococcus aureus; Mexico; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Inbred ICR; Mice, Knockout; Mice, Nude; Mice, SCID; Mice, Transgenic; Microarray Analysis; Microbial Sensitivity Tests; Microbiota; Micronutrients; MicroRNAs; Microscopy, Confocal; Microsomes, Liver; Middle Aged; Milk; Milk, Human; Minority Groups; Mitochondria; Mitochondrial Membranes; Mitochondrial Proteins; Models, Animal; Models, Molecular; Molecular Conformation; Molecular Docking Simulation; Molecular Dynamics Simulation; Molecular Epidemiology; Molecular Structure; Molecular Weight; Multilocus Sequence Typing; Multimodal Imaging; Muscle Strength; Muscle, Skeletal; Muscular Diseases; Mutation; Mycobacterium tuberculosis; Myocardial Stunning; Myristates; NAD(P)H Dehydrogenase (Quinone); Nanocomposites; Nanogels; Nanoparticles; Nanotechnology; Naphthalenes; Nasal Cavity; National Health Programs; Necrosis; Needs Assessment; Neoadjuvant Therapy; Neonicotinoids; Neoplasm Invasiveness; Neoplasm Metastasis; Neoplasm Proteins; Neoplasm Recurrence, Local; Neoplasm Staging; Neoplasm Transplantation; Neoplasms; Neoplastic Stem Cells; Netherlands; Neuroblastoma; Neuroprotective Agents; Neutrophils; NF-kappa B; NFATC Transcription Factors; Nicotiana; Nicotine; Nitrates; Nitrification; Nitrites; Nitro Compounds; Nitrogen; Nitrogen Dioxide; North Carolina; Nuclear Magnetic Resonance, Biomolecular; Nuclear Proteins; Nucleic Acid Hybridization; Nucleosomes; Nutrients; Obesity; Obesity, Morbid; Oceans and Seas; Oncogene Protein v-akt; Oncogenes; Oocytes; Open Reading Frames; Osteoclasts; Osteogenesis; Osteoporosis; Osteoporosis, Postmenopausal; Outpatients; Ovarian Neoplasms; Ovariectomy; Overweight; Oxazines; Oxidants; Oxidation-Reduction; Oxidative Stress; Oxides; Oxidoreductases; Oxygen; Oxygen Inhalation Therapy; Oxygenators, Membrane; Ozone; Paclitaxel; Paenibacillus; Pain Measurement; Palliative Care; Pancreatic Neoplasms; Pandemics; Parasympathetic Nervous System; Particulate Matter; Pasteurization; Patient Preference; Patient Satisfaction; Pediatric Obesity; Permeability; Peroxiredoxins; Peroxynitrous Acid; Pharmaceutical Services; Pharmacists; Pharmacy; Phaseolus; Phenotype; Phoeniceae; Phosphates; Phosphatidylinositol 3-Kinases; Phospholipid Transfer Proteins; Phospholipids; Phosphorus; Phosphorylation; Photoperiod; Photosynthesis; Phylogeny; Physical Endurance; Physicians; Pilot Projects; Piperidines; Pituitary Adenylate Cyclase-Activating Polypeptide; Plant Extracts; Plant Leaves; Plant Proteins; Plant Roots; Plaque, Atherosclerotic; Pneumonia; Pneumonia, Viral; Point-of-Care Testing; Polyethylene Glycols; Polymers; Polysorbates; Pore Forming Cytotoxic Proteins; Positron Emission Tomography Computed Tomography; Positron-Emission Tomography; Postprandial Period; Poverty; Pre-Exposure Prophylaxis; Prediabetic State; Predictive Value of Tests; Pregnancy; Pregnancy Trimester, First; Pregnancy, High-Risk; Prenatal Exposure Delayed Effects; Pressure; Prevalence; Primary Graft Dysfunction; Primary Health Care; Professional Role; Professionalism; Prognosis; Progression-Free Survival; Prolactin; Promoter Regions, Genetic; Proof of Concept Study; Proportional Hazards Models; Propylene Glycol; Prospective Studies; Prostate; Protein Binding; Protein Biosynthesis; Protein Isoforms; Protein Kinase Inhibitors; Protein Phosphatase 2; Protein Processing, Post-Translational; Protein Serine-Threonine Kinases; Protein Structure, Tertiary; Protein Transport; Proteoglycans; Proteome; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins c-myc; Proto-Oncogene Proteins c-ret; Proto-Oncogene Proteins p21(ras); Proton Pumps; Protons; Protoporphyrins; Pseudomonas aeruginosa; Pseudomonas fluorescens; Pulmonary Artery; Pulmonary Disease, Chronic Obstructive; Pulmonary Gas Exchange; Pulmonary Veins; Pyrazoles; Pyridines; Pyrimidines; Qualitative Research; Quinoxalines; Rabbits; Random Allocation; Rats; Rats, Sprague-Dawley; Rats, Wistar; Receptors, Histamine H3; Receptors, Immunologic; Receptors, Transferrin; Recombinant Proteins; Recurrence; Reference Values; Referral and Consultation; Regional Blood Flow; Registries; Regulon; Renal Insufficiency, Chronic; Reperfusion Injury; Repressor Proteins; Reproducibility of Results; Republic of Korea; Research Design; Resistance Training; Respiration, Artificial; Respiratory Distress Syndrome; Respiratory Insufficiency; Resuscitation; Retinal Dehydrogenase; Retreatment; Retrospective Studies; Reverse Transcriptase Inhibitors; Rhinitis, Allergic; Ribosomal Proteins; Ribosomes; Risk Assessment; Risk Factors; Ritonavir; Rivers; RNA Interference; RNA-Seq; RNA, Messenger; RNA, Ribosomal, 16S; RNA, Small Interfering; Rosuvastatin Calcium; Rural Population; Saccharomyces cerevisiae; Saccharomyces cerevisiae Proteins; Salivary Ducts; Salivary Gland Neoplasms; San Francisco; SARS-CoV-2; Satiation; Satiety Response; Schools; Schools, Pharmacy; Seasons; Seawater; Selection, Genetic; Sequence Analysis, DNA; Serine-Threonine Kinase 3; Sewage; Sheep; Sheep, Domestic; Shock, Hemorrhagic; Signal Transduction; Silver; Silymarin; Single Photon Emission Computed Tomography Computed Tomography; Sirolimus; Sirtuin 1; Skin; Skin Neoplasms; Skin Physiological Phenomena; Sleep Initiation and Maintenance Disorders; Social Class; Social Participation; Social Support; Soil; Soil Microbiology; Solutions; Somatomedins; Soot; Specimen Handling; Spectrophotometry, Ultraviolet; Spectroscopy, Fourier Transform Infrared; Spectrum Analysis; Spinal Fractures; Spirometry; Staphylococcus aureus; STAT1 Transcription Factor; 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YAP-Signaling Proteins; Yogurt; Young Adult; Zebrafish; Zebrafish Proteins; Ziziphus

Psychological problems are common among end-stage renal disease patients undergoing dialysis. We aim to evaluate whether high-dose vitamin D3 (VD3) supplementation has beneficial effects on depressive symptoms in dialysis patients. This prospective, randomized, and double-blind trial includes 746 dialysis patients with depression treated in 3 hospitals in Southeast China. Depression was diagnosed according to the Diagnostic and Statistical Manual of Mental Disorders criteria. Patients were randomly assigned to 52-week treatment of oral 50,000 IU/wk VD3 (cholecalciferol) (test group) or a placebo (control group). The presence of depressive symptoms was evaluated using the Chinese version of Beck Depression Inventory (BDI) II both before and after treatment. Sociodemographic data, clinical data, nutritional indexes, inflammatory biomarkers, and plasma VD3 concentrations were also determined. Finally, 726 patients completed the experiments, including 362 tested patients and 364 controls. After 52 weeks, the depressive symptoms were not significantly improved in the test group (mean BDI II scores changed from -1.1 ± 0.3 to -3.1 ± 0.6) versus the control group. Multivariable logistic regression showed BDI scores were not significantly improved in the test group versus the control group with adjustment for age, sex, comorbidity index, dialysis modality, or (OH)D levels (multivariable-adjusted mean change or MAMC [95% confidence interval (CI)], -2.3 [-2.48 to -1.83]) in the whole dialysis population. After stratification by depression types, the findings do support a significant relationship between the VD3 supplementation and the improvement in BDI II scores in dialysis patients with vascular depression (MAMC [95% CI], -4.4 [-5.08 to -2.76]), but the effect was not significant for major depressive disorders (MAMC [95% CI], -0.9 [-1.52 to -0.63]). The high-dose VD3 supplementation did not significantly reduce the depressive symptoms in our total dialysis population, but a beneficial effect on vascular depression was found, probably mainly based on the improvement of cardiovascular risk factors.

Topics: Administration, Oral; Adolescent; Adult; Aged; China; Cholecalciferol; Depression; Depressive Disorder, Major; Dietary Supplements; Double-Blind Method; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Prospective Studies; Renal Dialysis; Treatment Outcome; Vitamin D Deficiency; Young Adult

Active Vitamin D analogues are used clinically for prevention and treatment of secondary hyperparathyroidism (SHPT) in hemodialysis (HD) patients. Nutritional vitamin D supplementation is used for additional local parathyroid (PTH) suppression, with lower incidence of hypercalcemia and hyperphosphatemia. This study evaluates the possible beneficial effects of combined vitamin D treatment (paricalcitol and cholecalciferol).. Sixty HD patients with serum parathyroid hormone (iPTH) >300 pg/mL were enrolled. All patients administered 2 mcg/day of paricalcitol and were randomly allocated into control group (placebo) or study group (cholecalciferol) for 16 weeks. Serum 25(OH)D₃, iPTH and human cathelicidin (hCAP-18) were measured at baseline and during follow-up.. iPTH levels decreased in the study group appropriately and were more significantly decreased at 16 weeks. Study group had significantly increased 25(OH)D₃ levels. In addition, the study group had significantly increased serum hCAP-18 levels compared with control group. Correlation analysis showed a significant correlation between the percentage increase in serum hCAP-18 and 25(OH)D₃ levels.. Cholecalciferol, in combination with paricalcitol, additively lowers the iPTH levels in a significant number of patients after 16 weeks of supplementation. A dose of 5000 IU/week of cholecalciferol could maintain serum 25(OH)D₃ levels above 30 ng/dL as early as 8 weeks after beginning supplementation. Doubling of serum cathelicidin levels were noted after 16 weeks of cholecalciferol supplementation in 40% of study patients.

Topics: Aged; Antimicrobial Cationic Peptides; Calcifediol; Cathelicidins; Cholecalciferol; Drug Interactions; Drug Therapy, Combination; Ergocalciferols; Female; Humans; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Hormone; Placebos; Renal Dialysis; Treatment Outcome; Vitamin D

Elevated concentrations of fibroblast growth factor 23 (FGF23) are postulated to promote 25-hydroxyvitamin D (25[OH]D) insufficiency in CKD by stimulating 24-hydroxylation of this metabolite, leading to its subsequent degradation; however, prospective human studies testing this relationship are lacking.. An open-label prospective study was conducted from October 2010 through July 2012 to compare the effect of 8 weeks of oral cholecalciferol therapy (50,000 IU twice weekly) on the production of 24,25(OH)2D3 in vitamin D-insufficient patients with CKD (n=15) and controls with normal kidney function (n=15). Vitamin D metabolites were comprehensively profiled at baseline and after treatment, along with FGF23 and other mineral metabolism parameters.. Vitamin D3 and 25(OH)D3 concentrations increased equivalently in the CKD and control groups following cholecalciferol treatment (median D3 change, 8.6 ng/ml [interquartile range, 3.9-25.6 ng/ml] for controls versus 12.6 ng/ml [6.9-41.2 ng/ml] for CKD [P=0.15]; 25(OH)D3 change, 39.2 ng/ml [30.9-47.2 ng/ml] for controls versus 39.9 ng/ml [31.5-44.1 ng/ml] for CKD [P=0.58]). Likewise, the absolute increase in 1α,25(OH)2D3 was similar between CKD participants and controls (change, 111.2 pg/ml [64.3-141.6 pg/ml] for controls versus 101.1 pg/ml [74.2-123.1 pg/ml] for CKD; P=0.38). Baseline and post-treatment 24,25(OH)2D3 concentrations were lower in the CKD group; moreover, the absolute increase in 24,25(OH)2D3 after therapy was markedly smaller in patients with CKD (change, 2.8 ng/ml [2.3-3.5 ng/ml] for controls versus 1.2 ng/ml [0.6-1.9 ng/ml] for patients with CKD; P<0.001). Furthermore, higher baseline FGF23 concentrations were associated with smaller increments in 24,25(OH)2D3 for individuals with CKD; this association was negated after adjustment for eGFR by multivariate analysis.. Patients with CKD exhibit an altered ability to increase serum 24,25(OH)2D3 after cholecalciferol therapy, suggesting decreased 24-hydroxylase activity in CKD. The observed relationship between baseline FGF23 and increments in 24,25(OH)2D3 further refutes the idea that FGF23 directly contributes to 25(OH)D insufficiency in CKD through stimulation of 24-hydroxylase activity.

Topics: 24,25-Dihydroxyvitamin D 3; Adult; Aged; Bone Density Conservation Agents; Calcifediol; Calcitriol; Case-Control Studies; Cholecalciferol; Female; Fibroblast Growth Factor-23; Fibroblast Growth Factors; Glomerular Filtration Rate; Humans; Kidney Failure, Chronic; Male; Middle Aged; Prospective Studies; Vitamin D Deficiency

The role of cholecalciferol supplementation in end-stage renal disease (ESRD) patients has been questioned. The objective of this randomized double-blinded study is to assess whether cholecalciferol therapy can increase serum 25-hydroxyvitamin D [25(OH)D] levels in haemodialysed patients and the safety implications of this therapy on certain biological parameters and vascular calcifications score.. Forty-three haemodialysis patients were randomized to receive placebo or cholecalciferol (25,000 IU) therapy every 2 weeks. The biological parameters, serum calcium, phosphorus, 25(OH)D and parathormone (PTH) levels, were monitored monthly for 12 consecutive months. Vascular calcifications were assessed by lateral X-ray radiography.. At baseline, the mean serum 25(OH)D levels were low and similar in both groups. Thirty patients (16 treated and 14 placebo) completed the study: 11 patients died (5 placebo and 6 treated), 1 patient dropped out and 1 patient was transplanted (both from the placebo group). After 1 year, the percentage of 25(OH)D deficient patients was significantly lower in the treated group. None of the patients developed hypercalcaemia. The PTH levels tended to increase over the study period under placebo and to decrease in the cholecalciferol group. The median changes in PTH levels from baseline to 1 year were statistically different between the two groups [+80 (-58 to 153) and -115 (-192 to 81) under placebo and cholecalciferol treatment, respectively, P=0.02].The calcification scores increased equivalently in both groups (+2.3 per year).. Cholecalciferol is effective and safe, and does not negatively affect calcium, phosphorus, PTH levels and vascular calcifications. Additional studies are needed to compare the impacts of nutritional and active vitamin D agents on vascular calcification and mortality.

Topics: Aged; Bone Density Conservation Agents; Calcium; Cholecalciferol; Dietary Supplements; Double-Blind Method; Female; Glomerular Filtration Rate; Humans; Kidney Failure, Chronic; Male; Parathyroid Hormone; Phosphorus; Renal Dialysis; Vascular Calcification; Vitamin D; Vitamin D Deficiency

Recent understanding of extrarenal production of calcitriol has led to the exploration of native vitamin D treatment in dialysis patients. This paper reports the pharmacokinetics of 25-hydroxyvitamin D response to 10,333 IU cholecalciferol given weekly in subjects on chronic dialysis.. This randomized, double-blind, placebo-controlled trial of 15 weeks of oral cholecalciferol in subjects with stage 5 CKD requiring maintenance hemodialysis was conducted from November of 2007 to March of 2010. The time course of serum 25-hydroxyvitamin D was measured over the course of treatment. Additionally, blood was drawn at baseline and last visit for calcium, phosphorus, calcitriol, and parathyroid hormone levels.. The median (interquartile range) baseline 25-hydroxyvitamin D level was 13.3 (11.1-16.2) ng/ml for the treatment group and 15.2 (10.7-19.9) ng/ml for the placebo group. 25-hydroxyvitamin D steady state levels rose by 23.6 (19.2-29.9) ng/ml in the treatment group, and there was no change in the placebo group. Calcitriol levels also increased significantly in the treatment group. There were no significant changes in levels of calcium, albumin, phosphorus, and parathyroid hormone in either group.. Cholecalciferol (10,333 IU) given weekly in patients on chronic hemodialysis produces a steady state in 25-hydroxyvitamin D of approximately 24 ng/ml.

Topics: Administration, Oral; Aged; Biomarkers; Calcium; Chi-Square Distribution; Cholecalciferol; Dietary Supplements; Double-Blind Method; Drug Administration Schedule; Female; Humans; Kidney Failure, Chronic; Linear Models; Male; Middle Aged; Nebraska; Parathyroid Hormone; Phosphorus; Renal Dialysis; Treatment Outcome; Vitamin D; Vitamins

Vitamin D deficiency is a common health complication in patients with chronic kidney disease and can be treated with an abundance of classical and advanced pharmaceutics. However, the impact of bundling in dialysis clinics limits the use of the most optimal therapeutics and desired efficacy targets in end-stage renal disease patients. To address this issue, we investigated the benefits of adding a cost-effective antioxidant and vitamin D nutraceutical (MV-ONE, Nephrian Inc.) to patient regiments. This nutraceutical was used in an attempt to replete vitamin D levels and decrease inflammation that dialysis patients experience. Additionally, we investigated the potential of this therapy to reduce the need for erythropoietin-stimulating agents. Results indicate MV-ONE caused: (1) increases in 25-OH vitamin D (p = 0.0058), (2) decreases in ESA dose (p = 0.0475), and (3) no change in C-reactive protein (p = 0.3290). Overall, this suggests the addition of MV-ONE does benefit the vitamin D deficiency and anemia observed in ESRD patients.

Topics: Anemia; Antioxidants; C-Reactive Protein; Cholecalciferol; Cost-Benefit Analysis; Dietary Supplements; Drug Combinations; gamma-Tocopherol; Hematinics; Humans; Kidney Failure, Chronic; Renal Dialysis; Thioctic Acid; Vitamin D; Vitamin D Deficiency; Vitamins

Approximately 50% of patients with stage 3 Chronic Kidney Disease are 25-hydroxyvitamin D insufficient, and this prevalence increases with falling glomerular filtration rate. Vitamin D is now recognised as having pleiotropic roles beyond bone and mineral homeostasis, with the vitamin D receptor and metabolising machinery identified in multiple tissues. Worryingly, recent observational data has highlighted an association between hypovitaminosis D and increased cardiovascular mortality, possibly mediated via vitamin D effects on insulin resistance and inflammation. The main hypothesis of this study is that oral Vitamin D supplementation will ameliorate insulin resistance in patients with Chronic Kidney Disease stage 3 when compared to placebo. Secondary hypotheses will test whether this is associated with decreased inflammation and bone/adipocyte-endocrine dysregulation.. This study is a single-centre, double-blinded, randomised, placebo-controlled trial. Inclusion criteria include; estimated glomerular filtration rate 30-59 ml/min/1.73 m(2); aged >or=18 on entry to study; and serum 25-hydroxyvitamin D levels <75 nmol/L. Patients will be randomised 1:1 to receive either oral cholecalciferol 2000IU/day or placebo for 6 months. The primary outcome will be an improvement in insulin sensitivity, measured by hyperinsulinaemic euglycaemic clamp. Secondary outcome measures will include serum parathyroid hormone, cytokines (Interleukin-1beta, Interleukin-6, Tumour Necrosis Factor alpha), adiponectin (total and High Molecular Weight), osteocalcin (carboxylated and under-carboxylated), peripheral blood mononuclear cell Nuclear Factor Kappa-B p65 binding activity, brachial artery reactivity, aortic pulse wave velocity and waveform analysis, and indirect calorimetry. All outcome measures will be performed at baseline and end of study.. To date, no randomised controlled trial has been performed in pre-dialysis CKD patients to study the correlation between vitamin D status with supplementation, insulin resistance and markers of adverse cardiovascular risk. We remain hopeful that cholecalciferol may be a safe intervention, with health benefits beyond those related to bone-mineral homeostasis.. Australian and New Zealand Clinical Trials Registry ACTRN12609000246280.

Topics: Administration, Oral; Adult; Aged; Aged, 80 and over; Bone Density Conservation Agents; Cholecalciferol; Double-Blind Method; Female; Humans; Inflammation; Insulin Resistance; Kidney Failure, Chronic; Male; Placebo Effect; Treatment Outcome; Vitamin D Deficiency; Young Adult

By the time patients require dialysis replacement therapy, nearly all chronic kidney diseases (CKD) patients are affected with uremic bone diseases. High-turnover osteodystrophy can be prevented; patients with CKD should be monitored for imbalances in calcidiol (25 OH vitamin D), calcium, and phosphate homeostasis. We aimed to determine the effect of a monthly oral 300,000 IU vitamin D(3) (cholecalciferol) supplementation on the uremic bone diseases (UBD) markers such as iPTH and alkaline phosphatase in CKD patients. Among a total of 70 patients under treatment in the nephrology unit, 40 predialysis CKD patients (mean age of 49 +/- 14, male/female 20/20) were included the study. The patients were randomly divided into two groups. Treatment group included 20 patients (mean age of 51 +/- 14, male/female 9/11), and the control group comprised 20 patients (mean age of 47 +/- 14, male/female 9/11). Treatment group patients were given a single dose of Devit3 ampoule (300,000 U cholecalciferol) per month orally way. Patients in the control group did not take any vitamin D for a month. The level of calcidiol was lower than normal range in two groups. After a month, treatment group patient's calcidiol increased statistically significant (6.8 +/- 3.5 to 17.8 +/- 21.4 ng/mL, p < 0.001). After a month, iPTH level decreased in the treatment group statistically significantly (368 +/- 274 to 279 +/- 179 pg/ml, p < 0.001). At the 30(th) day of the treatment, in 9/20 of the treatment group patients (45%), the iPTH value decreased at least 30% (p < 0.001). We suggest that oral depot cholecalciferol treatment causes a statistically significant decrease of serum iPTH level but does not cause a statistically significant change in Ca, P, ratio of Ca x P, or urinary calcium creatinine rate in UBD predialysis CKD. This treatment can be used safely for the predialysis CKD patients, along with the cautious control of serum calcium and phosphor.

Topics: Absorptiometry, Photon; Administration, Oral; Adult; Bone Density; Bone Density Conservation Agents; Calcifediol; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Delayed-Action Preparations; Dose-Response Relationship, Drug; Drug Administration Schedule; Female; Follow-Up Studies; Humans; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Kidney Function Tests; Male; Middle Aged; Parathyroid Hormone; Probability; Prospective Studies; Reference Values; Renal Dialysis; Risk Assessment; Severity of Illness Index; Treatment Outcome

Vitamin D has emerged as an important survival factor in patients with chronic kidney disease. Non-activated vitamin D may also have beneficial effects on bone, cardiovascular and immune functions. Cholecalciferol is the prevalent non-activated vitamin D in Europe, but there is no valid prospective data available about its use in haemodialysis patients. Thus, we initiated a prospective study to evaluate dosing, safety and tolerability of cholecalciferol supplementation in haemodialysis patients.. The prospective study included 64 haemodialysis patients. During replenishment phase patients received 20 000 IU cholecalciferol/week for 9 months. In the open maintenance phase (15 months), patients were randomized to a treated group (20 000 IU cholecalciferol/month) and an untreated group, which did not receive cholecalciferol.. Calcidiol [25(OH)D] deficiency (<37.5 nmol/l; <15 microg/l) was detected in 61/64 patients (95%). During the replenishment phase, calcidiol increased significantly from 16.65 +/- 9.6 to 79.48 +/- 27.15 nmol/l (6.66 +/- 3.84 microug/l to 31.79 +/- 10.86 microg/l) (P < 0.001). Recommended levels (>75 nmol/l; >30 microg/l; K/DOQI) were achieved in 57% of patients. Calcium increased from 2.28 +/- 0.17 to 2.37 +/- 0.19 mmol/l (9.1 +/- 0.69 mg/dl to 9.49 +/- 0.75 mg/dl) (P<0.01). Phosphorus, calcium-phosphorus product and parathyroid hormone showed no significant changes. Fifty-nine patients progressed to the maintenance phase. Analysis per protocol showed a significant drop of calcidiol in the treated [83.98 +/- 31.73 versus 78.5 +/- 38.75 nmol/l (33.59 +/- 12.69 versus 31.4 +/- 15.5 microg/l) (P < 0.001)] and untreated groups [86.35 +/- 40.75 versus 53.4 +/- 26.2 nmol/l (34.54 +/- 16.3 versus 21.36 +/- 10.48 microg/l) (P < 0.001)]. The comparison of the treated and the untreated groups showed no significant differences at the beginning of the maintenance phase: 83.98 +/- 31.73 versus 86.35 +/- 40.75 nmol/l (33.59 +/- 12.69 versus 34.54 +/- 16.3 microg/l). At the end they differed significantly: 78.5 +/- 38.75 versus 53.4 +/- 26.2 nmol/l (31.4 +/- 15.5 versus 21.36 +/- 10.48 microg/l) (P < 0.001).. Vitamin D deficiency is present in a majority of haemodialysis patients. Supplementation with cholecalciferol is safe, well tolerated and reasonable to replenish vitamin D stores in haemodialysis patients. However, only 57% of patients achieved recommended calcidiol levels, thus favouring additional dose-finding studies.

Topics: Calcifediol; Cholecalciferol; Drug Tolerance; Female; Humans; Kidney Failure, Chronic; Male; Prospective Studies; Renal Dialysis; Vitamin D Deficiency

Renal osteodystrophy is the major complication in patients with end-stage renal failure. Oral or intravenous vitamin D3 (D3) is given to these patients, but severe hypercalcaemia sometimes interrupts this therapy. This study was undertaken to determine whether the effectiveness and safety of D3 also depend on its dosing time during a repeated treatment.. A higher dose (3 micro g) was given orally to 13 haemodialysis patients at 08.00 h or 20.00 h for 12 months by a randomized, cross-over design.. Three patients were withdrawn due to severe hypercalcaemia after switching from 08.00 h to 20.00 h dosings. The elevation in serum calcium concentration was significantly (P < 0.001) greater during the 08.00 h dosing in the remaining ten patients. Mean serum Ca concentration after the trial was 10.92 (95% confidence interval (CI) 10.79, 11.06) and 9.55 mg dl-1 (95% CI 9.30, 9.71) by 08.00 h and 20.00 h dosing, respectively. On the other hand, the suppression of the elevated serum parathyroid hormone (PTH) and subsequent increment in bone density were significantly greater during the 08.00 h dosing. Mean PTH concentration after the trial was 414 (95% CI 360, 475) and 220 pg ml-1 (95% CI 202, 249) by 08.00 h and 20.00 h dosing, respectively (P = 0.02). Mean increment of bone density after the trial was 22 (95% CI 8, 32) and 57 g cm-3 (95% CI 43, 83) by 08.00 h and 20.00 h dosing, respectively (P = 0.04).. These results indicate that a higher dose of oral D3 is more effective and safe after dosing at evening in patients with renal osteodystrophy.

Topics: Administration, Oral; Adult; Aged; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Chronotherapy; Cross-Over Studies; Double-Blind Method; Female; Humans; Hypercalcemia; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis

The blood pressure, the most influencing factor in cardiovascular disease in end-stage renal failure patients, follows a seasonal variation during the year. Since vitamin D(3) is known to be related to sun exposure, we wanted to evaluate the putative participation of the vitamin D(3) metabolism in blood pressure modifications.. We studied 22 stable hemodialysis patients (11 females and 11 males, mean age +/- SD 56 +/- 1 year) who had been continuously treated in our dialysis unit for more than 1 year between 1994 and 1997 and did not receive pulse vitamin D(3) treatment. Supine systolic and diastolic blood pressures were measured before every dialysis session (>12,000 measurements) and the intact parathormone (iPTH), 25-hydroxyvitamin D(3) [25(OH)D(3)], and 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] levels every 3 months (>300 determinations). The mean values of blood pressure per season and per patient were taken for analysis using a 4-year longitudinal study design.. The blood pressure varied during the years studied following a seasonal trend. It was highest during autumn and tended to decrease during spring and warmer months. Systolic as well as diastolic blood pressures were significantly correlated with the 25(OH)D(3) levels (p = 0.0291 and p = 0.0327, respectively). No correlation was observed between blood pressure and 1,25(OH)(2)D(3) or iPTH levels.. There is a link between blood pressure and 25(OH)D(3) level. This interrelation is not secondary to a iPTH modulation. Although it cannot be excluded that vitamin D(3) and blood pressure vary following a third factor with seasonal variations, since vitamin D(3) varies during the year, mainly following sun exposure, we suggest that vitamin D(3) is one of the factors participating in the seasonal variation of the blood pressure. Other factors known to control the blood pressure and particularly the extracellular volume overload may also participate.

Topics: Blood Pressure; Calcifediol; Calcitriol; Cholecalciferol; Female; Humans; Kidney Failure, Chronic; Longitudinal Studies; Male; Middle Aged; Parathyroid Hormone; Renal Dialysis; Seasons

Topics: Adult; Aged; Aged, 80 and over; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis

Secondary hyperparathyroidism is one of the severe complications of chronic renal failure. In this study, we investigated the cellular components of parathyroid tissue, with measurements of various serum parathyroid hormone (PTH) types in the circulation, and evaluated their clinical significance in hemodialysis patients. Thirty-eight patients who underwent both subtotal parathyroidectomy and autotransplantation in Tokai University Hospital from 1979 to 1994 were divided into two groups. Group 1 (G-1) was not administered active-type vitamin D3 (VD; 19 patients; 15 males and 4 females), and group 2 (G-2) was administered VD (19 patients; 10 males and 9 females). The parathyroid tissues which were obtained from G-1 and G-2 patients were classified into three classes based on the size of the oxyphilic cell area (class I < 25%, class II 25-50% and class III > 50%). Our results showed that the proliferation index of parathyroid tissues in the oxyphilic cell area was higher in G-2 than that in G-1. Immunohistochemically, MIB-1 staining was more intense than that in the chief cell area in G-2 patients. Moreover, the proliferative index in the same specimen was also higher in the oxyphilic cell area than in the chief cell area. It was suggested that the oxyphilic cells proliferated independently. Furthermore, synthesis of PTH in the oxyphilic cell area was revealed immunohistochemically by the presence of PTH and was confirmed by positive staining of PTH mRNA in the oxyphilic cell area with in situ hybridization. HS(M-terminal)- and C-PTH levels in the serum were significantly higher in class III than in class I (p < 0.01). No significant difference of HS- and C-PTH levels between class II and class III was noted. Moreover, no significant difference of intact-PTH levels was found in all three classes. From the above findings, it was suggested that proliferation of the parathyroid tissues or secretory state of PTH in hemodialysis-maintained patients with secondary hyperparathyroidism, which was closely related to the proliferation of oxyphilic cells, can be more accurately reflected by HS- and C-PTH levels than by the intact-PTH level. Therefore, it was suggested that HS- and C-PTH levels in the serum are important indices for accurate evaluation of the pathology and suitable therapy of secondary hyperparathyroidism, as well as observation of the clinical course.

Topics: Adult; Antibodies, Monoclonal; Cell Division; Cell Nucleus; Cholecalciferol; Female; Humans; Hyperparathyroidism, Secondary; Immunohistochemistry; In Situ Hybridization; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Hormone; Parathyroidectomy; RNA, Messenger

Seventeen undialysed adult patients with chronic renal failure took part in a controlled study of the effects of 1,25(OH)2D3 and D3. After a 6-month observation period the patients were allocated at random to 2 groups for 6 months of treatment with either 1,25(OH)2D3 (mean dose 0.5 micrograms daily) or D3 (dose 100 micrograms daily). Treatment was then discontinued and the patients were studied for a further 3 months. The patients as a group initially had a moderate renal osteodystrophy. During treatment serum iPTH decreased in both groups but most markedly in the 1,25(OH)2D3 group in which the iPTH values became normal. Serum creatinine increased during treatment in both groups, in the group receiving 1,25(OH)2D3 this was coupled with an increase in serum calcium to within the normal range. Our data demonstrate that 1,25(OH)2D3 treatment in patients with chronic renal failure leads to a further reduction in renal function, which may be partially reversible. Physicians should therefore be reluctant to give vitamin D analogues to patients with chronic renal failure unless they have severe symptomatic renal osteodystrophy.

Topics: Adult; Aged; Alkaline Phosphatase; Bone and Bones; Calcitriol; Cholecalciferol; Clinical Trials as Topic; Female; Humans; Hydroxycholecalciferols; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Hormone; Phosphates; Reference Values; Vitamin D

Seventeen undialysed adult patients with chronic renal failure took part in a controlled study of the effects of 1,25(OH)2D3 and D3. After a 6-month observation period the patients were allocated at random to two groups for 6 months of treatment with either 1,25(OH)2D3 (mean dose 0.5 microgram daily) or D3 (dose 100 microgram daily). Treatment was then discontinued and the patients were studied for a further 6 months. Serum iPTH was decreased in both groups but most markedly in the 1,25(OH)2D3 group in which the iPTH values became normal. Serum creatinine increased during treatment in both groups. In the group receiving 1,25(OH)2D3 this was coupled to an increase in serum calcium within the normal range. Our data demonstrate that 1,25(OH)2D3 treatment in patients with chronic renal failure leads to a further reduction in renal function, which may be partially reversible. Physicians should therefore be reluctant to give vitamin D analogues to patients with chronic renal failure unless they have severe symptomatic renal osteodystrophy.

Topics: Adult; Aged; Calcitriol; Cholecalciferol; Clinical Trials as Topic; Female; Humans; Kidney Failure, Chronic; Kidney Function Tests; Male; Middle Aged

Seventeen undialysed adult patients with chronic renal failure took part in a controlled study of the effects of 1,25(OH)2D3 and D3. After a 6-month observation period the patients were allocated at random to two groups for 6 months of treatment with either 1,25(OH)2D3 (mean dose 0.5 microgram daily) or D3 (dose 100 microgram daily). The treatment was then discontinued and the patients were studied for a further 3 months. In the 1,25(OH)2D3 group the mean serum concentration of 1,25(OH)2D rose significantly during treatment, whereas serum concentratins of 25OHD and 24,25(OH)2D remained unchanged. In the D3 group there was a highly significant increase in serum concentrations of 25OHD and 24,25(OH)2D, whereas serum 1,25(OH)2D remained unchanged. There was a significant fall in serum iPTH in both treatment groups. This fall was unrelated to serum calcium in the D3 group unlike the findings in the 1,25(OH)2D3 group. The data support previous experimental evidence that serum iPTH can be suppressed by 24,25(OH)2D3 and suggest that this analogue may be of clinical importance in the treatment of chronic renal failure without inducing hypercalcaemia.

Topics: 24,25-Dihydroxyvitamin D 3; Adolescent; Adult; Calcifediol; Calcitriol; Calcium; Cholecalciferol; Clinical Trials as Topic; Dihydroxycholecalciferols; Female; Humans; Hydroxycholecalciferols; Kidney Failure, Chronic; Male; Parathyroid Hormone

A controlled study of the effects of 1,25-dihydroxycholecalciferol (1,25[OH]2D3) and vitamin D3 (D3) was performed in 18 non-dialyzed patients with chronic renal failure (CRF) (creatinine clearance below 35 ml/min) and mild renal osteodystrophy. After 6 months observation of the spontaneous course, the patients were randomly allocated to 6 months oral treatment with either 1,25(OH)2D3 or D3 in initial daily doses of 1 and 100 microgram, respectively, combined with 0.5 g calcium (Calcium Sandoz). 1,25(OH)2D3 had a fast normalizing effect on the biochemical changes of calcium metabolism. D3 had similar, but less pronounced effects. The percent fall in creatinine clearance was greater during than before treatment in all patients on 1,25(OH)2D3 (p less than 0.01) and in 7 of 9 patients on D3 treatment (n.s.). Deterioration of renal function is a major limitation to clinical use of 1,25(OH)2D3 (and D3) in non-dialyzed patients with CRF. In fact, the decreased formation of 1,25(OH)2D3 seen in CRF might protect renal function through the abnormalities in mineral metabolism.

Topics: Alkaline Phosphatase; Bone and Bones; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Clinical Trials as Topic; Creatinine; Dihydroxycholecalciferols; Humans; Hydroxycholecalciferols; Kidney; Kidney Failure, Chronic; Parathyroid Hormone; Phosphates

A controlled study of the effects of the potent vitamin-D metabolite, 1, 25-dihydroxycholecalciferol (1,25[OH]2D3), and vitamin D3 was done in 18 non-dialysed patients with chronic renal failure (C.R.F.). Patients with a creatinine clearance below 35 ml/min and mild renal osteodystrophy were selected. After 6 months' observation of the spontaneous course the patients were randomly allocated to 6 months' oral treatment with either 1, 25 (OH)2D3 or vitamin D3 in initial daily doses of 1microgram and 4000 I.U., respectively, combined with 0.5 g calcium. 1,25(OH)2D3 quickly corrected hypocalcaemia, reduced serum-alkaline-phosphatases and serum-immunoreactive-parathyroid-hormone, and more than doubled the urinary excretion rate of calcium. D3 had similar, but less pronounced effects. 7 out of 8 patients on 1,25(OH)2D3, developed hypercalcaemia which necessitated a reduction in dosage. None of the patients on D3 treatment developed hypercalcaemia. The percentage fall in creatinine clearance was greater during treatment than before treatment in all patients on 1, 25 (OH)2D3 (P less than 0.01) and in 7 of 9 patients on vitamin D3 treatment (though the group change here was not significant). Deterioration of renal function is a major limitation of the clinical use of 1, 25(OH)2D3 and D3 in non-dialysed patients with C.R.F. In fact, the decrased formation of 1, 25(OH)2D3 seen in C.R.F. might protect renal function at the expense of abnormalities in mineral metabolism.

Topics: Administration, Oral; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydroxycholecalciferols; Drug Evaluation; Follow-Up Studies; Humans; Hydroxycholecalciferols; Hypercalcemia; Kidney; Kidney Failure, Chronic; Kidney Function Tests

1,25 dihydroxycholecalciferol [1,25(OH)2D3] was studied in a double-blind controlled fashion in patients on chronic dialysis. Serum calcium was unchanged in 16 patients on vitamin D3 (D3) (400 to 1200 IU/day). In 15 patients on 1,25(OH)2D3 (0.5 to 1.5 microgram/day), serum calcium increased from 9.05 +/- .15 to 10.25 +/- .20 mg/dl (p less than 0.001), returning to 9.37 +/- .16 mg/dl (p less than 0.001) in the post control period. Patients on D3 showed no reversible decrease in immunoreactive parathyroid hormone levels, but patients on 1,25(OH)2D3 did, from a control of 1077 +/- 258 to 595 +/- 213 microliter equivalents/ml (p less than 0.01), and returned to 1165 +/- 271 microliter equivalents/ml (p less than 0.005). Nine of 12 patients on D3 who underwent serial iliac-crest biopsies showed histologic deterioration, and six of seven who received 1,25(OH)2D3 were improved or unchanged (p less than 0.025). Bone mineral and calcium decreased in patients on D3 (p less than 0.05) but not in those on 1,25(OH)2D3. Hypercalcemia occurred in five of 15 patients. We conclude that 1,25(OH)2D3 has a calcemic effect in chronic dialysis patients, decreases levels of immunoreactive parathyroid hormone, and is associated with histologic improvement in bone disease. Thus, 1,25(OH)2D3 is a valuable adjunct to the management of renal osteodystrophy but requires monitoring of serum calcium to avoid hypercalcemia.

Topics: Adult; Alkaline Phosphatase; Antigens; Bone and Bones; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Clinical Trials as Topic; Dihydroxycholecalciferols; Double-Blind Method; Female; Humans; Hydroxycholecalciferols; Hypercalcemia; Kidney Failure, Chronic; Male; Middle Aged; Minerals; Parathyroid Hormone; Phosphorus; Renal Dialysis

Among the chronic diseases, chronic kidney failure is one of diseases that have the most difficulty in coping with oxidative stress due to the deterioration of the antioxidant system balance in the body. Beyond being a vitamin, 1. In this study, we evaluated the medical treatments of 69 PD patients who were followed up routinely. The patients were divided into 2 groups according to whether they used vitamin D3 or not. 49 of our patients were using vitamin D3. While requesting routine laboratory tests, we reserved a separate serum sample to measure serum TRX levels by double-antibody sandwich enzyme-linked immunosorbent assay for all patients.. Only one parameter has a significant statistical relationship with serum TRX level and the treatment protocol. The serum TRX level was significantly higher (211,62 U/l ± 314,46) in the group receiving vitamin D3 compared to the group which is not using Vitamin D3 (101,63 U/l ± 215,03) (. This study highlights the importance of appropriate dose of vitamin D3 replacement especially in PD patients who are under intense oxidative stress compared to healthy individuals.

Topics: Antioxidants; Cholecalciferol; Female; Humans; Kidney Failure, Chronic; Male; Oxidative Stress; Peritoneal Dialysis; Thioredoxins

Topics: Adult; Calciphylaxis; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Corneal Diseases; Female; Humans; Kidney Failure, Chronic; Male; Radiography

End-stage renal disease is strongly associated with progressive cardiovascular calcification (CVC) and there is currently no therapy targeted to treat CVC. SNF472 is an experimental formulation under development for treatment of soft tissue calcification. We have investigated the pharmacokinetics of SNF472 administration in rats and its inhibitory effects on CVC. SNF472 was studied in three rat models: (1) prevention of vitamin D3-induced CVC with an intravenous SNF472 bolus of 1 mg/kg SNF472, (2) inhibition of progression of vitamin D3-induced CVC with a subcutaneous SNF472 bolus of 10 or 60 mg/kg SNF472, starting after calcification induction, (3) CVC in adenine-induced uremic rats treated with 50 mg/kg SNF472 via i.v. 4h -infusion. Uremic rats presented lower plasma levels of SNF472 than control animals after i.v. infusion. CVC in non-uremic rats was inhibited by 60-70% after treatment with SNF472 and progression of cardiac calcification completely blocked. Development of CVC in uremic rats was inhibited by up to 80% following i.v. infusion of SNF472. SNF472 inhibits the development and progression of CVC in uremic and non-uremic rats in the same range of SNF472 plasma levels but using in each case the required dose to obtain those levels. These results collectively support the development of SNF472 as a novel therapeutic option for treatment of CVC in humans.

Topics: Animals; Calcinosis; Cardiovascular Diseases; Cholecalciferol; Disease Models, Animal; Disease Progression; Humans; Inositol; Kidney Failure, Chronic; Rats; Renal Insufficiency, Chronic; Uremia

In chronic kidney disease (CKD) a deficiency of 1,25-dihydroxyvitamin D is common. The aim of this review was to compare vitamin D status after oral supplementation of vitamin D3 to that of serial suberythemal irradiation in end-stage kidney disease (ESKD) patients.. Ninety-five patients, with a mean age of 62 (range=35-82) years, were treated with a mean dose of 35,000 (20,000-60,000) IU vitamin D3 per week for a period of 18 months. Fourteen patients, with a mean age of 51 (range=41-57) years, were whole-body UVB irradiated for over 6 months. From 3 hemodialysis patients skin biopsies were performed.. With oral supplementation 25(OH)D3 increased by 60%. With UV irradiation 25(OH)D3 increased by 400%. Gene expression analysis demonstrated an improvement in the vitamin D receptor (VDR) by 0.65 fold, in 1-alpha-hydroxylase (CYP27B1) by 1.0 fold, and in 25-hydroxylase (CYP2R) by 1.2 fold.. Serial suberythemal UVB irradiation of patients with CKD on dialysis is capable to improve serum 25(OH)D3 and 1,25(OH)2D3 by enhancing the skin's ability to activate vitamin D.

Topics: Adult; Aged; Aged, 80 and over; Calcifediol; Calcitriol; Cholecalciferol; Dietary Supplements; Humans; Kidney Failure, Chronic; Male; Middle Aged; Receptors, Calcitriol; Renal Dialysis; Renal Insufficiency, Chronic; Ultraviolet Rays; Vitamin D; Vitamin D Deficiency; Vitamin D3 24-Hydroxylase

Vitamin D3 can be metabolized in the skin to 25(OH)D and 1,25(OH)2D because the skin expresses vitamin D-25-hydroxylase, 25(OH)D-1-alpha-hydroxylase, and the vitamin D receptor. The aim of this review was to discuss the pleiotropic effects after serial suberythemal UVB irradiation with a sun-simulating UV spectrum in end-stage kidney disease patients.. Fourteen hemodialysis patients, with a mean age of 51 (range 41-57) years, were whole-body UV irradiated over 6 months.. Patients demonstrated an increase in their hematocrit and required less erythropoietin. An increase in maximal oxygen uptake and workload capacity was associated with decreased lactic acid production. The patients demonstrated a decreased heart rate and systolic and diastolic blood pressure with an increase in the R-R-interval and the beat-to-beat-differences.. Cardiovascular disease is the most important comorbidity. Exposure to simulated sunlight that contains both UVB and UVA reduce cardiovascular risk factors and improve quality of life.

Topics: Adult; Blood Pressure; Calcifediol; Cardiovascular Diseases; Cholecalciferol; Comorbidity; Heart Rate; Humans; Kidney Failure, Chronic; Middle Aged; Quality of Life; Renal Dialysis; Renal Insufficiency, Chronic; Risk Factors; Sunlight; Ultraviolet Rays; Vitamin D

Vitamin D reduces albuminuria in patients with chronic kidney disease (CKD) but its effects on glomerular podocytes are not entirely understood.. To evaluate if cholecalciferol supplementation reduces the levels of podocyte-associated urine mRNAs in patients with CKD.. A total of 27 patients with stages 2 to 4 CKD and suboptimal serum vitamin D [25(OH)D] levels were treated with cholecalciferol for 6 months. Serum 25(OH)D level, estimated glomerular filtration rate (eGFR), proteinuria, and urine mRNA of nephrin, podocin, podocalyxin, transient receptor potential cation channel 6, vascular endothelial growth factor A, and transforming growth factor beta were assessed before and after intervention.. eGFR declined at an average rate of -4.71 mL/min/1.73 m2 (p = 0.010 vs. baseline), being 28 ± 16 mL/min/1.73 m2 at six months. No changes in proteinuria or mineral and bone metabolism parameters were observed after cholecalciferol supplementation. Urinary podocyte-associated mRNAs did not change significantly after treatment. However, patients who achieved 25(OH)D level > 20 ng/mL at six months showed a trend of reduction of urinary nephrin and podocin mRNA levels; in patients with 25(OH)D that remained < 20 ng/mL there was a significant increase in urinary podocalyxin, and a trend of higher expression of urinary nephrin and podocin mRNA.. Six months of cholecalciferol supplementation had no effect on urine podocyte-associated mRNA profile of patients with advanced CKD. The protective effect of vitamin D or its analogues on the glomerular podocyte should be investigated in early stages of CKD with a longer treatment period.

Topics: Cholecalciferol; Dietary Supplements; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Podocytes; Prospective Studies; RNA, Messenger; Vitamins

Declining kidney function leads to progressively dysregulated mineral homeostasis and contributes to vascular calcification and a pro-inflammatory milieu, both of which play a critical role in loss of dialysis vascular access patency. We designed this study to examine the relationship between markers of bone and mineral metabolism, vitamin D replacement medications, and vascular access outcomes. We hypothesized that higher levels of calcium, phosphorous, parathyroid hormone (PTH), and albumin are independently associated with vascular access patency and that vitamin D supplementation is associated with lower risk of access failure.. We abstracted data on 204 consecutive patients referred for angiographic evaluation of their permanent arteriovenous access over a 25-month period. We followed patients from the time of access salvage until subsequent referral for access failure.. The incidence of vascular access failure did not differ by serum phosphorus, PTH, calcium, calcium-phosphorus product or albumin level. Patients receiving any vitamin D replacement therapy, however, had a lower incidence of access failure compared to those receiving no therapy. Those receiving vitamin D3 therapy with or without paricalcitol (Zemplar, Abbot Laboratories, Abbot Park, IL) or calcitriol had an adjusted HR = 0.18 compared to those receiving no vitamin D therapy.. This study suggests a relationship between vitamin D3 usage and better vascular access patency, independent of the effect of vitamin D on PTH. Though this relationship needs more rigorous investigation prior to clinical application, the known differences in the pro- and anti-inflammatory effects of various vitamin D metabolites provide a potential mechanism for these clinical observations.

Topics: Adult; Aged; Angiography; Arteriovenous Shunt, Surgical; Biomarkers; Blood Vessel Prosthesis; Blood Vessel Prosthesis Implantation; Calcium; Cholecalciferol; Female; Graft Occlusion, Vascular; Humans; Incidence; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Hormone; Phosphorus; Protective Factors; Renal Dialysis; Retrospective Studies; Risk Factors; Serum Albumin, Human; Time Factors; Treatment Outcome; Vascular Patency; Vitamin D; Vitamin D Deficiency; Wisconsin

Traditionally, secondary hyperparathyroidism (SHPT) due to low calcitriol synthesis in failing kidneys has been treated with synthetic vitamin D receptor (VDR) activators. Recently, also the importance of low native vitamin D status beyond the issue of SHPT has been recognized in these patients. The aim of this work was to evaluate the effect of cholecalciferol supplementation in haemodialysis patients with low vitamin D serum levels. Another aim was to evaluate dual vitamin D therapy (cholecalciferol supplementation plus paricalcitol) in haemodialysis patients with vitamin D deficiency and concomitant SHPT.. Ninety clinically stable maintenance haemodialysis patients were included. Supervised cholecalciferol supplementation was administered due to low vitamin D status. Patients with SHPT were also treated with synthetic VDR activator. Two pre hoc subgroups for statistical analysis were formed: patients treated solely with cholecalciferol (N=34; 5,000 IU once weekly) and patients treated with a combination of cholecalciferol (identical dose, i.e. 5,000 IU/week) plus paricalcitol (N=34, median dose 10 μg/week). Follow-up visit was scheduled 15 weeks later. Serum concentrations of calcidiol (25-D), parathyroid hormone (PTH) and beta-cross laps (CTX) were assessed at baseline and at follow-up. Serum calcium, phosphate and alkaline phosphatase (ALP) were monitored monthly. Only non-calcium gastrointestinal phosphate binders were administered. Dialysate calcium was 1.5 mmol/L in all patients, and no oral calcium-containing preparations were prescribed. Depending on data distribution, parametric or nonparametric statistical methods were used for comparison within each group (i.e. baseline vs. follow-up data) as well as between groups.. In the whole group of 90 patients, mean baseline 25-D serum level was 20.3 (standard deviation 8.7) nmol/L, and it increased to 66.8 (19) nmol/L (p<0.0001) after supplementation. In both preformed subgroups, the effect of vitamin D supplementation was almost identical. In cholecalciferol monotherapy, 25-D levels increased from 18.4 (8.2) to 68.6 (21.2) and in dual vitamin D therapy from 18.4 (5.0) to 67.6 (17.7) nmol/L (both p<0.0001). In addition, both treatment modalities decreased serum PTH levels importantly: from 21.7 (interquartile range 17.3; 35.4) to 18.1 pmol/L (15.3; 24.7) in monotherapy (p=0.05) and from 38.6 (31.8; 53.3) to 33.9 pmol/L (26.1; 47.5) in dual vitamin D therapy (p=0.01). Serum calcium, phosphate, ALP and CTX did not change. We have not observed any episode of hypercalcemia in any subject during the whole period of follow-up. At baseline, slightly lower 25-D levels were observed in diabetic than in non-diabetic patients. This difference disappeared after substitution. Vitamin D status and its changes were not related to the patient's age.. Low 25-D levels were very common in haemodialysis patients. They were safely and effectively corrected with supervised low-dose cholecalciferol supplementation. In patients with higher baseline PTH levels, dual vitamin D therapy (cholecalciferol plus paricalcitol) was safely and effectively used.

Topics: Aged; Alkaline Phosphatase; Bone Density Conservation Agents; Calcifediol; Calcium; Cholecalciferol; Dietary Supplements; Drug Therapy, Combination; Ergocalciferols; Female; Humans; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Hormone; Phosphates; Receptors, Calcitriol; Renal Dialysis; Vitamin D Deficiency; Vitamins

Is cholecalciferol (D3) superior to ergocalciferol (D2) in treating nutritional vitamin D deficiency in chronic kidney disease (CKD)? The answer to this question has not been fully explored.. A retrospective analysis of 57 patients with non-dialysis-requiring CKD was conducted to assess the relative effectiveness of D2 versus D3 replacement on circulating 25(OH)D levels. Levels of 25(OH) D were assessed at baseline, after attempted repletion with D2, and then after attempted repletion with D3. The relative paired differences of the drug treatment effects were tested using t-tests. Multiple regression modeling was used to determine the factors significantly associated with differential responsiveness to the drugs.. The mean (SEM) age was 66.4 ± 1.4 and mean eGFR was 40.5 ± 2.2 ml/min/1.73 m(2). The baseline 25(OH)D level was 15.3 ± 0.8 ng/ml. After standardizing to 100,000 units of drug, increases after cholecalciferol (2.7 ± 0.3 ng/ml) were more than twice as great as those from ergocalciferol (1.1 ± 0.3 ng/ml) (p < 0.0001). A sensitivity analysis, which pooled the results of an additional 109 individuals treated with ergocalciferol alone, revealed similar findings (standardized change 2.7 ± 0.3 vs. 1.6 ± 0.3 ng/ml, p = 0.0025). Factors associated with a superior response to cholecalciferol were lower baseline 25(OH) D level at the start of therapy (p = 0.015) and the interaction of sex and age (p = 0.0048), with younger females tending to benefit relatively more from cholecalciferol than older males did.. Cholecalciferol may be superior to ergocalciferol in treating nutritional vitamin D deficiency in non-dialysis CKD.

Topics: Aged; Cholecalciferol; Ergocalciferols; Female; Glomerular Filtration Rate; Humans; Kidney Failure, Chronic; Male; Vitamin D Deficiency

This study examined rates and determinants of vitamin D supplementation among Chronic Renal Insufficiency Cohort (CRIC) participants and determined the association between dose and 25-hydroxyvitamin D (25(OH)D) level. The 2010 Institute of Medicine Report noted a significant increase in vitamin D supplementation in the general population, but use in chronic kidney disease (CKD) is unknown.. CRIC is a multicenter prospective observational cohort study of 3,939 participants with a median baseline age of 60 and an estimated glomerular filtration rate (eGFR) of 42.1 mL/minute per 1.73 m2. Of the cohort, 54.9% was male, 42.1% were Black, and 48.4% were diabetic. Multivariable logistic generalized estimating equations were used to examine determinants of supplementation use assessed annually between 2003 and 2011. Cross-sectional linear regression models, based on a subset of 1,155 participants, assessed associations between supplement dose and 25(OH)D level, measured by high-performance liquid chromatography coupled with tandem mass spectrometry.. The proportion of participants reporting supplement use increased (P < .0001), from 10% at baseline to 44% at 7-year follow-up visits. This was largely due to initiation of products containing only ergocalciferol or cholecalciferol. The odds of supplementation were greater in older, female, non-Black, married participants with greater education and lower body mass index. Among participants taking supplementation, dose was positively associated with 25(OH)D level, adjusted for race, season, diabetes, dietary intake, eGFR, and proteinuria. Only 3.8% of non-Black and 16.5% of Black participants taking a supplement were deficient (<20 ng/mL), whereas 22.7% of non-Black and 62.4% of black participants not reporting supplement use were deficient.. Vitamin D supplementation rates rose significantly among CRIC participants over 7 years of follow-up and were associated with greater serum 25(OH)D levels. Studies of vitamin D levels on clinical outcomes in CKD and future vitamin D interventional studies should consider these changes in supplementation practices.

Topics: Age Factors; Aged; Cholecalciferol; Cohort Studies; Cross-Sectional Studies; Dietary Supplements; Ergocalciferols; Female; Glomerular Filtration Rate; Humans; Kidney Failure, Chronic; Linear Models; Male; Middle Aged; Parathyroid Hormone; Prospective Studies; Renal Insufficiency, Chronic; Sex Factors; Vitamin D

We reported previously that serum parathyroid hormone [PTH(1-84)]/intact PTH[PTH(1-84) + PTH(7-84)] ratio provides the better marker for parathyroid function and bone turnover state than serum PTH level itself. The present study demonstrated that higher PTH(1-84)/intact PTH ratio, but not serum PTH(1-84) and intact PTH, predicted higher all-cause mortality in 177 male hemodialysis patients.. We reported that PTH(1-84)/intact PTH ratio provides a clinically relevant marker for parathyroid function and the resultant bone turnover state. The purpose of our study was to investigate the association of PTH(1-84)/intact PTH ratio with all-cause mortality (ACM) in male hemodialysis patients.. The study was performed for 70 months. Serum PTH in 177 male hemodialysis patients was measured with PTH(1-84)-specific whole PTH assay and intact PTH assay which cross-reacts with N-truncated PTH including PTH(7-84).. The patients (n = 177) were divided into higher and lower halves based on serum levels of PTH(1-84)/intact PTH ratio (cutoff value, 0.484), intact PTH (143.8 pg/mL), and PTH(1-84) (64.1 pg/mL). In Kaplan-Meier analysis, the higher group in whole PTH/intact PTH ratio had significantly higher ACM than the lower group (P = 0.020 by log-rank test), in contrast with the insignificant difference between the higher and lower groups in intact PTH and PTH(1-84). Multivariate Cox regression hazard analysis identified higher log [PTH(1-84)/intact PTH ratio], but not log intact PTH or log PTH(1-84) as a significant independent predictor [hazard ratio 14.428 (95% CI 2.486-83.728)] for ACM after adjustment for various factors including age, hemodialysis duration, presence/absence of diabetes mellitus, BMI, log C-reactive protein, serum albumin, calcium, and phosphate. The association existed between log [PTH(1-84)/intact PTH ratio] and ACM in those without vitamin D administration (n = 95).. Higher PTH(1-84)/intact PTH ratio, which provides a relevant marker for parathyroid function, may be a significant predictor of ACM in male hemodialysis patients.

Topics: Aged; Biomarkers; Cholecalciferol; Humans; Japan; Kaplan-Meier Estimate; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Hormone; Peptide Fragments; Prognosis; Proportional Hazards Models; Prospective Studies; Renal Dialysis

Associations between 25 hydroxy vitamin D [25(OH)D], adipokines levels, and insulin resistance have been reported. The aim of this study was to explore the effects of cholecalciferol supplementation on vitamin D levels, insulin resistance, leptin, and adiponectin levels in vitamin D-deficient peritoneal dialysis (PD) patients.. In nineteen vitamin D-deficient PD patients, who were treated with cholecalciferol, fasting serum glucose, insulin, adiponectin, leptin, 25(OH)D and parathyroid hormone (PTH) were measured before and after cholecalciferol replacement therapy. Eighteen (94.7 %) PD patients with vitamin D deficiency were receiving active vitamin D compounds (alphacalciferol) for PTH control. Alphacalciferol dosing was kept constant during treatment with cholecalciferol.. While mean 25(OH)D significantly increased from (10.2 ± 4.9 ng/ml) to (82.9 ± 56.5 ng/ml) (p < 0.05), mean homeostatic model assessment-insulin resistance index significantly decreased from (4.6 ± 3.6) to (2.8 ± 2.0) after cholecalciferol replacement therapy (p < 0.05). Serum leptin levels (12.9 ± 17.6 ng/ml) significantly increased (18.1 ± 19.5 ng/ml) (p < 0.05), while there was no change in serum adiponectin, calcium, and phosphate after vitamin D replacement. Serum PTH levels significantly decreased from 551.9 ± 276.6 pg/ml to 434.0 ± 273.4 ng/ml.. Cholecalciferol replacement therapy significantly decreases PTH levels and insulin resistance. The results of this study need to be confirmed in larger clinical trials.

Topics: Adipokines; Cholecalciferol; Female; Follow-Up Studies; Humans; Insulin Resistance; Kidney Failure, Chronic; Leptin; Male; Middle Aged; Peritoneal Dialysis; Pilot Projects; Prospective Studies; Vitamin D; Vitamin D Deficiency; Vitamins

Hypovitaminosis D is highly prevalent among patients with chronic kidney disease (CKD) and has been associated with poor outcome. We aimed to test the effect of a protocol of cholecalciferol supplementation on the restoration of vitamin D status and on parathyroid hormone (PTH) levels in patients with CKD.. This was a prospective interventional study of 6 months. Forty-five CKD patients (stages 3 and 4) with 25-hydroxyvitamin D deficiency [25(OH)D <15 ng/ml] were included. Patients received a weekly dose of 50,000 IU of cholecalciferol during 3 months, and 50,000 IU/month thereafter for those who had achieved 25(OH)D ≥30 ng/ml.. At 3 months, 78% of the patients restored their vitamin D status. At 6 months, only 43% of those patients maintained adequate vitamin D status. PTH decreased at 3 months (p = 0.02) but returned to baseline levels after 6 months. Fibroblast growth factor 23 increased at 3 months (p = 0.001) and returned to initial levels at 6 months. No changes were found in serum 1,25(OH)(2)D, ionized calcium and phosphorus.. A weekly dose of 50,000 IU of cholecalciferol for 3 months restored the vitamin D status of most patients and led to a reduction in PTH. The monthly dose of 50,000 IU appears not to be sufficient to maintain the levels of 25(OH)D.

Topics: Adult; Aged; Body Composition; Brazil; Calcium; Cholecalciferol; Dietary Supplements; Female; Follow-Up Studies; Humans; Kidney Failure, Chronic; Logistic Models; Male; Middle Aged; Nutritional Status; Parathyroid Hormone; Phosphorus; Prospective Studies; Vitamin D; Vitamin D Deficiency

VitD deficiency and bone disease are common after Tx. Prevalence and risk factors for low VitD and BMD and response to VitD therapy were investigated in pediatric renal Tx recipients. 25-hydroxy VitD levels of 71 Tx were compared to 54 healthy AA children. DXA of 44 Tx were compared to 47 AA controls. Of Tx, 59% were AA. Majority (59.1%) of Tx were VitD deficient (23.9%) or insufficient (35.2%). Prevalence of low VitD levels was double in AA (73.9%) vs. non-AA Tx (37.7%), (p = 0.003). Low VitD among Tx was associated with AA ethnicity (p < 0.01), winter (p < 0.05), older age (p < 0.05), males (p < 0.05) and time <6 months post Tx (p < 0.05). Tx with low VitD were treated with oral ergocalciferol or cholecalciferol (23 each); 13% treated with ergocalciferol vs. 82.6% treated with cholecalciferol achieved repletion (p < 0.0001). Of 36 Tx with whole body DXA, 19.5% had BMD (z < -1) after height adjustment. AA Tx had 3.4-fold higher risk of low BMD vs. controls (p < 0.05). Low VitD and BMD are prevalent in children after renal Tx. Better repletion of VitD is achieved with cholecalciferol.

Topics: Absorptiometry, Photon; Administration, Oral; Adolescent; Black or African American; Bone Density; Bone Density Conservation Agents; Child; Child, Preschool; Cholecalciferol; Ergocalciferols; Female; Humans; Infant; Kidney Failure, Chronic; Kidney Transplantation; Male; Risk Factors; Vitamin D; Vitamin D Deficiency; Young Adult

CaCO3 alone and CaCO3 plus vitamin D3 metabolites are commonly prescribed in CKD patients. The objective of this study is to analyze the changes in Ca x P product, calcium level and phosphorus level in CKD patients receiving calcium carbonate alone and calcium carbonate with vitamin D3 in combination.. A prospective, cross sectional study among CKD patients under maintenance hemodialysis two times a week were studied over a period of one year. The patients were divided into two groups receiving oral CaCO3 alone and CaCO3 plus vitamin D3 once a day. The patients were followed for 1 month and result of Ca x P product was analyzed accordingly.. Mean decrease of Ca x P product in CaCO3 group is (50.42+/-8.85 to 47 +/-6.63) in one month, p value =0.001(0.6-5) and CI- 95%. There is also significant reduction of phosphorus level in CaCO3 group than CaCO3 plus vitamin D3 group. Mean decrease in phosphorus in CaCO3 group is (5.51+/-0.76 to 5.17+/- 0.05) in one month. P value =0.01(0.14-0.53) and CI 95%.. There is a significant decrease in Ca x P product and phosphorus level was observed in CKD patients taking CaCO3 alone.

Topics: Adult; Antacids; Calcium; Calcium Carbonate; Cholecalciferol; Cross-Sectional Studies; Drug Therapy, Combination; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Nepal; Phosphorus; Prospective Studies; Renal Dialysis; Vitamins

In vitro, monocyte 1alpha-hydroxylase converts 25-hydroxyvitamin D [25(OH)D] to 1,25-dihydroxyvitamin D to regulate local innate immune responses, but whether 25(OH)D repletion affects vitamin D-responsive monocyte pathways in vivo is unknown. Here, we identified seven patients who had 25(OH)D insufficiency and were undergoing long-term hemodialysis and assessed changes after cholecalciferol and paricalcitol therapies in both vitamin D-responsive proteins in circulating monocytes and serum levels of inflammatory cytokines. Cholecalciferol therapy increased serum 25(OH)D levels four-fold, monocyte vitamin D receptor expression three-fold, and 24-hydroxylase expression; therapy decreased monocyte 1alpha-hydroxylase levels. The CD16(+) "inflammatory" monocyte subset responded to 25(OH)D repletion the most, demonstrating the greatest increase in vitamin D receptor expression after cholecalciferol. Cholecalciferol therapy reduced circulating levels of inflammatory cytokines, including IL-8, IL-6, and TNF. These data suggest that nutritional vitamin D therapy has a biologic effect on circulating monocytes and associated inflammatory markers in patients with ESRD.

Topics: 25-Hydroxyvitamin D3 1-alpha-Hydroxylase; Antimicrobial Cationic Peptides; Calcitriol; Cathelicidins; Cholecalciferol; Cytokines; Dietary Supplements; Humans; Interleukin-6; Interleukin-8; Kidney Failure, Chronic; Mixed Function Oxygenases; Monocytes; Prospective Studies; Receptors, Calcitriol; Renal Dialysis; Steroid Hydroxylases; Toll-Like Receptor 2; Tumor Necrosis Factor-alpha; Vitamin D Deficiency; Vitamin D3 24-Hydroxylase

Vitamin D3 has diverse biological effects extending beyond the maintenance of calcium and phosphorus homeostasis and ensuring the proper functioning of the body.. This study evaluated the levels of vitamin D3 and its association with nutritional status, immunological activity, and selected markers of cardiovascular disease in patients on long-term hemodialysis (HD).. We measured 25-hydroxyvitamin D3 (25(OH)D3) levels in a group of 84 patients (mean age, 65 years; average time on dialysis, 32.5 months) and investigated correlations between 25(OH)D3 levels and the following parameters: albumin, body mass index, hemoglobin (Hb), interleukin 6 (IL-6), interleukin 10, C-reactive protein, asymmetric dimethylarginine (ADMA), N-terminal pro-B-type natriuretic peptide (NT-proBNP), and comorbidity score.. A mean 25(OH)D3 level was 15.4 +/-7.2 ng/ml and only 5% of patients had 25(OH)D3 levels above the normal value of 30 ng/ml. There was no statistically significant difference in 25(OH)D3 levels between women and men (P = 0.06). A negative correlation was observed between 25(OH)D3 and IL-6 (R = -0.31, P = 0.009) and ADMA (R = -0.26, P = 0.03), as well as a positive correlation between 25(OH)D3 and Hb (R= 0.21, P = 0.05). There was no association between 25(OH)D3 levels and nutritional status.. A significant vitamin D3 deficiency observed in the majority of patients undergoing long-term HD contributes to the development of chronic inflammation, anemia, and indirectly, to endothelial cell injury.

Topics: Aged; Cardiovascular Diseases; Cholecalciferol; Female; Humans; Inflammation; Kidney Failure, Chronic; Male; Nutritional Status; Renal Dialysis; Vitamin D Deficiency

Few studies have been conducted to investigate the influence of recombinant human erythropoietin (rhEPO) on the long-term prognosis of end-stage renal disease (ESRD).. A retrospective cohort study.. The largest regional hospital renowned for haemodialysis in northern Taiwan.. A total of 702 ESRD patients undergoing haemodialysis between 1993 and 2002 were evaluated.. The rate of overall use of rhEPO, vitamin D3 or Fe therapy was 62 %. The 10-year survival rate in patients with rhEPO supplementation was statistically more favourable than that in patients without rhEPO (hazard ratio (HR) = 0.38, 95 % CI 0.30, 0.47, P < 0.0001). Similar findings were noted for patients receiving vitamin D3 (HR = 0.36, 95 % CI 0.21, 0.64, P = 0.0004) and Fe (HR = 0.45, 95 % CI 0.33, 0.61, P < 0.0001). After adjusting for age, education and aetiology, the administration of rhEPO resulted in statistically significant improvements in long-term survival rate either with (HR = 0.30, 95 % CI 0.22, 0.42) or without (HR = 0.48, 95 % CI 0.38, 0.61) combined use of Fe or vitamin D3.. We demonstrated a reduction in long-term mortality related to supplementation therapy with rhEPO, vitamin D3 and Fe. The findings provide a justification for the administration of combined supplement therapy in patients undergoing haemodialysis.

Topics: Adolescent; Adult; Aged; Child; Child, Preschool; Cholecalciferol; Cohort Studies; Dietary Supplements; Erythropoietin; Female; Follow-Up Studies; Humans; Infant; Infant, Newborn; Iron; Kaplan-Meier Estimate; Kidney Failure, Chronic; Male; Middle Aged; Multivariate Analysis; Prognosis; Recombinant Proteins; Renal Dialysis; Retrospective Studies; Young Adult

Although immune-mediated pathogenesis in adriamycin (ADR)-induced nephropathy has been proposed recently, studies are lacking about the effects of immunmodulators, such as vitamin D, on ADR-induced nephrotoxicity. We hypothesized that vitamin D(3) (cholecalciferol) would be beneficial on ADR-induced nephropathy because of its immunmodulatory properties. Eighteen male Wistar rats were divided into three groups (n = 6): group 1 (control), group 2 (single ADR injection intravenously), and group 3 (similar single ADR injection intravenously + daily oral cholecalciferol for 21 days) were used in the study. A single high dose of ADR resulted in increased urinary protein: creatinine ratio for all three weeks of the experiment in both groups 2 and 3 compared with the controls. Histological examination of the kidney tissue revealed distinct tubular lesions as tubular necrosis, hyaline casts in tubular lumen, tubular degeneration, tubular dilatation, and tubular vacuolization in group 2 compared with group 1. These tubular lesions were significantly reduced in group 3 compared to group 2. The results of this study indicate that cholecalciferol causes satisfactory tubulointerstitial recovery in ADR-induced nephrotoxicity in rats.

Topics: Analysis of Variance; Animals; Antioxidants; Cholecalciferol; Disease Models, Animal; Dose-Response Relationship, Drug; Doxorubicin; Immunohistochemistry; Injections, Intravenous; Kidney Failure, Chronic; Kidney Function Tests; Male; Probability; Random Allocation; Rats; Rats, Wistar; Reference Values

Vitamin D functions in the body through both an endocrine mechanism (regulation of calcium absorption) and an autocrine mechanism (facilitation of gene expression). The former acts through circulating calcitriol, whereas the latter, which accounts for more than 80% of the metabolic utilization of the vitamin each day, produces, uses, and degrades calcitriol exclusively intracellularly. In patients with end-stage kidney disease, the endocrine mechanism is effectively disabled; however, the autocrine mechanism is able to function normally so long as the patient has adequate serum levels of 25(OH)D, on which its function is absolutely dependent. For this reason, calcitriol and its analogs do not constitute adequate replacement in managing vitamin D needs of such patients. Optimal serum 25(OH)D levels are greater than 32 ng/mL (80 nmol/L). The consequences of low 25(OH)D status include increased risk of various chronic diseases, ranging from hypertension to diabetes to cancer. The safest and most economical way to ensure adequate vitamin D status is to use oral dosing of native vitamin D. (Both daily and intermittent regimens work well.) Serum 25(OH)D can be expected to rise by about 1 ng/mL (2.5 nmol/L) for every 100 IU of additional vitamin D each day. Recent data indicate that cholecalciferol (vitamin D(3)) is substantially more potent than ergocalciferol (vitamin D(2)) and that the safe upper intake level for vitamin D(3) is 10,000 IU/d.

Topics: Administration, Oral; Animals; Calcitriol; Cardiovascular Diseases; Cholecalciferol; Communicable Diseases; Diabetes Mellitus; Ergocalciferols; Humans; Kidney Failure, Chronic; Neoplasms; Nutrition Policy; Osteoporosis; Receptors, Calcitriol; Signal Transduction; Vitamin D; Vitamin D Deficiency; Vitamins

Parathyroidectomy is the only effective therapy for osteitis fibrosa cystica in hyperparathyroidism.. The objective of this study was to describe the changes of skeletal and nonskeletal manifestations in a patient with hyperparathyroidism and renal failure after oral vitamin D therapy.. This was a descriptive case report.. The patient was followed up in a referral center.. A 55-yr-old male patient with moderate renal failure was referred for expansile lytic lesions affecting several ribs and the spinous process of T12. His creatinine was 1.8 mg/dl; calcium, 8.9 mg/dl; PTH, 666 pg/ml; and 1,25 dihydroxy-vitamin D, 27 pg/ml. Bone mineral density (BMD) Z-scores by dual-energy x-ray absorptiometry were -4.1 at the spine, -1.7 at the hip, and -4.3 at the forearm.. The main outcome measures were the skeletal manifestations of hyperparathyroidism.. At 10 months of therapy, calcium level was 10 mg/d, PTH level declined to 71 pg/ml, and BMD increased by 12% at the spine and 18% at the hip. Computerized tomography (CT) cuts revealed marked regression in the lytic lesions. At 2 yr, BMD increased by an additional 6% at the spine, and there were no further changes in the lytic lesions by CT. The vitamin D receptor genotype using the restriction enzymes Bsm1, Taq1, and Apa1 was Bb, tt, and AA.. We showed regression of severe skeletal abnormalities of hyperparathyroidism documented by serial CT images in response to oral vitamin D therapy. It is possible that the vitamin D receptor genotype of the patient modulated this response.

Topics: Bone Density; Bone Diseases; Calcium; Cholecalciferol; Genotype; Humans; Hydroxycholecalciferols; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Male; Middle Aged; Osteitis Fibrosa Cystica; Osteoporosis; Receptors, Calcitriol; Thalassemia; Tomography, X-Ray Computed; Vitamin D

Secondary hyperparathyroidism (2HPT), which is related to renal osteodystrophy (ROD), may occur in patients in the comparatively early stage of chronic renal failure (CRF). Secondary hyperparathyroidism patients with parathyroid hyperplasia showed resistance to vitamin D(3) treatment during long-term dialysis. At present, evaluation by ultrasonography is considered to be useful for confirming parathyroid hyperplasia. There are no clinical data associated with imaging evaluation of 2HPT in CRF patients. In the present study, the relationship among clinical and biochemical data, and parathyroid hyperplasia by ultrasonography, was evaluated in 12 patients (six males and six females) with end-stage renal failure (ESRF) before and at initiation of dialysis. Five patients showed an enlargement of parathyroid glands in ultrasonography. Levels of serum-intact parathyroid hormone (PTH) in patients with parathyroid hyperplasia (positive group) were significantly higher than in those without hyperplasia (negative group; 97.6 +/- 36.65 vs 17.4 +/- 4.45 pmol/L; P < 0.05). The levels of intact PTH were above 35.0 pmol/L in all five patients with hyperplasia. All patients in the positive group had never taken vitamin D(3) supplements. Calcium-containing phosphate binders were not prescribed before the present study, except in one patient. Parathyroid hyperplasia caused by 2HPT was recognized in patients before and at initiation of dialysis in this study. It appears that untreated 2HPT in CRF patients may progress to advanced 2HPT in ESRF before and/or after the early stage of dialysis. The levels of serum intact PTH are useful in predicting parathyroid hyperplasia.

Topics: Adult; Aged; Alkaline Phosphatase; Biomarkers; Calcium; Calcium Carbonate; Cholecalciferol; Dialysis; Female; Humans; Hyperparathyroidism, Secondary; Hyperplasia; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Glands; Parathyroid Hormone; Ultrasonography, Doppler, Color; Vitamins

In spite of essential enrichment of our pathophysiological knowledge in the field of the calcium-phosphate metabolism and bone alterations in renal transplant patients, both diagnosis and therapy of these abnormalities still remain a challenge for nephrologists and transplantologists. The present study aimed to establish the diagnostic value of traditional and contemporary markers of Ca-P metabolism and bone alterations in kidney transplant patients 4 or more years after Tx and the main factors responsible for osteodystrophy after Tx respectively. 61 patients and 21 controls were examined. The assessed parameters were: serum levels of total (Ca) and ionized calcium (Ca2+), serum concentration of phosphorus (P), intact PTH, calcitonin, osteocalcin, 25-OH-D3, collagen type I cross-linked C-telopeptide and activity of alkaline phosphatase (total and bone isoenzyme). In all subjects bone densitometry of the total body, L2-L4 vertebrae and femoral neck were performed. In kidney transplant patients routinely assessed markers of calcium-phosphate metabolism (Ca, Ca2+, P, alkaline phosphatase total and bone fraction) were in the normal range while significantly elevated serum concentrations of PTH, osteocalcin and CTx were found. In more than 20% of renal transplant patients osteoporosis and in further 50% patients osteopenia were found by DEXA. The intensity of bone abnormalities was dependent on the duration of dialysis therapy before Tx, time after Tx, degree of impairment of the graft, intensity of hyperparathyroidism and total dose of corticosteroids. From results obtained in this study estimation of serum concentration of 25-OH-D3, PTH, CTx and the BMD respectively is mandatory to detect Ca-P abnormalities and osteoporosis or osteopenia in Tx patients.

Topics: Absorptiometry, Photon; Adult; Biomarkers; Bone and Bones; Bone Density; Bone Diseases, Metabolic; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Female; Follow-Up Studies; Humans; Kidney Failure, Chronic; Kidney Transplantation; Male; Osteoporosis; Parathyroid Hormone; Phosphates; Poland; Prospective Studies; Renal Dialysis

The treatment of the secondary hyperparathyroidism of chronic renal failure patients has greatly improved during the last 2 decades. Significant progress has been made, in particular in the indication of 1alpha-hydroxylated vitamin D derivatives and patient management using these compounds. Treatment and prevention should start early during the development of chronic renal insufficiency. One of the major remaining problems in more advanced stages of renal failure is that control of plasma phosphate often remains extremely difficult. New inert oral phosphate binders are needed. The nephrology community is still waiting for the advent of nonhypercalcemic and nonhyperphosphatemic vitamin D analogs with PTH suppressive activity equal to the parent compound calcitriol or its immediate precursor, alfacalcidol.

Topics: Administration, Oral; Calcitriol; Cholecalciferol; Humans; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Vitamin D

In the present study, we investigated the kinetics of bone metabolism by determining serum bone metabolic markers and quantifying bone mineral density by dual-energy X-ray absorptiometry to clarify the effect of long-term use of low-calcium hemodialysate on bone metabolism. After changing the calcium concentration in the dialysate from 3.0 mEq/l to 2.5 mEq/l, serum intact parathyroid hormone level, serum highly sensitive parathyroid hormone level, and serum bone metabolic markers were determined in ten patients with chronic nondiabetic renal insufficiency during 1 year. The doses of an oral phosphate binder and activated vitamin D were carefully regulated to control serum ionized calcium levels and serum inorganic phosphorus levels. Bone mineral density was determined at the distal 1/3 and 1/6 of the radius on the nonshunt side. As a result, the required amount of oral phosphate binder was increased; however, there was no need to significantly increase the amount of activated vitamin D. Intact parathyroid hormone showed no significant variation, but the highly sensitive parathyroid hormone was significantly increased. There were no significant changes in any bone metabolic markers or in bone mineral density. From these study results, it was found that it was difficult to increase the dose of activated vitamin D even if low-calcium hemodialysate was used, and that during use of the low-calcium hemodialysate the serum level of parathyroid hormone tended to increase but led to neither acceleration of bone turnover nor a decrease in bone mineral density.

Topics: Absorptiometry, Photon; Adult; Aged; Alkaline Phosphatase; Biomarkers; Bone and Bones; Bone Density; Calcium; Calcium Carbonate; Cholecalciferol; Female; Hemodialysis Solutions; Humans; Hydroxycholecalciferols; Isoenzymes; Kidney Failure, Chronic; Kinetics; Male; Middle Aged; Parathyroid Hormone; Peptide Fragments; Phosphorus; Procollagen; Renal Dialysis

Vitamin D compounds are usually indicated for the treatment of secondary hyperparathyroidism in dialysis patients. The possibility to induce a reversal of hyperparathyroidism with calcium supplementation alone is controversial. The present study was conducted to assess if oral calcium carbonate may constitute a therapeutic option for the control of hyperparathyroidism in patients with high PTH concentrations at the beginning of the treatment with chronic hemodialysis.. Thirty-one patients with end-stage renal failure with an intact PTH concentration above 250 pg/ml at the beginning of chronic hemodialysis therapy were treated with high doses of calcium carbonate; no patient received either aluminium-containing binders or vitamin D compounds. To minimize hypercalcemia, a calcium dialysate concentration of 2.5 mEq/l was used in all patients. The goal of the study was to reduce the intact PTH concentration to 250 pg/ml with oral calcium carbonate supplements alone.. Throughout the first year on hemodialysis treatment, the intact PTH concentration decreased from 538 +/- 256 to 251 +/- 218 pg/ml (p < 0.001). By the end of the study, the therapeutic objective was achieved in 22 patients (71%) ('responder' group). The remaining 9 patients were classified as the 'treatment failure' group. The basal intact PTH concentration was not different between both groups (508 +/- 235 vs. 612 +/- 303 pg/ml, respectively, p = n.s.), but 5 'treatment failure' patients admitted to take a dose of calcium carbonate lower than that prescribed. There were 40 episodes of hyperphosphatemia (11% of all measurements) in 7 of 31 patients, 5 of them belonged to the noncompliance 'treatment failure' patients. Only 15 episodes (4% of all measurements) of transient hypercalcemia (range 11.1 - 11.9 mg/dl) were detected in 8 patients.. Secondary hyperparathyroidism in hemodialysis patients can often be reverted by oral calcium carbonate alone. But a good adherence to treatment is absolutely necessary.

Topics: Administration, Oral; Calcium Carbonate; Cholecalciferol; Female; Humans; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Hormone; Renal Dialysis

Calciphylaxis occurred in a 40-year old female patient with end-stage renal failure. The patient developed livedo racemosa ("livedo reticularis") with painful skin necrosis and ulcers involving multiple areas of the hip and legs after 22 years of hemodialysis. X-ray-examinations revealed calcinosis of peripheral arteries, especially of the pelvis, thigh and hands, while histological examinations showed a fibrosis and calcinosis of small subcutaneous arteries. A generalized cutaneous microangiopathy could be demonstrated by transcutaneous oxygen pressure measurements. Laboratory data showed a moderate secondary hyperparathyroidism with mild elevation of calcium-phosphate product. In addition to the hemodialysis an attempt was made to improve the microcirculation by vasoactive drugs. The clinical course was characterized by slow healing of the ulcers and occurrence of new areas of cutaneous necrosis. Calciphylaxis is a rare late complication in patients with advanced, often end-stage renal failure. It has characteristic histopathological features and is frequently, but not always, associated with a disturbed calcium and phosphorus metabolism and mildly elevated levels of parathyroid hormone. Calciphylaxis is classified as a special type of metastatic calcinosis.

Topics: Adult; Aluminum Hydroxide; Calciphylaxis; Calcium; Cholecalciferol; Disseminated Intravascular Coagulation; Ergocalciferols; Erythropoietin; Female; Humans; Ischemia; Kidney Failure, Chronic; Long-Term Care; Necrosis; Parathyroid Hormone; Renal Dialysis; Skin Diseases, Vascular

Valvular calcification in chronic haemodialysis patients has already been reported in the literature, particularly the abnormally high incidence of aortic stenosis. In this study, 112 haemodialysis patients were followed up by Doppler echocardiography for a period of 36 months. Sixteen patients developed aortic valvular calcification with aortic stenosis over an 18.7 +/- 7.5 months period. The indexed aortic valve surface area decreased from 1.24 +/- 0.9 cm2/m2 to 0.66 +/- 0.21 cm2/m2 with abnormally rapid progression. Eight patients with aortic stenosis died during the 3 year study period. These results reflect the abnormal extra-skeletal calcification of chronic haemodialysis patients. Several predisposing factors were demonstrated: age (68.5 +/- 11.1 years versus 57.1 +/- 16.3 years in patients without calcifications), male gender, a longer period of dialysis than the patients without aortic stenosis (8.1 +/- 5.3 versus 5.9 +/- 5.7 years), abnormalities of calcium and phosphate metabolism, increased of the phosphocalcic product by hyperphosphoraemia and not by hypercalcaemia, hypoparathyroidism in 62% and hyperparathyroidism in 38% an increase in vitamin D 3 (19.7 +/- 14 ng/ml versus 9.6 +/- 6.3 ng/ml) biological signs of adynamic osteodystrophy. Calcific aortic stenosis is a commonly observed valvular lesion in haemodialysis patients: its progression may be very rapid, associated with a poor prognosis. Old age, male gender, duration of haemodialysis, hyperphosphataemia associated with hypoparathyroidism and raised Vitamin D3 are predisposing factors.

Topics: Aged; Aged, 80 and over; Aortic Valve Stenosis; Calcinosis; Calcium Metabolism Disorders; Cholecalciferol; Female; Follow-Up Studies; Humans; Kidney Failure, Chronic; Male; Middle Aged; Phosphorus Metabolism Disorders; Prognosis; Renal Dialysis; Risk Factors; Ultrasonography

To evaluate the natural history of bone mineral density after successful renal transplantation (TPL) modulated by therapeutic strategies in pediatric patients we have studied peripheral and partially proximal quantitative computed radius tomography (XCT) differentiating between trabecular (TBD), cortical (CBD) and total bone density (BD) cross-sectionally in a group of 24 subjects (mean age 17.1 +/- 7.0 y, mean Scr 1.66 +/- 0.89), 66.1 months (5-260) post transplant and compared the results with 12 controls. After TPL median TBD was elevated (182.5 vs. 155.5 mg/cm3) whereas the opposite was true for CBD (361.8 vs. 437.8 mg/cm3). The physiologic age dependency of BD had got lost after TPL but could be reassumed by the measurement of proximal CBD. TBD correlated with the cumulative calcitriol dosage (r = 0.60, p < 0.05), bone alkaline phosphatase (r = 0.55, p < 0.01), the Ca x P product (r = 0.43, p < 0.05) and inversely with the time after TPL (r = -0.45, p < 0.05), but no significant correlation could be detected with the cumulative steroid dose. It was found to be higher in calcitriol treated than in vitamin D3 treated patients. Proximal CBD was inversely correlated with bone alkaline phosphatase (r = -0.71, p < 0.01) and intact PTH (r = -0.59, p < 0.05). In conclusion CBD in kidney grafted pediatric patients seems to be more or less reduced by secondary hyperparathyroidism whereas the increase of TBD appears to be induced by anticipated calcitriol treatment under dialysis regimen and gradually normalizes after TPL.

Topics: Adolescent; Alkaline Phosphatase; Biopsy; Bone Density; Bone Resorption; Calcitriol; Cholecalciferol; Cross-Sectional Studies; Female; Follow-Up Studies; Glucocorticoids; Humans; Kidney Failure, Chronic; Kidney Transplantation; Male; Parathyroid Hormone; Prednisone; Tomography, X-Ray Computed

Twelve dialysis patients received oral pulse therapy with 1-alpha-hydroxyvitamin D3 in a dose of 0.1 microgram/kg body weight twice weekly and daily calcium carbonate (1.5-3.5 g) for a period of 8-12 months. This treatment was very effective in suppressing secondary hyperparathyroidism without causing hypercalcaemia and/or hyperphosphataemia.

Topics: Administration, Oral; Adolescent; Adult; Alkaline Phosphatase; Calcium; Child; Child, Preschool; Cholecalciferol; Female; Humans; Hyperparathyroidism, Secondary; Immunoradiometric Assay; Kidney Failure, Chronic; Male; Parathyroid Hormone; Peritoneal Dialysis, Continuous Ambulatory; Phosphorus; Renal Dialysis

Pulse vitamin D3 (3-5 micrograms po, twice a week) has been proposed for individuals with hyperparathyroidism resistant to daily po vitamin D3 therapy. While pulse vitamin D3 is effective, concerns regarding oversuppression of parathyroid hormone (PTH) values leading to adynamic bone disease have arisen. In view of these concerns, minibolus vitamin D3 po therapy was utilized in dosages varying from 0.25-1.0 micrograms twice a week in an effort to control elevated PTH values in patients who failed standard daily vitamin D3 therapy. Eleven patients were changed to minibolus vitamin D3 therapy from standard daily treatment (6 women, 5 men; mean age 55.8 +/- 14 years), on continuous ambulatory peritoneal dialysis (CAPD) for an average of 28.4 +/- 23 months. The mean intact PTH (iPTH) values on 0.25 microgram/day decreased by 54.5 +/- 167.8 pg/mL compared to pretreatment values. The mean iPTH on minibolus vitamin D3 therapy decreased by 165.1 +/- 104 pg/mL. The response to minibolus vitamin D3 was not truly predicted by the baseline PTH values. While the average decrease in PTH was greatest on 1.0 microgram two times a week, 2 patients experienced a decrease greater than 200 pg/mL in PTH on a lower dose. The greatest effect on PTH with minipulse vitamin D3 occurred when iPTH was < or = 500 pg/mL. While total calcium increased on daily vitamin D3, there was no significant change with minipulse therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Administration, Oral; Cholecalciferol; Drug Administration Schedule; Female; Humans; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Hormone; Peritoneal Dialysis, Continuous Ambulatory

We analyzed transiliac bone biopsy specimens from 30 end-stage renal failure patients, taken at the time of admission for CAPD training. Results were compared with values of iPTH, bone alkaline phosphatase, 1,25-dihydroxyvitamin D3, skeletal survey, quantitative computed tomography (QCT) and single photon absorptiometry (SPA) bone density measurements. Osteitis fibrosa was the most common histological diagnosis, present in 15 of the 30 patients (50%), with eight classified as "severe" and seven as "mild." Eight patients (27%) had adynamic bone lesion, four mixed renal osteodystrophy (13%), and two (7%) osteomalacia. The mean age of the adynamic group was higher than the osteitis fibrosa group (41 +/- 12.1 vs. 56 +/- 10.2 years; P < 0.01), and than the mixed group (39 +/- 7.5 vs. 56 +/- 10.2 years; P < 0.02). Levels of iPTH enabled discrimination between groups, but not between individual patients, and values correlated with bone alkaline phosphatase (r = 0.62; P < 0.001). Erosion of the terminal phalanges was seen on the plain X-rays of 7 of 15 patients with mild or severe OF, and in three patients with another diagnosis. The majority of patients (> 90%) had bone density measurements within the normal range. No significant correlation existed between QCT or SPA scores and any of the histomorphometric parameters, or iPTH. We conclude that iPTH is the most helpful non-invasive investigation in this group of patients. Plain X-ray of the hands is the most useful radiological investigation, but single measurements of bone density are not diagnostic.

Topics: Adult; Aged; Biopsy; Bone and Bones; Bone Density; Cholecalciferol; Female; Fibrous Dysplasia of Bone; Humans; Kidney Failure, Chronic; Male; Middle Aged; Osteomalacia; Parathyroid Hormone; Radioimmunoassay; Tomography, X-Ray Computed

Topics: Adult; Amyloidosis; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Kidney Transplantation; Male; Renal Dialysis

We measured 24,25-dihydroxyvitamin D [24,25(OH)2D] levels in patients treated with chronic ambulatory peritoneal dialysis (CAPD), before and after receiving vitamin D2 or 1 alpha-hydroxyvitamin D3 (1 alpha-OH-D3). Vitamin D2 administration led to an increase in 25-hydroxyvitamin D (25-OH-D) and a concomitant rise in 24,25(OH)2D. No change was observed in 1,25-dihydroxyvitamin D [1,25(OH)2D]. Administration of 1 alpha-OH-D3 resulted in an increase in 1,25(OH)2D3, and a concomitant rise in 24,25(OH)2D, but no change in 25-OH-D3. Thus, 24,25(OH)2D levels may be increased in CAPD patients by raising 25-OH-D levels, or by raising 1,25(OH)2D3 levels. Since the latter enhances specifically the renal 24-hydroxylase enzyme, we conclude that this enzyme is present in CAPD patients with kidneys in situ, and may be stimulated by adequate 1,25(OH)2D3 levels. Thus, administration of 1 alpha-OH-D3 to CAPD patients with kidneys in situ seems to be sufficient to obtain normal levels of 1,25(OH)2D3 and 24,25(OH)2D3. However, anephric patients require vitamin D2 in addition as a source of 25-OH-D, the substrate for extrarenal production of 24,25(OH)2D.

Topics: Calcifediol; Calcitriol; Cholecalciferol; Dihydroxycholecalciferols; Humans; Kidney Failure, Chronic; Peritoneal Dialysis, Continuous Ambulatory; Renal Dialysis

In 16 patients with a chronic renal insufficiency at the stage of the compensated retention and 13 test persons of the chronic haemodialysis programme determinations of the total calcium and of the ionized calcium fraction as well as investigation of the intestinal calcium absorption by means of the isotope 47Ca were performed. In these cases the influence of vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol) on these parameters of the calcium metabolism was compared. Under the treatment with vitamin D a normalization of the serum calcium levels concerning the total calcium concentration as well as with regard to the ionized calcium fraction was achieved; this effect took place parallel to the improvement of the intestinal calcium absorption. Vitamin D3, had a more favourable effect than vitamin D2. The necessary doses are below 40,000 U a day.

Topics: Blood Urea Nitrogen; Calcium; Cholecalciferol; Creatinine; Ergocalciferols; Humans; Intestinal Absorption; Kidney Failure, Chronic; Middle Aged; Phosphates; Renal Dialysis; Vitamin D Deficiency

Topics: Adolescent; Adult; Aged; Alkaline Phosphatase; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Female; Humans; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Long-Term Care; Male; Middle Aged; Osteomalacia; Parathyroid Glands; Parathyroid Hormone; Phosphorus; Radiography; Receptors, Calcitriol; Receptors, Steroid; Renal Dialysis

Two patients with moderate renal failure sustained spontaneous bilateral hip fractures during treatment with fluoride, calcium, and vitamin D for osteoporosis. They had been taking sodium fluoride (40-60 mg/day) for 11 and 21 months, respectively. Histological examination of a specimen of the bone showed severe fluorosis in the first case, and quantitative analysis of bone showed osteomalacia and skeletal fluorosis in the other case. These abnormalities were considered to be the consequence of excessive retention of fluoride due to renal insufficiency. As bilateral femoral neck fractures are very rare these data suggest a causal link between fractures and fluoride in patients with renal failure. Thus fluoride should be given at a lower dosage, if at all, to patients with even mild renal failure.

Topics: Aged; Bone and Bones; Calcium; Cholecalciferol; Drug Therapy, Combination; Female; Femoral Neck Fractures; Fractures, Spontaneous; Humans; Kidney Failure, Chronic; Osteomalacia; Osteoporosis; Sodium Fluoride

Topics: Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Kidney; Kidney Failure, Chronic

Topics: Animals; Child; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Growth; Growth Disorders; Humans; Kidney Failure, Chronic; Rats

Here we report the use of newly developed and established techniques for the determination of plasma levels of a broad spectrum of vitamin D3 metabolites, including vitamin D3 and 25OHD3-lactone, in normal humans, chronic renal failure patients, and anephric subjects. The methodology described consisted of methanol-methylene chloride extraction, Lipidex-5000 chromatography with stepwise gradient elution, normal-phase HPLC with concave gradient elution, and sensitive ligand-binding assays. The results of the study strongly suggest an extrarenal source(s) for 24,25(OH)2D3 and 25,26(OH)2D3 and indicate that both 25OHD3-lactone and 1,25(OH)2D3 may be produced solely in the kidney of the human. Significant reductions or nondetectable plasma levels of vitamin D3 in the renal disease patients may reflect abnormalities in the hepatobiliary-intestinal and/or cutaneous metabolism of vitamin D.

Topics: 24,25-Dihydroxyvitamin D 3; Calcifediol; Calcitriol; Cholecalciferol; Dihydroxycholecalciferols; Humans; Hydroxycholecalciferols; Kidney Failure, Chronic; Methods; Nephrectomy

The serum levels of 25-hydroxycholecalciferol (25-OHD3) and 1,25-dihydroxycholecalciferol[1,25-(OH)2D3] were measured simultaneously in nephrectomized patients on maintenance haemodialysis, in haemodialyzed patients with preserved kidneys who were receiving different vitamin D supplement, and in patients who had undergone renal transplantation. The results indicate that the production of 1,25-(OH)2D3 can be stimulated in patients with minimal residual renal excretory function by increasing the serum levels of 25-OHD3. Successful renal transplantation was followed by a rise in serum 1,25-(OH)2D3 concentrations.

Topics: Antigens; Calcium; Cholecalciferol; Dihydroxycholecalciferols; Glomerular Filtration Rate; Humans; Hydroxycholecalciferols; Kidney; Kidney Failure, Chronic; Kidney Transplantation; Magnesium; Nephrectomy; Parathyroid Hormone; Phosphorus; Renal Dialysis; Transplantation, Homologous

These studies were performed to see if jejunal malabsorption of magnesium in patients with chronic renal disease was influenced by therapy with 1 alpha, 25-dihydroxyvitamin D3 [1,25-(OH)2D3; 2 microgram/day by mouth for 7 days]. This treatment restored normal serum concentrations of the vitamin D metabolite from 0.9 +/- 0.2 to 4.2 +/- 0.6 ng/dl. Jejunal absorption of magnesium, measured by a triple-lumen constant-perfusion technique, was enhanced in each of the seven patients by this therapy. The mean value rose from 0.04 +/- 0.02 to 0.13 +/- 0.02 mmol . 30 cm-1 . h-1. This last value is similar to the magnesium absorption rate in untreated normal subjects. These results demonstrate that magnesium absorption in the human jejunum is dependent on vitamin D, and they show that 1 alpha,25-dihydroxyvitamin D3 therapy in patients with chronic renal failure is associated with an enhanced jejunal absorption of magnesium.

Topics: Adult; Cholecalciferol; Female; Humans; Jejunum; Kidney Failure, Chronic; Magnesium; Male; Parathyroid Hormone; Radioimmunoassay

Growth arrest and renal osteodystrophy is a major problem in renal insufficiency of children. The present report describes our experiences in managing renal osteodystrophy by using vitamin D3 for 24 months. Values in plasma of Ca, Mg, alkaline phosphatase, iPTH, 25-OH-D were determined regularly. Skeletal X-rays and analysis of iliac crest bone biopsies were obtained in each child. In treatment with vitamin D3 no hypercalcemia was seen despite high serum levels of 25-OH-D. Plasma-Ca, alkaline phosphatase, and iPTH normalized nearly. Radiographic abnormalities improved. Bone biopsies showed improvement in signs of secondary hyperparathyroidism and ostitis fibrosa, whereas osteomalacia remained unchanged. Osteoblast population showed a small reduction. No real increment in body growth was seen.

Topics: Alkaline Phosphatase; Aluminum Hydroxide; Calcium; Child; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Kidney Failure, Chronic; Phosphates; Renal Dialysis

Topics: Adolescent; Age Determination by Skeleton; Body Height; Child; Child, Preschool; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dietary Proteins; Energy Intake; Female; Growth; Humans; Infant; Kidney Failure, Chronic; Male; Peritoneal Dialysis; Puberty; Renal Dialysis

Topics: Animals; Bicarbonates; Cholecalciferol; Extracorporeal Circulation; Forecasting; Humans; Kidney Failure, Chronic; Kidneys, Artificial

Topics: Animals; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dogs; Humans; Hyperparathyroidism, Secondary; Intestine, Small; Kidney; Kidney Failure, Chronic; Myocardium; Parathyroid Hormone; Vitamin D

A competitive protein binding assay for 1,25-dihydroxycholecalciferol has been developed using the hormone's nuclear receptor protein from chick intestinal mucosa. This nuclear receptor protein can be stored at -70 degrees C for several months and bound and free hormone can be separated easily with dextran coated charcoal. Results obtained using this assay agree well with those reported by other groups of workers. Serum levels of other vitamin D-3 metabolites, namely 25-hydroxycholecalciferol and 24,25-dihydroxycholecalciferol have also been measured and are shown in relation to 1,25-(OH)2D3 levels.

Topics: Animals; Cell Nucleus; Cholecalciferol; Dihydroxycholecalciferols; Humans; Hydroxycholecalciferols; Hyperparathyroidism; Intestinal Mucosa; Kidney Failure, Chronic; Kinetics; Microchemistry; Osteomalacia; Radioligand Assay; Receptors, Drug

Topics: Anemia; Blood Pressure; Cell Differentiation; Cholecalciferol; Erythropoiesis; Erythropoietin; Humans; Juxtaglomerular Apparatus; Kallidin; Kallikreins; Kidney; Kidney Failure, Chronic; Natriuresis; Prostaglandins; Renin

Topics: Adult; Bone and Bones; Bone Diseases, Metabolic; Calcium; Cholecalciferol; Female; Humans; Hyperparathyroidism; Kidney Failure, Chronic; Male; Renal Dialysis; Vitamin D Deficiency

The corneas of 15 children on intermittent long-term dialysis for renal failure were studied, first during a period of treatment with high doses of vitamin D3 and subsequently during a study with the vitamin D metabolite 1,25 DHCC. Metastatic calcification of the limbus or increased limbic deposits only occurred during the second treatment phase, with vitamin 1,25 DHCC. In 5 of these children phases with plasma calcium levels were recorded which were closely related to the times when corneal changes occurred. In 3 children phosphate values were also increased. Only one child presented with normal calcium values and merely an increase in phosphate concentration. Regression of corneal deposits following normalization of calcium metabolism seems possible in the light of observations so far.

Topics: Adolescent; Calcium; Child; Cholecalciferol; Cornea; Dihydroxycholecalciferols; Humans; Kidney Failure, Chronic; Phosphates; Renal Dialysis

Twelve children with chronic renal failure (CRF) and sixteen children receiving regular dialysis therapy (RDT) were treated with between 10,000 and 50,000 IU of vitamin D daily. This was associated with an increase in serum calcium levels and reduction in PTH levels. In the children with CRF, secondary hyperparathyroidism was improved with treatment but its development was not completely prevented nor was healing complete. In the patients receiving RDT, treatment with vitamin D improved the changes associated with secondary hyperparathyroidism in 50% of cases but these features sometimes reappeared despite continuing treatment. Hypercalcaemia or metastatic calcification was not seen. Subsequently, 1,25(OH)2D3 was administered to 14 children receiving RDT. This was associated with the return of serum calcium levels to normal, inhibition of PTH synthesis and an improvement in intestinal calcium absorption. Fibro-osteoclasia was cured and there was improvement in actual bone resorption. There was also improvement in osteoidosis in those children who showed disturbances of mineralisation. Calcification in the limbus area of the eyes may occur and hypercalcaemia was seen commonly. Treatment with 1,25(OH)2D3 should only be offered to children with severe renal bone disease. Neither vitamin D3 nor 1,25(OH)2D3 can guarantee complete recovery of osteodystrophy and of growth arrest in uraemic children.

Topics: Adolescent; Alkaline Phosphatase; Bone and Bones; Bone Diseases; Calcium; Child; Cholecalciferol; Humans; Kidney Failure, Chronic; Phosphates; Renal Dialysis

Topics: 25-Hydroxyvitamin D3 1-alpha-Hydroxylase; Animals; Calcium; Chickens; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydroxycholecalciferols; Dogs; Humans; Intestinal Absorption; Kidney; Kidney Failure, Chronic; Parathyroid Glands; Parathyroid Hormone; Phosphorus; Vitamin D

Topics: Child; Child, Preschool; Cholecalciferol; Female; Follow-Up Studies; Growth; Growth Disorders; Humans; Kidney Failure, Chronic; Renal Dialysis

In 58 patients with end-stage renal failure before commencement of regular hemodialyses treatment (RTD) and 58 patients under RTD bone mineral content (BMC) was determined by the use of the photon absorptiometry. Further the effect of a treatment with bitamin D3 and 5,6-trans-25-OH-vitamin D3 on BMC was studied. There existed a negative correlation between the duration of chronic renal failure or of RDT as well as of the serum parathyroid hormone level to BMC. No correlation was found between BMC and serum calcium level. During a 14 months-course treatment with vitamin D3 or 5,6-trans-25-OH-vitamin D3 BMC increased. The method of photon absorptiometry presented itself as an easy and well reproducible technique for routine examinations.

Topics: Adolescent; Adult; Age Factors; Aged; Bone and Bones; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Densitometry; Elementary Particles; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Minerals; Parathyroid Hormone; Radius; Renal Dialysis; Spectrum Analysis; Time Factors; Ulna

Chronic renal disease in man and animals is associated with disturbances in calcium homeostasis which are resistant to vitamin D-therapy. Partially nephrectomized and intact rats were used to evaluate the effect of uremia on the response of bone to vitamin D. Serum calcium, serum phosphorus and blood urea nitrogen levels were higher in uremic rats than in intact rats, both given vitamin D. Metaphyseal bone in uremic rats was resistant to vitamin D-induced bone resorption; osteoblasts and osteocytes appeared less active ultrastructurally and osteoclass were infrequent. Calcitonin synthesis and release evaluated electron microscopically was greater in uremic rats. It is suggested that the altered response of bone to vitamin D in uremic rats was due in part to elevated serum phosphorus and increased calcitonin release. The present model does not refute experimental and clinical data that metabolism of vitamin D is altered in renal disease. It does, however, emphasize that in chronic renal failure other parameters (phosphorus levels, calcitonin release, uremia) are operating which may influence end organ response to pharmacologic doses of vitamin D. The partially nephrectomized rat may be a useful model for evaluating end-organ resistance to vitamin D in uremia.

Topics: Animals; Blood Urea Nitrogen; Bone and Bones; Calcitonin; Calcium; Cholecalciferol; Disease Models, Animal; Kidney Failure, Chronic; Male; Parathyroid Glands; Phosphates; Rats; Uremia; Vitamin D Deficiency

A survey is given on the present state of the animal-biochemical research concerning the effectivity of the D-vitamins. The vitamin D3 is transferred in 25-hydroxycholecalciferol in the microsome fraction of the liver. Then in the kidneys a transformation into the physiologically active forms - the 1,25- and the 24,25-hydroxycholecalciferol - takes place. The kind of transformation depends on the Ca- and P-supply as well as on the level of the parathormone secretion. In the mucous membrane of the small intestine the 1,25- and the 24,25-hydroxycholecalciferol stimulate the formation of the Ca-transport protein. The 1,25-hydroxycholecalciferol is above all formed in hypocalcaemia or hypophosphataemia and furthers the mobilisation of Ca- and phosphate-ions from the bones. In a liver damage disturbances of the formation of 25-hydroxycholecalciferol and in renal damage disturbances of the formation of 1,25- and 24,25-hydroxycholecalciferol may appear. A reduction of the formation of the active forms of the D-vitamins leads to a decrease of the Ca-utilisation as well as of the growth of bones.

Topics: Biological Availability; Bone and Bones; Calcium; Cholecalciferol; Humans; Hydroxycholecalciferols; Hydroxylation; Kidney Failure, Chronic; Phosphates; Rickets

Many clinical similarities between renal osteodystrophy and nutritional rickets have suggested that a defect in either the metabolism or action of vitamin D exists in chronic renal failure. The discovery of the kidney as the organ that manufactures the active metabolite of vitamin D has provided direct evidence for a relationship between renal failure and altered vitamin D metabolism. Other observations suggest that an abnormality of vitamin D action could underlie both osteomalacia and osteitis fibrosa (secondary hyperparathyroidism) observed in patients with chronic renal failure. The administration of the active vitamin D analogs, 25(OH)D3, 1,25(OH)2D3, and lalpha(OH)D3, to uremic patients with symptomatic bone disease is capable of reversing many of the abnormalities of divalent ion metabolism. The widespread availability of these agents in the future may provide the clinician the means to correct or even prevent the serious bone disease that frequently complicates the course of chronic renal failure.

Topics: Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydroxycholecalciferols; Humans; Hydroxycholecalciferols; Hyperparathyroidism, Secondary; Kidney; Kidney Failure, Chronic; Phosphorus; Vitamin D

Topics: Calcium Phosphates; Chemical Phenomena; Chemistry; Cholecalciferol; Dihydrotachysterol; Drug Resistance; Female; Homeostasis; Humans; Kidney Failure, Chronic; Middle Aged; Vitamin D

Topics: Animals; Calcium; Carbon Radioisotopes; Chickens; Cholecalciferol; Chromatography; Dihydroxycholecalciferols; Intestinal Absorption; Intestinal Mucosa; Kidney Failure, Chronic; Ligation; Tritium; Uremia; Ureter

Topics: Adult; Calcium; Calcium Radioisotopes; Cholecalciferol; Feces; Female; Humans; Intestinal Absorption; Kidney Failure, Chronic; Male; Metabolic Clearance Rate; Middle Aged; Phosphorus; Uremia

Topics: Calcium; Calcium Radioisotopes; Cholecalciferol; Dihydrotachysterol; Feces; Female; Humans; Intestinal Absorption; Isomerism; Kidney Failure, Chronic; Magnetic Resonance Spectroscopy; Male; Renal Dialysis; Spectrophotometry, Infrared; Spectrophotometry, Ultraviolet

Topics: Aluminum; Calcium Carbonate; Cholecalciferol; Humans; Hypocalcemia; Kidney Failure, Chronic; Male; Middle Aged; Phosphates

Topics: Animals; Bone Diseases; Calcium; Chemical Phenomena; Chemistry; Cholecalciferol; Dihydrotachysterol; Dihydroxycholecalciferols; Disease Models, Animal; Humans; Hydroxycholecalciferols; Isomerism; Kidney Failure, Chronic; Microradiography; Osteitis Fibrosa Cystica; Osteomalacia; Phosphates; Rats; Renal Dialysis; Uremia; Vitamin D

Topics: Calcium; Carbon Isotopes; Cholecalciferol; Chromatography; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydroxycholecalciferols; Humans; Hydroxycholecalciferols; Intestinal Absorption; Kidney; Kidney Failure, Chronic; Osteomalacia; Tritium; Vitamin D Deficiency

Topics: Animals; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Intestinal Absorption; Kidney Failure, Chronic; Rats

Topics: Aluminum; Animals; Calcium; Carbonates; Cholecalciferol; Diet Therapy; Dogs; Glomerular Filtration Rate; Humans; Hydroxides; Hyperparathyroidism, Secondary; Kidney; Kidney Failure, Chronic; Kidney Tubules; Nephrons; Parathyroid Hormone; Phosphorus

Topics: Anticonvulsants; Bone and Bones; Bone Resorption; Calcium; Cholecalciferol; Humans; Hydroxycholecalciferols; Hydroxylation; Intestinal Absorption; Intestinal Mucosa; Kidney Failure, Chronic; Liver; Osteomalacia; Vitamin D; Vitamin D Deficiency

Topics: Adult; Alkaline Phosphatase; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Ergocalciferols; Female; Humans; Kidney Failure, Chronic; Male; Parathyroid Glands; Parathyroid Hormone; Phosphorus; Radiography; Renal Dialysis; Vitamin D

Topics: Calcium; Cholecalciferol; Homeostasis; Humans; Hydroxycholecalciferols; Intestinal Absorption; Kidney Failure, Chronic; Uremia

Topics: Animals; Biological Transport; Blood Urea Nitrogen; Bone Diseases; Calcium; Chickens; Cholecalciferol; Intestinal Absorption; Intestine, Small; Kidney; Kidney Failure, Chronic; Ligation; Male; Nephrectomy; Rats; Uremia; Ureter; Vitamin D

Topics: Calcium; Calcium Isotopes; Calcium, Dietary; Cholecalciferol; Feces; Humans; Hydroxycholecalciferols; Intestinal Absorption; Kidney; Kidney Failure, Chronic; Male; Middle Aged; Phosphorus; Time Factors; Uremia; Vitamin D Deficiency

Topics: Calcium; Calcium Isotopes; Cholecalciferol; Creatinine; Humans; Hydroxycholecalciferols; Intestinal Absorption; Kidney Failure, Chronic; Peritoneal Dialysis; Phosphates; Renal Dialysis

Topics: Adolescent; Adult; Aged; Carbon Isotopes; Cholecalciferol; Chromatography; Female; Humans; Kidney Failure, Chronic; Malabsorption Syndromes; Male; Middle Aged; Osteomalacia; Silicon Dioxide; Tritium; Vitamin D; Vitamin D Deficiency

Topics: Biological Transport, Active; Calcium; Child; Cholecalciferol; Ergocalciferols; Humans; Intestinal Absorption; Kidney Failure, Chronic; Pigmentation; Protein Biosynthesis; Rickets; Skin; Vitamin D

Topics: Adolescent; Adult; Calcium; Cholecalciferol; Dihydrotachysterol; Female; Follow-Up Studies; Humans; Hydroxyproline; Hypoparathyroidism; Kidney Failure, Chronic; Male; Middle Aged; Spectrum Analysis; Thyroidectomy; Vitamin D

Topics: Animals; Bone and Bones; Bone Diseases; Bone Resorption; Carbon Isotopes; Cholecalciferol; Collagen; Hydroxyproline; Kidney Failure, Chronic; Male; Parathyroid Hormone; Proline; Rats; Skin; Tibia; Uremia

Topics: Animals; Bone and Bones; Bone Development; Bone Diseases; Bone Resorption; Calcitonin; Calcium Isotopes; Cholecalciferol; Culture Techniques; Dactinomycin; Hydroxyproline; Kidney Failure, Chronic; Parathyroid Hormone; Phosphates; Rats; RNA; Uremia

Topics: Animals; Bone and Bones; Bone Diseases; Calcium; Cholecalciferol; Humans; Kidney; Kidney Failure, Chronic; Liver; Rats; Uremia; Vitamin D

Topics: Animals; Biological Transport, Active; Bone Diseases; Calcium; Cholecalciferol; Duodenum; Intestinal Absorption; Intestinal Mucosa; Kidney Failure, Chronic; Male; Protein Binding; Rats; Tritium; Uremia; Vitamin D

Topics: Adolescent; Adult; Carbon Isotopes; Cholecalciferol; Chromatography; Female; Humans; Injections, Intravenous; Kidney Failure, Chronic; Male; Middle Aged

Topics: Alkanes; Animals; Carbon Isotopes; Cholecalciferol; Chromatography; Ethyl Ethers; Humans; Kidney Failure, Chronic; Methanol; Methods; Rats; Silicon Dioxide; Tritium

Topics: Adult; Calcium; Cholecalciferol; Humans; Intestinal Mucosa; Kidney Failure, Chronic; Liver; Tritium; Uremia

Topics: Bone Diseases; Cholecalciferol; Humans; Kidney Failure, Chronic; Uremia

The absorption and metabolism of vitamin D(3)-(3)H was studied in eight patients with chronic renal failure. Although the intestinal absorption of vitamin D(3)-(3)H was normal, the metabolic fate of the vitamin was abnormal as characterized by a twofold increase in fractional turnover rate, an abnormal accumulation of biologically inactive lipid-soluble metabolites, and the urinary excretion of both vitamin D(3)-(3)H and biologically inactive metabolites. Neither alterations in water-soluble vitamin D(3) metabolites nor qualitative abnormalities in protein-binding of vitamin D(3) were observed in the uremic subjects. Although hemodialysis proved ineffectual in reversing the observed abnormalities in vitamin D(3) metabolism and excretion, renal homotransplantation was completely successful in this regard. These experiments support the conclusion that the resistance to therapeutic doses of vitamin D often seen in patients with chronic renal failure and renal osteodystrophy results from an acquired defect in the metabolism and excretion of vitamin D.

Topics: Adult; Alkaline Phosphatase; Animals; Biological Assay; Blood Urea Nitrogen; Chloroform; Cholecalciferol; Chromatography; Electrophoresis; Feces; Female; Glomerulonephritis; Humans; Kidney Failure, Chronic; Kidney Transplantation; Male; Nephrotic Syndrome; Proteinuria; Pyelonephritis; Rats; Renal Dialysis; Transplantation, Homologous; Tritium