Long-term therapy of uremic osteodystrophy in adults with calcitriol.
Patients with end-stage renal failure develop osteodystrophy in part due to defective production of 1,25-dihydroxycholecalciferol by the kidney. We treated eight adults with chronic renal failure and osteodystrophy with 1,25-dihydroxycholecalciferol (calcitriol) for 30-44 months. Seven of these patients were also symptomatic with bone pain and/or muscle weakness. Striking amelioration of muscle weakness occurred, and bone pain was considered to be significantly improved in four of seven patients. Hypercalcemia was noted in all the patients, necessitating a reduction in the daily dose of calcitriol to a range of 0.125 to 0.5 microgram/day. While serum alkaline phosphatase fell during therapy, serum iPTH did not show any significant change. Bone mineral content improved in four patients, though it still remained below normal. Radiographic changes of osteodystrophy showed definite improvement in only three.
D000328:Adult; D000469:Alkaline Phosphatase / Q000097:blood; D001842:Bone and Bones / Q000378:metabolism; D002117:Calcitriol; D002118:Calcium / Q000097:blood; D012080:Chronic Kidney Disease-Mineral and Bone Disorder / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000378:metabolism; D004100:Dihydroxycholecalciferols / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D006887:Hydroxycholecalciferols / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D008903:Minerals / Q000378:metabolism; D010281:Parathyroid Hormone / Q000276:immunology; D011859:Radiography; D011884:Radius / Q000378:metabolism
D004100:Dihydroxycholecalciferols; D006887:Hydroxycholecalciferols; D008903:Minerals; D010281:Parathyroid Hormone; D000469:Alkaline Phosphatase; D002117:Calcitriol; D002118:Calcium