24-25-dihydroxyvitamin-d-3 and Chronic-Kidney-Disease-Mineral-and-Bone-Disorder

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

Evidence has emerged over the last several years indicating that aluminum accumulation in patients with chronic renal failure can cause certain forms of renal osteodystrophy, in particular osteomalacia and an aplastic lesion. The lines of evidence include epidemiological associations, chemical measurement and histological staining of bone aluminum, animal models of aluminum loading, and a favorable response to the removal of aluminum by chelation therapy. The primary sources of aluminum are dialysate solutions prepared from water with a high aluminum content and the oral ingestion of aluminum-containing phosphate binders. Desferrioxamine, a chelating agent with a high affinity for aluminum, can be used to remove aluminum during dialysis by increasing ultrafilterable plasma aluminum; preliminary results show that symptomatic patients markedly improve, both clinically and in their bone histology, after long-term chelation therapy with desferrioxamine. Treating water to ensure that aluminum levels are appropriately reduced in dialysate and the development of non-aluminum-containing phosphate binders are necessary to prevent aluminum-related osteodystrophy.

Topics: 24,25-Dihydroxyvitamin D 3; Aluminum; Animals; Bone and Bones; Calcitriol; Caseins; Chronic Kidney Disease-Mineral and Bone Disorder; Deferoxamine; Diet; Dihydroxycholecalciferols; Dogs; Drug Therapy, Combination; Humans; Osteomalacia; Parathyroid Hormone; Parenteral Nutrition, Total; Protein Hydrolysates; Rats; Renal Dialysis; Syndrome; Water Supply

Topics: 24,25-Dihydroxyvitamin D 3; Acidosis; Calcitriol; Calcium; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydroxycholecalciferols; Humans; Intestinal Absorption; Kidney Failure, Chronic; Phosphorus; Uremia; Vitamin D

Topics: 24,25-Dihydroxyvitamin D 3; Absorption; Adrenal Cortex Hormones; Anticonvulsants; Calcifediol; Calcitriol; Calcium; Chemical Phenomena; Chemistry; Chronic Kidney Disease-Mineral and Bone Disorder; Digestive System Diseases; Dihydroxycholecalciferols; Fanconi Syndrome; Female; Humans; Hydroxycholecalciferols; Hypocalcemia; Hypoparathyroidism; Hypophosphatemia, Familial; Infant, Newborn; Kidney Diseases; Kinetics; Liver Diseases; Menopause; Neoplasms; Osteomalacia; Osteoporosis; Rickets; Vitamin D

Topics: 24,25-Dihydroxyvitamin D 3; Adolescent; Adult; Aged; Animals; Bone and Bones; Calcifediol; Calcium; Child; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydroxycholecalciferols; Female; Humans; Hydroxycholecalciferols; Kidney Diseases; Middle Aged; Osteomalacia; Phosphates; Pregnancy; Rickets; Vitamin D

Twenty-three patients with end-stage renal failure on maintenance haemodialysis were treated with 1,25-dihydroxy vitamin D3 or 24-25-dihydroxy vitamin D3 for 3-32 months (total 232 patient months). Treatment with 1,25-dihydroxy vitamin D3 was marked by symptomatic, biochemical and histological improvements in the majority of patients. In contrast, treatment with 24,25-dihydroxy vitamin D3 produced no biochemical or histological improvements and such patients developed severe symptomatic bone disease. Successful renal transplantation resulted in rapid improvement in symptoms, biochemistry and bone histology in nine of 10 patients irrespective of whether prior treatment was with 1,25-dihydroxy vitamin D3, 24,25-dihydroxy vitamin D3 or both. During treatment with 1,25-dihydroxy vitamin D3 progressive reduction in dosage was required in the majority of patients because of hypercalcaemia, which was rapidly corrected by stopping treatment for a few days. Hypercalcaemia did not occur until serum alkaline phosphatase (AP) and amino terminal parathyroid hormone (N-PTH) had fallen towards normal. Treatment failure was uncommon in 1,25-dihydroxy vitamin D3-treated patients and was characterized by the early development of hypercalcaemia. Addition of 24,25-dihydroxy vitamin D3 in such patients rendered the hypercalcaemia more manageable but did not lead to any further improvement in biochemistry or bone histology. Treatment with 24,25-dihydroxy vitamin D3 was accompanied by the development of severe symptomatic bone disease in the majority of patients and a characteristic pattern of biochemical abnormalities with hypocalcaemia and rises in AP and N-PTH. Substitution of 1,25-dihydroxy vitamin D3 treatment for 24,25-dihydroxy vitamin D3 in these patients resulted in prompt improvement in clinical, biochemical and histological abnormalities. Successful renal transplantation was accompanied by rapid resolution of clinical, biochemical and histological features of renal osteodystrophy irrespective of whether previous treatment was with 1,25-dihydroxy vitamin D3 or 24,25-dihydroxy vitamin D3. Hypophosphataemia was common in the early months after renal transplantation without evidence of continuing hyperparathyroidism. The studies have confirmed that 1,25-dihydroxy vitamin D3 is effective in controlling clinical, biochemical and histological features of renal osteodystrophy while 24,25-dihydroxy vitamin D3 did not have a useful therapeutic effect in the dose used.

Topics: 24,25-Dihydroxyvitamin D 3; Adult; Bone and Bones; Calcitriol; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydroxycholecalciferols; Drug Therapy, Combination; Humans; Hypercalcemia; Kidney Failure, Chronic; Kidney Transplantation; Middle Aged; Time Factors

This study compares the effects of 1,25(OH)2D3 and 24,25(OH)2D3 alone or in combination on renal osteodystrophy in rats with chronic renal failure (CRF).. One month subsequent to 5/6 nephrectomy animals were divided into four groups and treated for one or four weeks with either vehicle, 1,25(OH)2D3, 24,25(OH)2D3 or 1,25(OH)2D3 + 24,25(OH)2D3. A sham-operated group with normal renal function matched for age and weight was used as control. At the termination of the study blood chemistry, parathyroid hormone (PTH) level and bone histomorphometry were analyzed.. The main findings were: amelioration of 1,25(OH)2D3-induced hypercalcemia by 24,25(OH)2D3, and similar suppression of PTH by the two metabolites of vitamin D when administered alone or in combination. Bone histomorphometry showed that 1,25(OH)2D3 alone exerts a potent proliferative effect on the osteoblasts but severely depresses their mineralizing capacity in a dose- and time-dependent manner. By contrast, 24,25(OH)2D3 improved the mineralizing activity with only a limited effect on osteoblast proliferation. Addition of 24,25(OH)2D3 potentiated the beneficial effect of 1,25(OH)2D3 on bone-resorbing parameters and corrected the mineralization failure.. Based on the above observations we suggest that the combined treatment with 1,25(OH)2D3 and 24,25(OH)2D3 markedly improves the morphologic and metabolic abnormalities of renal osteodystrophy.

Topics: 24,25-Dihydroxyvitamin D 3; Animals; Bone and Bones; Calcitriol; Calcium Channel Agonists; Chronic Kidney Disease-Mineral and Bone Disorder; Drug Therapy, Combination; Kidney Failure, Chronic; Male; Rats

We have previously established an uremic rat model which is suitable for investigating the effect of various treatment modalities on the progression of renal osteodystrophy [1]. Four months subsequent to 5/6 nephrectomy, animals were treated three times a week for 3 months with either vehicle, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], 1,25(OH)2D3 + 24,25-dihydroxyvitamin D3 [24,25(OH)2D3], 1,25(OH)2D3 + calcitonin (CT), or 1,25(OH)2D3 + 24,25(OH)2D3 + CT. At termination of the study, clinical chemistry, chemical composition, and mechanical properties of femurs, calvarial parathyroid hormone (PTH)-elicited adenylate cyclase (AC), and phospholipase C (PL-C) activities, femoral cross-sectional area, and bone histomorphometry were analyzed. The main findings were that 1,25(OH)2D3 +/- 24,25(OH)2D3 treatment enhanced elasticity as well as time to fracture at the femoral metaphysis. CT potentiated the increase in elasticity obtained by 1,25(OH)2D3 +/- 24,25(OH)2D3 treatment. Only 24,25(OH)2D3 administration rectified the supernormal PTH-stimulated uremic bone AC, and only 1,25(OH)2D3 medication normalized the diminished CT-elicited AC. The obliterated uremic bone PTH-sensitive PL-C was fully normalized by all drug regimens. Femoral shaft inner zone diameter was enhanced by uremia, however, all drug treatments normalized it. Ditto effect was registered with either drug treatment on the subnormal outer and inner zone widths. Histomorphometrical analyses showed that 1,25(OH)2D3 administration reduced both eroded and osteoid surfaces. Most prominently, adjuvant 24,25(OH)2D3 or CT administration potentiated the beneficial effect of 1,25(OH)2D3 on fibrosis and osteomalacia. We assert that vitamin D3 treatment markedly reverses the development of renal osteodystrophy, and CT potentiates the effect of vitamin D3.

Topics: 24,25-Dihydroxyvitamin D 3; Adenylyl Cyclases; Animals; Bone and Bones; Bone Density; Calcitonin; Calcitriol; Calcium; Chronic Kidney Disease-Mineral and Bone Disorder; Creatinine; Disease Models, Animal; Drug Administration Schedule; Female; Femur; Rats; Rats, Wistar; Type C Phospholipases; Uremia

A prospective study was made of sequential changes in the metabolism of vitamin D and calcium in 19 allograft recipient during the first year after successful renal transplantation. All but one of the patients received cyclosporine A combined with corticosteroids and azathioprine as immunosuppressive therapy. Shortly after transplantation most patients showed transient hypocalcemia and hypophosphatemia. At the time of transplantation 17 of 19 patients had an elevated plasma intact parathyroid hormone (PTH) level, and at the close of follow-up one in four patients. In six other patients intact PTH was within the reference range, but high in relation to simultaneously measured serum ionized calcium. According, one year after transplantation less than half of the patients showed complete resolution of hyperparathyroidism. The change towards normal in the metabolism of vitamin D began within the first post-transplantation week irrespective of the onset of diuresis. One to two weeks after transplantation 1,25(OH)2D3 and 24,25(OH)2D3 reached the lower limit of normal range. In these renal allograft recipients who received cyclosporine A the long-term values of serum 1,25(OH)2D3 did not differ from those of normal subjects.

Topics: 24,25-Dihydroxyvitamin D 3; Adult; Calcifediol; Calcitriol; Calcium; Chronic Kidney Disease-Mineral and Bone Disorder; Creatinine; Female; Follow-Up Studies; Humans; Kidney Failure, Chronic; Kidney Function Tests; Kidney Transplantation; Male; Middle Aged; Osteocalcin; Parathyroid Hormone; Phosphates; Postoperative Complications; Prospective Studies; Serum Albumin; Vitamin D

An increasing body of experimental data suggests a role for 24,25(OH)2D3 in bone metabolism. The present study was carried out to assess a possible therapeutic role of this vitamin D metabolite in renal osteodystrophy. Twenty-two chronic dialysis patients, most of whom were previously maintained on 1 alpha (OH)D3 therapy, received additional treatment with 10 micrograms/day 24,25(OH)2D3 and were compared to 19 patients receiving 1 alpha (OH)D3 alone. Analysis of transiliac bone biopsies obtained at study entry and following 10-16 months of treatment revealed that the combined therapy produced a decrease in bone turnover. Specifically, the addition of 24,25(OH)2D3 inhibited an increase in trabecular bone volume (BV/TV) and suppressed osteoclastic parameters. Thus BV/TV increased from 26.2 +/- 8.6 to 32.1 +/- 7.5% (p < 0.01) in the 1 alpha (OH)D3 group, but it remained unchanged in the combined therapy group. In contrast, the eroded surface (ES/BS), the osteoclast surface (Oc.S/BS), and the osteoclast numbers were significantly suppressed in patients receiving both 24,25(OH)2D3 and 1 alpha (OH)D3, as compared with those receiving 1 alpha (OH)D3 alone (p < 0.01, p < 0.01, and p < 0.001, respectively). These improvements were independent of changes in 1 alpha (OH)D3 dosage. The extent of bone aluminium deposits was unrelated to the administration of 24,25(OH)2D3 or to its effect. 24,25(OH)2D3 therapy was not associated with any adverse effects.

Topics: 24,25-Dihydroxyvitamin D 3; Adult; Aged; Alkaline Phosphatase; Bone Density; Calcium; Chronic Kidney Disease-Mineral and Bone Disorder; Creatinine; Drug Therapy, Combination; Female; Humans; Hydroxycholecalciferols; Male; Middle Aged; Phosphates; Renal Dialysis

The rate of aluminium accumulation in bone may be related to the presence of vitamin D metabolites. The present study investigated the effect of 1,25(OH)2D3 (24 pmol/d s.c.) and 24R,25(OH)2D3 (480 pmol/day), combined or alone, on the deposition of aluminium (119 mumol/kg per day) in bone of uraemic rats during concomitant parenteral administration of aluminium for 9 weeks. Bone histomorphometry of trabecular bone revealed a severe low-turnover osteodystrophy in aluminium-treated uraemic rats, as evidenced by a decrease in osteoblastic osteoid surfaces and mineral apposition rates. 1,25(OH)2D3 as well as 24R,25(OH)2D3 decreased stainable bone aluminium and the aluminium content of trabecular bone and, in parallel, the number of osteoblasts and osteoclasts increased. Additional treatment with one or both vitamin D metabolites 14 days prior to the aluminium load further improved these results. Despite these effects, dynamic histomorphometric parameters remained suppressed and osteoidosis persisted. Serum PTH concentrations were significantly elevated in aluminium-loaded uraemic rats treated with 24R,25(OH)2D3 alone compared to controls. In conclusion, administration of 1,25(OH)2D3 or 24R,25(OH)2D3 reduces the accumulation of aluminium in trabecular bone in uraemic rats and prevents some of its excess toxicity. The mechanism of action may be different for either vitamin D metabolite; however, combined treatment does not result in further reduction of the accumulation rate of aluminium in bone in this model.

Topics: 24,25-Dihydroxyvitamin D 3; Aluminum; Animals; Bone and Bones; Calcitriol; Chronic Kidney Disease-Mineral and Bone Disorder; Male; Premedication; Rats; Rats, Inbred Strains; Uremia

Uraemic rats maintained on either a high or a low phosphate diet for 12 weeks were allocated to one of the following oral vitamin D treatment groups and received: 1,25-dihydroxycholecalciferol [1, 25-(OH)2D3], 24,25-dihydroxycholecalciferol [24,25-(OH)2D3], both 1,25-(OH)2D3 and 24,25-(OH)2D3, or no vitamin D supplements. Mean serum creatinine concentrations were elevated to a similar extent in all groups. Mean serum concentrations of calcium, phosphate and alkaline phosphatase were not significantly different from normal in any of the groups. In the group receiving the high phosphate diet and no vitamin D supplements, calcified bone area measured by quantitative computerized histomorphometry was significantly lower than in the group receiving the low phosphate diet and no vitamin D supplements (0.01 greater than P greater than 0.001), and in the groups receiving high phosphate diet and either 1,25-(OH)2D3 (0.01 greater than P greater than 0.001) or 24,25-(OH)2D3 (0.01 greater than P greater than 0.001). We conclude that uraemic rats maintained on a high phosphate diet for 12 weeks develop skeletal demineralization, this process does not occur in rats on a low phosphate diet, and a decrease in calcified bone area may be prevented by treatment with either 1,25-(OH)2D3 or 24,25-(OH)2D3.

Topics: 24,25-Dihydroxyvitamin D 3; Animals; Bone Diseases, Metabolic; Calcinosis; Calcitriol; Chronic Kidney Disease-Mineral and Bone Disorder; Creatinine; Dihydroxycholecalciferols; Male; Nephrectomy; Phosphates; Rats; Rats, Inbred Strains; Uremia

Twenty-three patients with end-stage renal failure treated by hemodialysis or transplantation were followed for up to 10 years. Sequential full thickness iliac crest bone biopsies were obtained to assess the effects on bone disease of hemodialysis, treatment with 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] and 24,25-dihydroxycholecalciferol [24,25-(OH)2D3] and renal transplantation. The biopsies were analyzed by a computerized histomorphometric technique which allowed accurate measurements of calcified bone and osteoid areas. Serum aluminum and parathyroid hormone concentrations were also monitored. Hemodialysis was associated with a loss of calcified bone and an increase in osteoid areas. The progressive bone loss was arrested but not reversed following treatment with either 1,25-(OH)2D3 or 24,25-(OH)2D3. Osteoid area was unchanged or reduced following treatment with 1,25-(OH)2D3 in all but three patients who had serum aluminum concentrations in excess of 5 mumol/l. 24,25-(OH)2D3 was not effective in reducing osteoid area, and combined treatment with 1,25 and 24,25-(OH)2D3 had no effect beyond that expected with 1,25-(OH)2D3 alone. Bone biopsies showed loss of calcified bone and an increase in osteoid areas one year and more after successful renal transplantation in five patients. Nineteen of the 23 patients developed serum aluminum concentrations greater than 3 mumol/l, probably because of the use of oral aluminum hydroxide as a phosphate binding agent. In these patients serum parathyroid hormone concentrations greater than 600 pg/ml appeared to prevent the development of osteopenia.

Topics: 24,25-Dihydroxyvitamin D 3; Aluminum; Bone and Bones; Calcitriol; Chronic Kidney Disease-Mineral and Bone Disorder; Computers; Dihydroxycholecalciferols; Drug Therapy, Combination; Follow-Up Studies; Histological Techniques; Humans; Kidney Failure, Chronic; Kidney Transplantation; Parathyroid Hormone; Renal Dialysis

The effect of administration of 25 micrograms 24,25-dihydroxyvitamin D3 (24,25(OH)2D) combined with dihydrotachysterol (DHT2) on clinical, radiological, biochemical and bone histological parameters was assessed in ten children on chronic hemodialysis. Eight children had been treated with DHT2 prior to administration of 24,25(OH)2D. Addition of 24,25(OH)2D to the treatment resulted in a decrease in serum calcium values. Therefore higher doses of DHT2 were required to maintain serum-calcium levels between 2.4-2.8 mmol/l. Administration of 24,25(OH)2D did not modify the quality of bone, but histomorphometric investigation did show a significant reduction of the surface percentage of bone trabecula, in the iliac crest, covered with osteoclasts (oc%). Following the administration of 24,25(OH)2D an increase in bone mineralization was shown by X-rays of the wrists and measured by dual photonabsorptiometry. Addition of 24,25(OH)2D to the DHT2 treatment resulted in an increase in serum concentration of 24,25(OH)2D and a decrease in DHT2 levels. The present study suggests that administered 24,25(OH)2D interferes with DHT2 metabolism and increases DHT2 tolerance. Increased bone mineralization may be related to 24,25(OH)2D, a higher dose of DHT2 or both.

Topics: 24,25-Dihydroxyvitamin D 3; Adolescent; Bone and Bones; Calcium; Child; Child, Preschool; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydrotachysterol; Dihydroxycholecalciferols; Drug Therapy, Combination; Female; Humans; Kidney Failure, Chronic; Male; Minerals; Renal Dialysis

Controversy exists as to whether 24,25(OH)2D3 has a direct inhibitory effect on parathyroid hormone (PTH) secretion. Therefore, the present investigation examined the effect of long-term administration of 24,25(OH)2D3 on immunoassayable PTH levels (iPTH) and bone histology in dogs with chronic renal failure. Chronic renal failure was produced in 16 dogs, half of which served as controls whereas the other half received 2.5 micrograms/day of 24,25(OH)2D3, orally. Serum iPTH, serum total, ionized calcium, serum phosphorus, and creatinine were followed at weekly or biweekly intervals in both groups. Also, creatinine clearances, serum levels of 25(OH)D3, 24,25(OH)2D3, and 1,25(OD)2D3 and the intestinal absorption of calcium were measured. After 1 year of chronic renal failure the dogs were sacrificed and rib biopsy specimens were obtained for histological examination and measurement of mineral content. Serum iPTH increased equally in the two dog groups with no effect at any time of 24,25(OH)2D3 treatment, despite a significant increase in the serum levels of 24,25(OH)2D3 and a concomitant decrease of the 1,25(OH)2D3 levels. There was no difference in the levels of serum calcium or in the calcium content of bone. Furthermore, after 8 months of uremia three control dogs were switched to the group treated with 24,25(OH)2D3 and followed for another 7 months. No suppressive effect of administering 24,25(OH)2D3 on the iPTH levels could be demonstrated in these three dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: 24,25-Dihydroxyvitamin D 3; Animals; Bone and Bones; Calcium; Chronic Kidney Disease-Mineral and Bone Disorder; Creatinine; Dihydroxycholecalciferols; Dogs; Female; Intestinal Absorption; Kidney Function Tests; Magnesium; Osteoclasts; Parathyroid Hormone; Uremia

We measured peritoneal losses of the active vitamin D metabolites 1,25(OH)2D3 and 24,25(OH)2D3 in patients receiving continuous ambulatory peritoneal dialysis (CAPD). The serum concentration of 24,25(OH)2D3 was considerably lower than in hemodialysis patients. The serum concentration of 1,25(OH)2D3 was undetectable and rose to levels similar to those in hemodialysis patients only after loading with much higher oral doses of 1-alpha-vitamin D3 than those received by hemodialysis patients. Losses of both metabolites in peritoneal fluid were considerable, averaging approximately 6-8% of the plasma pool per day. These losses lead to low serum levels of these active vitamin D metabolites in CAPD patients, which may be an important factor in exacerbating renal osteodystrophy. Our results indicate the need for increased replacement doses of vitamin D metabolites in CAPD patients.

Topics: 24,25-Dihydroxyvitamin D 3; Ascitic Fluid; Blood Proteins; Calcitriol; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydroxycholecalciferols; Humans; Kidney Failure, Chronic; Peritoneal Dialysis; Peritoneal Dialysis, Continuous Ambulatory

Topics: 24,25-Dihydroxyvitamin D 3; Calcifediol; Calcitriol; Calcium; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydroxycholecalciferols; Ergocalciferols; Humans; Hydroxycholecalciferols; Hypoparathyroidism; Intestinal Absorption; Osteomalacia; Osteoporosis; Rickets; Tetany; Vitamin D

Histomorphometric studies of bone biopsies were performed on 12 hemodialyzed patients before and after six months of treatment with 25-(OH) and 1 alpha-(OH) vitamin D3. Patients could be classified into three groups according to bone resorption: Group I with normal bone resorption; Group II with elevated initial bone resorption unresponsive to vitamin D treatment; group III with elevated initial bone resorption sensitive to vitamin D treatment. None of the patients had histological signs of osteomalacia. In Group I, plasma concentrations of 24,25-(OH)2D and the ratio of 24,25-(OH)2D to 25-(OH) D remained in the normal range throughout the study; in Group II these parameters were subnormal initially and did not increase above normal except in one case; in Group III, plasma concentrations of 24,25-(OH)2D were high before or at the beginning of vitamin D administration and normal at the time of the second biopsy and wide variations were observed in the ratio of 24,25-(OH)2D to 25-(OH)D. No difference was found between these last two groups with regard to the cumulative dose of vitamin D derivatives administered or the changes in plasma PTH, CT, calcium and phosphate. These observations suggest a specific regulation of plasma 24,25-(OH)2D concentrations in hemodialyzed patients and a possible link (independent of circulating PTH, CT, or phosphate) between this regulation and healing of bone resorption. However, no correlation was found between plasma 24,25-(OH)2D and either one of the simultaneously measured biochemical or histological parameters.

Topics: 24,25-Dihydroxyvitamin D 3; Adult; Bone Resorption; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydroxycholecalciferols; Female; Humans; Male; Middle Aged; Parathyroid Hormone; Renal Dialysis

24,25(OH)2D3 has been compared with 1,25(OH)2D3 in the treatment of renal osteodystrophy. Treatment with 24, 25(OH)2D3 2 micrograms/day for 5-7 months was accompanied by deterioration in clinical, biochemical, radiological and histological features of osteodystrophy with no increase in Ca absorption. In contrast, treatment with 1,25(OH)2D3 0.25--1 microgram/day for 6-15 months resulted in rapid improvement in clinical, biochemical, radiological and histological features and a return of Ca absorption to normal. It is concluded that in the dose used 24,25(OH)2D3 alone is not an effective treatment for renal osteodystrophy.

Topics: 24,25-Dihydroxyvitamin D 3; Adult; Alkaline Phosphatase; Calcitriol; Calcium; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydroxycholecalciferols; Humans; Hydroxycholecalciferols; Middle Aged; Phosphates

Topics: 24,25-Dihydroxyvitamin D 3; Adult; Bone and Bones; Bone Resorption; Calcifediol; Calcitriol; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydroxycholecalciferols; Female; Humans; Hydroxycholecalciferols; Male; Middle Aged; Nephrectomy; Renal Dialysis; Uremia