cholecalciferol and Glomerulonephritis

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

We aimed to determine the effect of a monthly oral vitamin D on the serum 25-hydroxyvitamin D levels and iPTH levels in patients with CKD.. This was a prospective controlled trial of 48 patients with CKD stage 3-4. Patients were divided into two groups Group1 the cholecalciferol treatment group, Group 2, the control group. One patient in Group 1, and 3 patients in Group2 were excluded after the baseline 25(OH)D levels were determined to be greater than 30ng/ml. Two patients in Group1, and one patient in Group 2 were excluded after the baseline iPTH was determined to be less than 70 pg/ml and greater than 300 pg/ml. Five patients in both groups were lost to follow-up. Thus, a total of 16 patients in Group 1 and 15 patients in Group2 completed the three month study. Group1 patients received 300,000 IU month oral cholecalciferol.. The mean serum 25(OH)D concentration of the group1 was significantly higher at baseline (P=0.039). At the end of the three months; serum 25 (OH) D level increased significantly in Group1 (P=0.001). iPTH level of Group1 was significantly lower at baseline (P=0.034). The values of the group1 before and end of third month was compared, serum Ca (P=0.011), P (P=0.013) level showed significant increase, but no significant increase in the Group 2 (P>0.05). The groups had not a clinically significant change in serum Ca and P level (P>0.05).. Oral cholecalciferol supplementation can be used safely and effective in reducing iPTH levels and correcting vitamin D insufficiency/deficiency in patients with CKD.

Topics: Administration, Oral; Adult; Aged; Bone Density Conservation Agents; Cholecalciferol; Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Diabetic Nephropathies; Female; Follow-Up Studies; Glomerulonephritis; Humans; Hyperparathyroidism; Hypertension; Male; Middle Aged; Parathyroid Hormone; Prospective Studies; Renal Insufficiency, Chronic; Risk Factors; Treatment Outcome; Vitamin D

Although vitamin K2 has been shown to prevent prednisolone-induced loss of bone mineral density of the lumbar spine in patients with chronic glomerulonephritis, the magnitude of this effect remains to be clarified. The aim of this prospective study is to compare the protective effect of vitamin K2 with that of vitamin D3 on prednisolone-induced loss of bone mineral density in patients with chronic glomerulonephritis.. Sixty patients (28 men, 32 women) were randomly divided into 4 groups (n = 15 each group): control (group C), vitamin D3 alone (alfacalcidol, 0.5 microg/d; group D), vitamin K2 alone (menatetrenone, 45 mg/d; group K), and vitamins D3 plus K2 (group D + K). Alfacalcidol and menatetrenone therapy were started at the same time as prednisolone. Bone mineral density of the lumbar spine (L2 to L4) was determined by means of dual-energy X-ray absorptiometry, and various biochemical parameters of calcium and bone homeostasis were assessed before and at the end of week 8 of treatment.. Treatment with prednisolone alone caused loss of bone mineral density, which could be fully prevented in groups D, K, and D + K. However, marked reductions in levels of several biochemical markers of both bone formation and resorption also were observed in all groups. The preventive effect in groups K and D + K on loss of bone mineral density induced by prednisolone was similar to that in group D. The elevation in serum calcium levels observed in group D was attenuated in group D + K.. Protective effects of vitamin K2 or vitamins D3 and K2 on prednisolone-induced loss of bone mineral density are similar to that of vitamin D3.

Topics: Adolescent; Adult; Bone Density; Bone Resorption; Cholecalciferol; Chronic Disease; Female; Glomerulonephritis; Glucocorticoids; Humans; Lumbar Vertebrae; Male; Middle Aged; Parathyroid Hormone; Prednisolone; Prospective Studies; Vitamin K 2

The aim of this study was to assess vitamin D status and bone density in steroid-treated children with glomerulopathies and to evaluate the effect of prophylactic vitamin D and calcium supplementation.. Retrospective analysis was performed on 55 children aged 4-18 yrs with glomerulopathies. The following data were analyzed: antropometrical parameters, bone densitometries, parathormone, 25-hydroxyvitamin D (25-OHD), urinary calcium excretion and medications received for prevention of low bone mass.. A significant number of children (38%) had decreased spinal bone mineral density (BMD z-score < -2.0) and the majority of them (89%) had hypovitaminosis D (25-OHD < 30 ng/ml), 75% were vitamin D insufficient (25-OHD < 20 ng/ml) and 16% were vitamin D deficient (25-OHD < 10 ng/ml). The mean serum 25-OHD concentration was comparable to that of controls (19.32 ± 12.87 vs. 15.05 ± 8.52 ng/ml). Nearly all patients (82%) were receiving preparations of calcium and/or vitamin D to improve bone health. Patients on cholecalciferol had higher mean concentration of 25-OHD compared to those who were not receiving it (p=0.027) and to the controls (p=0.047). In 23 children on vitamin D and calcium supplementation for an average 6-month time, we observed an increase in the mean BMD values (p=0.004), however, mean BMD z-score and 25-OHD concentrations did not significantly change over time.. Vitamin D and bone density deficits are remarkably common in steroid-treated children with glomerulopathies, despite vitamin D and calcium repletion. In order to enhance the effectiveness of vitamin D supplementation for improvement of bone density, we suggest regular assessment of serum concentration of 25-OHD that can guide subsequent dose adjustment of vitamin D.

Topics: Adolescent; Bone Density; Calcium; Cholecalciferol; Dietary Supplements; Female; Glomerulonephritis; Humans; Male; Retrospective Studies; Vitamin D

Light chain deposit disease is a plasma cell disorder characterized by production of a large amount of monoclonal immunoglobulin light chain or part of it, which is usually deposited as an amorphous substance in the kidneys. Immunotactoid glomerulopathy is an uncommon disease, which might be related to plasma cell dyscrasia, and characteristically manifest as organized glomerular ultra structural fibrils or microtubules. In this article, we report a case of a combined presentation of light chain disease and immunotactoid glomerulopathy in a patient with multiple myeloma and reversible advanced renal failure.

Topics: Anemia; Angiotensin-Converting Enzyme Inhibitors; Cholecalciferol; Erythropoietin; Glomerular Filtration Rate; Glomerulonephritis; Humans; Immunoglobulin kappa-Chains; Immunoglobulin Light Chains; Kidney Glomerulus; Male; Middle Aged; Recombinant Proteins; Treatment Outcome

To study possible correction of bone disorders (osteopenia, Ca/P-imbalance, bone pain, limited volume of indolent movements) which are still a serious complication associated with renal diseases and pathogenic therapy (steroids).. The bone disorders were treated in 10 uremic hemodialyzed patients (8 men, 2 women; group 1) with vitamin D3 (calcitriol made in Russia) + rhEPO (recormon; Boehringer Mannheim), in 15 patients (15 women, 0 men) with lupus-nephritis (group 2) with vitamin D3 (n = 5, group 2a) or miscalcic (Sandoz) (n = 10, group 2b), in 2 patients (2 men, 0 women) with glomerulonephritis (group 3) with vitamin D3 + miacalcic. Additionally all the patients received Ca salts. In groups 2 and 3 renal function was normal. The duration of the treatment was 3-6 months.. In all the groups we obtained an analgetic effect (attenuation of bone pain and more indolent movements), improvement of life quality, diminished need in analgetics, elevation of serum Ca level (p > 0.05).. Treatment of renal patients with bone affection with vitamin D3 and miacalcic has an analgetic effect, improves life quality.

Topics: Adult; Analgesics; Bone Diseases; Calcitonin; Calcium; Cholecalciferol; Drug Therapy, Combination; Erythropoietin; Female; Glomerulonephritis; Humans; Lupus Nephritis; Male; Middle Aged; Quality of Life; Recombinant Proteins; Renal Dialysis; Treatment Outcome; Uremia

Mercuric chloride (HgCl2) induces a lymphoproliferative disorder and autoimmune glomerulonephritis in Brown Norway (BN) rats. This syndrome is the consequence of T cell-dependent polyclonal B cell activation and autoantibody production. We have previously shown that HgCl2-induced autoimmune perturbations can be prevented in BN rats by the administration of cyclosporin A (CsA). The most potent vitamin D3 metabolite 1,25(OH)2 D3 (Vit D3) shares certain immunomodulatory properties with CsA. We therefore chose to compare the effects of Vit D3 to those of CsA in BN rats treated with HgCl2 in order to establish whether Vit D3 either alone or in combination with CsA can attenuate an autoimmune syndrome in vivo.. BN rats were treated with HgCl2 according to a standard protocol. Subgroups of rats were also given CsA alone, Vit D3 or synthetic analogues of Vit D3 alone, or combinations of both agents. Different doses and routes of administration were compared. The following markers of disease activity were evaluated: mortality, peak proteinuria, serum IgE concentrations, and renal immunoglobulin deposition.. Disease activity was markedly attenuated in all rats treated with CsA alone. Vit D3 and certain of its synthetic analogues administered alone also tempered the autoimmune process, but to a lesser extent than did CsA. The effect of CsA alone was so potent, that no additive or synergistic effects could be demonstrated when CsA was administered in combination with Vit D3.. Despite similar described immunomodulatory effects in vitro, CsA is clearly more effective than Vit D3 in preventing HgCl2 autoimmune disease in BN rats. This suggests that there is a difference in the cellular targets of these two agents in vivo, and/or a difference in the potency with which HgCl2-triggered immune activation is suppressed.

Topics: Animals; Autoimmune Diseases; Autoimmunity; Calcium; Cholecalciferol; Cyclosporine; Drug Therapy, Combination; Female; Glomerulonephritis; Immunoglobulin E; Immunosuppressive Agents; Lymphoproliferative Disorders; Male; Mercuric Chloride; Proteinuria; Rats; Rats, Inbred BN; Serum Albumin

Topics: Adolescent; Affective Symptoms; Age Factors; Cardiovascular Diseases; Child; Child, Preschool; Cholecalciferol; Depression; Erythropoiesis; Family; Female; Glomerulonephritis; Growth Disorders; Humans; Infant; Kidney Transplantation; Male; Renal Dialysis; Seizures; Terminal Care; Transplantation, Homologous; 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