Renal Osteodystrophy with Special Emphasis on Secondary Hyperparathyroidism

Chronic uraemia is associated with severe disturbances in the calcium, phosphorus and vitamin D homeostasis, leading to the development of secondary hyperparathyroidism (HPT) with increased biosynthesis and secretion of parathyroid hormone (PTH) and hyperplasia of the parathyroid glands. Renal osteodystrophy (ROD) is a frequent and serious complication in chronic uraemic patients, which in a majority of patients is secondary to the severe disturbances in parathyroid homeostasis with high PTH levels leading to a high turnover bone disease, osteitis fibrosa, and with low PTH levels leading to a low turnover bone disease, the adynamic bone disease. Therapeutic strategies with a beneficial preRenal osteodystrophy with special emphasis on secondary hyperparathyroidism Ewa Lewin, Jinxing Huan, Klaus Olgaard Nephrological Department B, the Copenhagen County Hospital in Herlev, and Nephrological Department P, Rigshospitalet, Copenhagen, Denmark. Artigo Original ventive and/or therapeutic effect on HPT and the accompanying ROD in chronic uraemia include phosphate restriction, phosphate binders, low calcium dialysate, vitamin D analogs and calcimimetics. SECONDARY HYPERPARATHYROIDISM IN URAEMIA Secondary hyperparathyroidism (sec. HPT) develops early in renal insufficiency and may affect the function of several organs. The stimuli for the development of sec. HPT of relevance to renal failure are hypocalcaemia, hyperphosphatemia and low levels of 1,25(OH)2D . Hypocalcaemia increases the PTH gene expression per parathyroid cell, in-