cholecalciferol and Chronic-Kidney-Disease-Mineral-and-Bone-Disorder

The prevalence of vitamin D deficiency in hemodialysis patients is high. While most hemodialysis patients are treated with activated vitamin D (1,25[OH]2D) to prevent renal osteodystrophy, clinical practices of the screening and treatment of 25(OH)2D deficiency are highly variable. It is unclear if nutritional vitamin D supplementation with D2 or D3 provides an additional clinical benefit beyond that provided by activated vitamin D treatment in this population.. We will conduct a systematic review of nutritional vitamin D (D2/D3) supplementation and health-related outcomes in hemodialysis patients according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The primary objective is to assess the impact of nutritional vitamin D supplementation on clinical outcomes relevant in hemodialysis patients, such as mortality, cardiovascular events, infections, and fractures. Secondary outcomes will include anemia, hyperparathyroidism, medication use (erythrocyte-stimulating agents, activated vitamin D), and quality of life. We will search MEDLINE, Scopus, Web of Science, and ClinicalTrials.gov for randomized, controlled trials of nutritional vitamin D supplementation (ergocalciferol/D2 or cholecalciferol/D3) in chronic hemodialysis patients. The Cochrane Risk Assessment Tool will be used to assess the quality of eligible studies. We will perform meta-analyses using standard techniques for the outcomes listed above if pooling is deemed appropriate/sufficient. The results of this systematic review may highlight gaps in our knowledge of the relevance of nutritional vitamin D in end-stage renal disease, allowing for the informed design of clinical trials assessing the impact of nutritional vitamin D therapy in the hemodialysis population in the future.. PROSPERO CRD42014013931.

Topics: Cardiovascular Diseases; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Clinical Protocols; Dietary Supplements; Ergocalciferols; Fractures, Bone; Humans; Infections; Renal Dialysis; Renal Insufficiency, Chronic; Research Design; Systematic Reviews as Topic; Vitamin D Deficiency; Vitamins

Renal osteodystrophy is the damage of bone morphology by CKD and treatment and occurred abnormal bone metabolism through renal dysfunction. It demonstrated that the control of P and Ca improves to normalization of mineral metabolism. Protein energy wasting and malnutrition are common in patients with CKD stage 5 and has been associated with life prognosis. In CKD patients, nutritional management is a critical role of treatment. Also it may be important of nutritional management that control P and Ca and improve nutritional status in renal osteodystrophy patients.

Topics: Bone and Bones; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Diphosphonates; Humans; Nutrition Therapy; Nutritional Status; Osteoporosis; Phosphorus; Prognosis; Protein-Energy Malnutrition; Renal Insufficiency, Chronic

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

Topics: 24,25-Dihydroxyvitamin D 3; Animals; Bone Resorption; Calcifediol; Calcitriol; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydroxycholecalciferols; Humans; Intestinal Absorption; Rickets; Vitamin D; Vitamin D Deficiency

Topics: 25-Hydroxyvitamin D 2; Calcitriol; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydrotachysterol; Ergocalciferols; Humans; Intestinal Absorption; Osteomalacia; Parathyroid Hormone; Vitamin D

It is now accepted that vitamin D is an integral part of a complex endocrine system, one with far-reaching implications in mineral metabolism. Reviews of the sources, functions and metabolism of vitamin D, as currently understood, are presented as a prelude to discussions of the role of vitamin D in calcium and phosphorous homeostatis and possible specific roles for vitamin D in mineralized tissues. Data describing a possible regulatory function for vitamin D in bone and bone protein metabolism are presented. Some of the controversy which presently exists regarding the biochemical mechanism of the action of this vitamin is discussed. Finally, the possible relationship of vitamin D and disorders of skeletal tissues is described.

Topics: Animals; Bone and Bones; Bone Resorption; Calcium; Cell Nucleus; Chemical Phenomena; Chemistry; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Glucocorticoids; Humans; Hydroxylation; Intestinal Mucosa; Kidney; Osteogenesis; Osteoporosis; Parathyroid Hormone; Proteins; Rats; Vitamin D; Vitamin D Deficiency; Vitamin D-Binding Protein

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

Topics: Animals; Bone Resorption; Calcitonin; Calcium; Cat Diseases; Cats; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dog Diseases; Dogs; Female; Hyperparathyroidism; Hyperparathyroidism, Secondary; Hypoparathyroidism; Kidney; Liver; Male; Parathyroid Diseases; Parathyroid Glands; Parathyroid Hormone; Parathyroid Neoplasms; Pregnancy; Tetany

During the past decade, an explosion of information has become available on the metabolism and function of vitamin D which is of great importance to clinicians in the treatment of metabolic bone disease. We have learned that vitamin D is the precursor of at least one hormone and that this hormone carries out functions in calcium and phosphorus metabolism bringing about mineralization of bone on one hand, and the prevention of hypocalcaemic tetany on the other. It may also function in the prevention of such degenerative bone diseases as osteoporosis. An important analogue of this hormone, 1alpha-hydroxyvitamin D3 has been prepared and is used successfully in the treatment of a variety of clinical conditions. This presentation will summarize these findings and their possible implications in these metabolic bone diseases.

Topics: Aged; Aging; Animals; Bone and Bones; Calcification, Physiologic; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Estradiol; Humans; Hydroxycholecalciferols; Kidney; Middle Aged; Osteoporosis; Parathyroid Hormone; Phosphorus; Rats; Vitamin D

Vitamin D3 gives rise to at least one hormone in which the kidney is utilized as an endocrine system. This hormone arises from 25-OH-D3 which in turn is synthesized in the liver from vitamin D3. The production of this calcium and phosphorus mobilizing hormone, namely 1,25-(OH)2D3, is strongly regulated by the need for calcium and phosphorus. The regulation of its production can occur only after initial 1,25-(OH)2D3 is made and brings about the appearance of 25-OH-D3-24hydroxylase. The need for calcium brings about a stimulation of parathyroid hormone secretion. The parathyroid hormone suppresses the 24-hydroxylase and stimulates the 1-hydroxylase. Alternatively, the need for phosphorus directly stimulates the 1-hydroxylase and suppresses the 24-hydroxylase. The 24-hydroxylation appears to be the initial reaction leading to the inactivation and excretion of vitamin D whereas the 1-hydroxylation is the reaction bringing about the activation of the molecule to 1,25-(OH)2D3. The 1,25-(OH)2D3, the 25-OH-D3 and an analog of 1,25-(OH)2D3, namely 1alpha-OH-D3, are potentially extremely useful in the treatment of metabolic bone diseases such as renal osteodystrophy, hepatically related disorders of calcium and bone metabolism, hypoparathyroidism, and vitamin D dependency disease. The 1alpha-OH-D3 is effective by virtue of its conversion to 1,25-(OH)2D3. The 25-hydroxylation of both 1alpha-OH-D3 and vitamin D3 itself occurs predominantly in the liver. Finally, it is not entirely settled whether 1,25-(OH)2D3 is active directly in all of the functions of viramin D or whether it must be further converted metabolically. A new metabolic pathway for vitamin D has been discovered in which 1,25-(OH)2D3 loses its 26 and 27 carbons to carbon dioxide, producing an unknown metabolite. It is not certain whether this pathway represents degradation of the 1,25-(OH)2D3 or its further activation.

Topics: 25-Hydroxyvitamin D3 1-alpha-Hydroxylase; Animals; Bone Development; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydroxycholecalciferols; Humans; Hydroxycholecalciferols; Intestinal Mucosa; Kidney; Liver; Muscles; Parathyroid Glands; Phosphorus; Steroid Hydroxylases; Structure-Activity Relationship; 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

Current status of our understanding of the metabolism of vitamin D and its implications in metabolic bone disease is reviewed. The details of metabolism of vitamin D3 to 25-hydroxyvitamin D3 in the liver and its further conversion in the kidneys to either 1,25-dihydroxyvitamin D3 or 24,25-dihydroxyvitamin D3 are presented. The latter conversions are regulated by the vitamin D status, serum calcium through the parathyroid gland system, and serum inorganic phosphorus concentration. The 1,25-dihydroxyvitamin D3 can now be regarded as a calcium- and a phosphate-mobilizing hormone and must be considered as one of the most important serum calcium-regulating hormones. Disruption of the vitamin D metabolic sequence or the signal system for 1,25-dihydroxyvitamin D3 results in several bone and calcium metabolism disorders such as renal osteodystrophy, hypoparathyroidism, pseudohypoparathyroidism, and vitamin D-dependency rickets. The use of the synthetic analogs of 1,25-dihydroxyvitamin D3 as well as 1,25-dihydroxyvitamin D3 itself in the management of these disease states is discussed.

Topics: Animals; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Endocrine Glands; Ergocalciferols; Homeostasis; Humans; Hyperparathyroidism, Secondary; Intestinal Absorption; Kidney; Phosphates; Vitamin D

Topics: Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Ergocalciferols; Feedback; Humans; Hypocalcemia; Kidney Diseases; Liver; Osteomalacia; Parathyroid Hormone; Rickets; Seasons; Ultraviolet Rays; Vitamin D

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

Topics: Bone and Bones; Bone Diseases; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Hydroxycholecalciferols; Hypoparathyroidism; Hypophosphatemia, Familial; Kidney; Liver Cirrhosis; Parathyroid Hormone; Phosphates; Protein Precursors; Pseudohypoparathyroidism; Vitamin D

Topics: Animals; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydrotachysterol; Dihydroxycholecalciferols; Humans; Hydroxycholecalciferols; Hypophosphatemia, Familial; Rats; Rickets; Vitamin D; Vitamin D Deficiency

Topics: Animals; Biological Transport; Bone and Bones; Calcium; Calcium, Dietary; Chemical Phenomena; Chemistry; Chickens; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydroxycholecalciferols; Feedback; Humans; Hydroxycholecalciferols; Hydroxylation; Intestinal Absorption; Kidney; Liver; Parathyroid Hormone; Phosphates; Rats; Skin; Vitamin D

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: Aluminum; Bone Regeneration; Calcium; Calcium Carbonate; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydrotachysterol; Dihydroxycholecalciferols; Ergocalciferols; Humans; Hydroxycholecalciferols; Intestinal Absorption; Osteitis Fibrosa Cystica; Osteomalacia; Parathyroid Glands; Phosphorus; Secretory Rate; 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: Aged; Anemia; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Double-Blind Method; Drug Administration Schedule; Female; Hepcidins; Humans; Male; Middle Aged; Polymorphism, Single Nucleotide; Renal Dialysis; Vitamin D

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

Topics: Alkaline Phosphatase; Calcium; Calcium Carbonate; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dialysis; Drug Therapy, Combination; Female; Humans; Hyperparathyroidism, Secondary; Male; Parathyroid Hormone; Phosphorus; Polyamines; Practice Guidelines as Topic; Sevelamer

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

Parathyroid hormone increases due to hypocalcemia even in the early phases of renal insufficiency. At the same time, hyperphosphatemia develops due to decreasing renal excretion which, in turn, intensifies secondary hyperparathyroidism. The cornerstones for prevention and therapy of renal osteopathy are, therefore, efficient lowering of phosphate levels and the early substitution of vitamin-D3 metabolites. In a post marketing surveillance (PMS) of almost 2,000 dialysis patients with renal osteopathy, the course of therapy with Alfacalcidol (Bondiol) was observed over a 6-month period. In 55.9% of cases, Alfacalcidol was administered at a daily dose of 0.25 microg. In 26.6% of patients, Alfacalcidol was administered every second day at a dose of 0.25-1 microg/d. In 16.1% of patients, Alfacalcidol was administered as pulse-therapy, mostly at a dose of 1-2 microg once or twice per week. To lower phosphate levels, 54.8% of patients received calcium compounds, 9.2% aluminium compounds, and 21.7% aluminium compounds in combination with calcium compounds. 14.3% of patients did not receive phosphate binding agents. Two thirds of patients had received active vitamin-D3-metabolites prior to commencing therapy with alfacalcidol, most frequently calcitrol. In 58.1%, the dialysis solution used had a calcium concentration of 1.5 mmol/l (44.8%) or lower; whereas in 41.9%, a higher calcium concentration was used--mostly 1.75 mmol/l (3 8%). During the observation period, serum concentrations of calcium and phosphate remained constant, suggesting that the risk of hypercalcemia due to therapy with Alfacalcidol was not increased. It was found that elevated alkaline phosphatase and parathyroid hormone levels could be significantly lowered (statistically). These effects could be observed both in patients who had been previously treated with vitamin-D3-metabolites and in patients without prior therapy. Efficacy and tolerability of therapy with Alfacalcidol was assessed to be very high by the attending nephrologists.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Alkaline Phosphatase; Aluminum Compounds; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Female; Humans; Hydroxycholecalciferols; Male; Middle Aged; Parathyroid Hormone; Phosphates; Product Surveillance, Postmarketing; Renal Dialysis; Treatment Outcome

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

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

We conducted a 7-month randomized, single, double, single-blind comparison of calcitriol (1,25(OH)2D3) with vitamin D3 in 22 hemodialysis patients to study the effects on the biochemical abnormalities associated with osteodystrophy. Calcitriol was given for 3 mo. All patients had initial prestudy calcium values less than or equal to 9.5 mg/100 ml, and phosphate values less than or equal to 4.5 mg/100 ml. Data were analyzed using the Normalized Trend Index (NTI). Calcitriol induced a rise in calcium (8.7 to 10.25 mg/100 ml) (p less than 0.001) and a fall in alkaline phosphatase (p less than 0.005), while D3 had no appreciable effect. The mean dose of calcitriol during treatment was 0.579 microgram/day while that for D3 was 706 IU/day. The effect on serum phosphate concentration was variable. Hypercalcemia as high as 13.2 mg/100 ml occurred in 2 of 13 patients on 1,25(OH)2D3, but in every instance promptly returned to normal with dose reduction. No other adverse effects were noted with therapy. We conclude that calcitriol reverses the biochemical abnormalities of osteodystrophy. Since its effects are rapidly reversed with discontinuation, the drug is probably safe as well as effective.

Topics: Adult; Aged; Alkaline Phosphatase; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Clinical Trials as Topic; Dihydroxycholecalciferols; Double-Blind Method; Female; Humans; Hydroxycholecalciferols; Male; Middle Aged; Renal Dialysis

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

Topics: Adult; Aspartate Aminotransferases; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Clinical Trials as Topic; Dihydroxycholecalciferols; Double-Blind Method; Female; Humans; Hydroxycholecalciferols; Hypercalcemia; Male; Middle Aged; Renal Dialysis

Abnormalities related to mineral and bone metabolism are a common finding in chronic kidney disease (CKD). Vitamin D compounds are often prescribed to CKD patients with the purpose to control secondary hyperparathyroidism and reduce the risk of high-turnover bone disease. However, data on the effect of vitamin D sterols on bone histology in non-dialysis CKD is limited.. A prospective controlled study was conducted on a cohort of 56 patients with CKD stages 3 and 4. 19 patients on calcitriol and 12 patients on cholecalciferol were compared to a group of 25 age- and sex-matched controls. Participants underwent a tetracycline double-labelled transiliac bone biopsy before starting therapy and again 12 months later. Changes from baseline in circulating biomarkers and bone histomorphometric parameters were analyzed.. Low-turnover bone disease was the most common pattern of renal osteodystrophy on the initial biopsy. There was no difference in biochemical or histomorphometric values between the three study groups at baseline. Serum intact parathormone (iPTH) and bone formation rate decreased significantly in calcitriol-treated patients, with prevalence of low-turnover bone disease doubling from baseline. In contrast, no significant changes were noted in cholecalciferol-treated and control subjects.. Calcitriol was effective in preventing secondary hyperparathyroidism and high-turnover bone disease. However, it was associated with an increased risk of developing or aggravating low-turnover bone disease. In the absence of a bone biopsy, calcitriol use in pre-dialysis CKD should be reserved for patients with a progressive rise in iPTH levels, in whom high-turnover bone disease is suspected.

Topics: Calcitriol; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dialysis; Humans; Hyperparathyroidism, Secondary; Parathyroid Hormone; Prospective Studies; Renal Dialysis; Renal Insufficiency, Chronic; Sterols; Vitamin D; Vitamins

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

Chronic kidney disease (CKD) is a progressive condition characterized by irreversible loss of functional nephron mass due to variety of causes; an inevitable complication of CKD is metabolic bone disease, and this pathology is called as renal osteodystrophy (ROD). In this study, we aimed to determine the levels of serum sRANKL and intracellular NF-κB levels in peripheral blood osteoclast precursor cells in patients with stage 3 CKD.. Forty-one male patients aged 35-60 with CKD identified as stage 3 according to GFR calculated on the basis of creatinine values and 27 healthy male subjects with age ranging from 40 to 60 as control group were included in this study. Levels of biochemical parameters, vitamin D3, parathyroid hormone, bone mineral density, sRANKL and NF-κB were determined by using photometric, electrochemiluminescence, HPLC, ELISA and flow cytometric methods in control and patient groups, respectively.. When stage 3 CKD patients were compared with controls, patients with stage 3 CKD had statistically significantly higher iPTH levels, but they had statistically significantly lower vitamin D3 levels. However, the other biochemical parameters, bone mineral density, sRANKL and NF-κB levels did not reveal any significance.. In conclusion, vitamin D3 and iPTH levels seem to be important parameters for evaluating the early stages of ROD. The lack of statistically significant differences in the levels of sRANKL and NF-κB suggests that these parameters are not sufficient in the evaluation of bone metabolism in the early stages of renal failure.

Topics: Adult; Bone Density; Case-Control Studies; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Male; Middle Aged; NF-kappa B; Osteoclasts; Parathyroid Hormone; RANK Ligand; Renal Insufficiency, Chronic; Stem Cells

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

Topics: Calcitriol; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Drug Therapy, Combination; Humans

During the course of chronic renal failure (CRF) in man, renal osteodystrophy (osteitis fibrosa and/or osteomalacia) gradually develops. The present study aimed to establish a similar type of CRF leading to renal osteodystrophy in rats. During progressive CRF development over 225 days after 5/6 nephrectomy, the following serum variables were measured: creatinine, immunoreactive parathyroid hormone (iPTH), 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), a25-hydroxyvitamin D3, (25(OH)D3), alkaline phosphatase, albumin, phosphate, urea nitrogen, total calcium, and other blood electrolytes. Subsequent to sacrifice, mechanical properties of the rat femur, bone histomorphometry (osteoid and eroded surfaces) and bone contents of calcium, phosphate and hydroxyproline were also examined. Serum creatinine in rats with CRF gradually escalated by some 70%, while circulating 1,25(OH)2D3 was reduced beneath detection level. Total plasma calcium and phosphate concentrations were, however, almost unchanged indicating that PTH-induced bone remodeling due to moderate hyperparathyroidism sustained calcium homeostasis. Alkaline phosphatase levels were reduced by some 50%, which reflects chronically impeded bone formation. Bone histomorphometry assessment revealed substantial elevation of resorption with moderate accompanying fibrosis in about 70% of afflicted animals. Bone calcium, phosphate and hydroxypyrroline contents remained unaltered. However, hydroxyproline/calcium ratio was marginally reduced. These results, together with altered mechanical bending stress characteristics and diminished diaphysis cross section area, confirm development of mixed bone lesions in the uremic animals. Our results are compatible with the early development of CRF in man. The established rat model is therefore useful in elucidating the precipitation and early treatment of renal osteodystrophy in humans.

Topics: Alkaline Phosphatase; Animals; Biomarkers; Bone and Bones; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Disease Models, Animal; Female; Hydroxyproline; Hyperparathyroidism, Secondary; Nephrectomy; Parathyroid Hormone; Rats; Rats, Wistar; Second Messenger Systems; Stress, Mechanical; Uremia

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

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

Topics: Calcitonin; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Ion Channels; Parathyroid Hormone; Phosphates

The generic term "Renal Osteodystrophy" is used to denote a complex of skeletal and metabolic impairments found in nephropathic patients. Neither dialytic treatment nor transplant is always capable of limiting the worsening evolution; transplantation, on the contrary, while it does not in many cases bring the phospho-calcic metabolism back to full normality, introduces new elements of imbalance arising as a result of the inevitable immunosuppressive therapy. After outlining the main post-transplant metabolic problems, the Authors discuss the manifestations of orthopaedic interest, in particular the most severe complication, i.e. aseptic necrosis.

Topics: Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Femur Head Necrosis; Hip Prosthesis; Humans; Kidney Transplantation; Metabolic Diseases; Nephrotic Syndrome; Osteonecrosis; Osteosclerosis; Parathyroid Hormone; Postoperative Complications; Radiography

Recognition over the last ten years of the fact that vitamin D does not act as such, but must be converted into a hormonal form, has filled in the picture physiological endocrine regulation of calcium and phosphate homeostasis. While vitamin D has thus lost the dietetic significance associated with it for over 50 years. Nevertheless, new interpretations of the aetiopathogenesis of many demineralizing bone diseases are of much greater utility. Nor is it futuristic to suppose that all the biochemical parameters establishing one of the metabolisms that are under strict homeostatic control in the body, such as that of calcium and that of phosphate, are understood.

Topics: Bone Diseases; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Glucocorticoids; Humans; Hypoparathyroidism; Iatrogenic Disease; Intestinal Absorption; Osteomalacia; Osteoporosis; Phosphates; Rickets; Vitamin D

Topics: Adult; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dietary Proteins; Energy Intake; Female; Humans; Male; Middle Aged; Renal Dialysis; Uremia

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

Elucidation of the vitamin D endocrine system and the availability of potent metabolites have led to new approaches to vitamin D therapy. The traditional management of exogenous (sunlight) or endogenous (malabsorption) vitamin D deficiency without evidence of disordered vitamin D metabolism has not changed, since it consists of treatment with vitamin D itself--a therapy which preserves the normal intrinsic mechanisms for regulating the rate of production of 1,25-dihydroxycholecalciferol. 1,25-DHCC and the analogue compound 1 alpha-CC should be reserved for treatment of hypocalcemia consequent on chronic renal failure or hypoparathyroidism, where 1-hydroxylation is lacking or impaired. Hypophosphatemic rickets has been treated with 1-hydroxylated compounds, with promising results; this use of the latter metabolites warrants further investigation. The use of vitamin D metabolites and of pharmacological doses of vitamin D itself must be regarded as substitution of a hormone or hormone precursors. Therefore, careful monitoring of serum and urine calcium is required in every patient receiving these compounds, in order to avoid excessive dosage. Special attention must be paid to patients with sarcoidosis since they often develop hypercalcemia after vitamin D or UV-light exposure, as a result of an intrinsic regulation defect in 1,25-DHCC synthesis.

Topics: Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydroxycholecalciferols; Humans; Hydroxycholecalciferols; Hypoparathyroidism; Osteomalacia; Phosphates; Vitamin D; Vitamin D Deficiency

Topics: Calcium Metabolism Disorders; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Ergocalciferols; Humans; Hypoparathyroidism; Osteomalacia; Osteoporosis; Phosphorus Metabolism Disorders; Renal Dialysis; Vitamin D

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

The comparative effectiveness of vitamin D3 and its derivatives in curing hyperparathyroidism and osteodystrophic bone lesions was examined in a laboratory model of renal osteodystrophy associated with marked secondary hyperparathyroidism in rats. The experimental model was prepared by a single injection of homologous glycopeptide. Plasma levels of 1 alpha,25-dihydroxyvitamin D3 [1 alpha,25(OH)2D3] appeared to decrease in the rats receiving glycopeptide. Various doses of vitamin D3 derivatives [2 or 10 microgram/kg D3, 2 microgram/kg 25-hydroxyvitamin D3 (25OHD3), 0.1 microgram/kg 1 alpha,25(OH)2D3, and 0.1 or 0.2 microgram/kg 1 alpha-hydroxyvitamin D3 (1 alpha OHD3)] were daily administered orally to the nephritic rats for 23 days before sacrifice. 1 alpha,25(OH)2D3 and 1 alpha OHD3 were much more potent than 25OHD3 and D3 in reducing the hyperplasia of parathyroir glands. The potency of 1 alpha OHD3 in curing the histological changes of osteodystrophy appeared to be greater than that of 1 alpha,25(OH)2D3. The same dose level of 1 alpha OHD3 was more effective than 1 alpha,25(OH)2D3 in enhancing plasma 1 alpha,25(OH)2D3 levels.

Topics: Animals; Bone and Bones; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydroxycholecalciferols; Disease Models, Animal; Glycopeptides; Hydroxycholecalciferols; Parathyroid Glands; Parathyroid Hormone; Rats; Structure-Activity Relationship

A half century ago, vitamin D was recognized as a vitamin. Now it has become clear that it is also a hormone--indeed the biochemical cornerstone of a major hormonal system involved in regulating the body's calcium economy. The active metabolite, calcitriol, produced in the kidney, acts on bone and intestine and has been found effective in therapy of osteodystrophy and perhaps other metabolic bone diseases.

Topics: Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Hypoparathyroidism; Hypophosphatemia, Familial; Osteoporosis; Phosphates; Phosphorus; Vitamin D

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

We evaluated oral 1,25-vitamin D3 for as long as 26 months in six prepubescent children with renal osteodystrophy previously treated with vitamin D2. Therapy was given at 14 to 41 ng per kilogram per day to correct hypocalcemia and reverse bone disease. Serum levels of 1,25-vitamin D3 were initially reduced at 15 +/- 5 pg per milliliter (mean +/- S.E.M.) and after treatment rose to 54 +/- 13. Serum calcium rose from 7.5 +/- 1.6 mg per deciliter (mean +/- S.D.) to 9.8 +/- 0.6 after one month (P less than 0.02). Alkaline phosphatase activity fell from 536 +/- 298 to 208 +/- 91 IU per liter after 12 months (P less than 0.05). Serum immunoreactive parathyroid levels fell from 900 +/- 562 microliter eq per milliliter 411 +/- 377. Healing of rickets and subperiosteal erosions was found. Remineralization of bone was demonstrated by the photon absorption technic. In four patients growth velocity, evaluated for 12 months before and after therapy, increased from 2.6 +/- 0.8 to 8.0 +/- 3.2 cm per year. Growth velocity per year increased from less than third percentile in each to the 10th to 97th percentile after therapy. Height increment ranged from 27 to 113 per cent of that expected for change in chronologic age and 40 to 114 per cent expected for change in bone age after therapy. This trial demonstrates that oral 1,25-vitamin D3 can reverse renal bone disease and increase growth in uremic children.

Topics: Administration, Oral; Adolescent; Alkaline Phosphatase; Body Height; Bone and Bones; Calcium; Child; Child, Preschool; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Female; Growth; Humans; Hypocalcemia; Infant; Magnesium; Male; Minerals; Parathyroid Hormone; Phosphorus; Radiography

Topics: Child; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans

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: Adolescent; Adult; Animals; Bone and Bones; Bone Resorption; Calcium; Child; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Hypoparathyroidism; Intestinal Mucosa; Kidney; Liver Cirrhosis, Biliary; Malabsorption Syndromes; Osteomalacia; Parathyroid Glands; Phosphorus; Rats; Renal Tubular Transport, Inborn Errors; Vitamin D

Topics: Adult; Aged; Bone and Bones; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Color; Drug Evaluation; Female; Humans; Male; Middle Aged; Radionuclide Imaging; Television

Topics: Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Hydroxycholecalciferols; Kidney; Kidney Diseases; Phosphates; Vitamin D

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

Topics: Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Methods; Parathyroid Glands

Importance sequelae of uremia are hormonal changes in calcium homeostasis combined with chronic calcium imbalance causing structural alteration and functional insufficiency of bone. Morphological findings of the so called renal osteodystrophy are osteomalacia, osteitis fibrosa and osteoporosis. Osteitis fibrosa and abnormal skeletal metabolism (changes of collagen turnover, insufficient maturation of stable bone crystals) impair the mechanical qualities of bone. Probably the uremia per se influences the collagen metabolism; additional factors such as secondary hyperparathyroidism and deficiency of vitamin D3 are discussed.

Topics: Animals; Bone and Bones; Bone Resorption; Calcification, Physiologic; Calcium Phosphates; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Collagen; Humans; Hydroxyapatites; Parathyroid Hormone; Protein Conformation; Uremia

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: Animals; Appetite Regulation; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Financing, Government; Graft Rejection; Growth Disorders; Humans; Kidney Transplantation; Kidneys, Artificial; Rats; Research; Transplantation, Homologous; Uremia

Topics: Biopsy, Needle; Bone and Bones; Calcium, Dietary; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Parathyroid Glands; Phosphates; Renal Dialysis; Uremia

Topics: Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Kidney; Liver; Terminology as Topic

Topics: Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Phosphorus

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: 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