25(OH)D3 in the Treatment of Juvenile Renal Osteodystrophy

Abstract

The previous speakers in this symposium have clearly and forcefully delineated the major clinical issues confronting pediatric nephrologists when they deal with azotemic renal osteodystrophy in childhood. These are as follows: (1) since chronic renal failure is no longer a fatal condition in children, renal osteodystrophy has emerged as one of its major but treatable complications (Houston, Mehls, Chesney); (2) when evaluated with increasingly sensitive and sophisticated laboratory techniques such as measurement of serum PTH and quantitative bone histology, patterns of subclinical renal osteodystrophy emerge relatively early in the course of chronic renal failure (Houston, Mehls); (3) it remains controversial as to whether or not subclinical renal osteodystrophy should be treated with vitamin D agents, or one should wait for the appearance of clinical abnormalities such as radiologic evidence of hyperparathyroidism (Houston); (4) our information about the spectrum of skeletal manifestations of juvenile renal osteodystrophy, particularly histology, is woefully inadequate and in need of improvement (Mehls); (5) now seems to be the time to test the hypothesis that aggressive therapy with vitamin D agents in very young children (under 5 years) with azotemic renal osteodystrophy may improve long-term growth by a sustained increase in growth velocity (Chesney, Norman); and (6) although each of the major vitamin D metabolites [25(OH)D; 24,25(OH)₂D₃; 1,25(OH)₂D] have been shown to improve one or more of the abnormalities in azotemic renal osteodystrophy, we do not yet know how to select the best metabolite or combination of metabolites to treat individual patients. Here the pattern of skeletal histology may play an important role (Houston, Norman).