Renal osteodystrophy--pathogenesis and treatment.
Histologic bone changes of osteitis fibrosa and osteomalacia are commonly present in patients with end-stage renal disease. Although many patients are not symptomatic from these bone changes, some patients are severely disabled. Altered metabolism of vitamin D, calcium, phosphorus, and parathyroid hormone occurs in renal failure and contributes to the development of uremic bone disease. This article reviews the current theories of pathogenesis and treatment of renal osteodystrophy. In addition, the clinical presentation, pathogenesis, and treatment of the various aluminum-associated osteomalacic syndromes in uremia are discussed.
D000535:Aluminum / Q000009:adverse effects; D001842:Bone and Bones / Q000033:anatomy & histology / Q000473:pathology; D002117:Calcitriol / Q000627:therapeutic use; D002118:Calcium / Q000378:metabolism; D002136:Calcium, Dietary / Q000008:administration & dosage; D012080:Chronic Kidney Disease-Mineral and Bone Disorder / Q000209:etiology / Q000378:metabolism / Q000628:therapy; D006801:Humans; D007676:Kidney Failure, Chronic / Q000378:metabolism; D010002:Osteitis Fibrosa Cystica / Q000209:etiology / Q000473:pathology; D010018:Osteomalacia / Q000209:etiology / Q000473:pathology / Q000628:therapy; D010281:Parathyroid Hormone / Q000378:metabolism; D010758:Phosphorus / Q000378:metabolism; D006435:Renal Dialysis; D014807:Vitamin D / Q000378:metabolism
D002136:Calcium, Dietary; D010281:Parathyroid Hormone; D014807:Vitamin D; D010758:Phosphorus; D000535:Aluminum; D002117:Calcitriol; D002118:Calcium