Patients with end-stage renal failure present with various debilitating forms of renal osteodystrophy characterized either by high bone turnover with or without mineralization defect or low bone turnover, that is, adynamic bone disease. Alterations in parathyroid hormone and calcitriol production do not completely account for the abnormalities in bone turnover. This suggest that other factors or mediators, or both, are involved in the regulation of bone turnover. Among them, the cytokine systems are of particular interest because of the following: cytokine production is altered in uremic patients; there are interactions between parathyroid hormone, calcitriol, and cytokines; and cytokines modulate bone cell number or activity, or both. Preliminary results of direct assessment of cytokines in bone of uremic patients are promising. Future research in this field should advance our knowledge of the intricate mechanisms that regulate bone turnover in renal osteodystrophy. This could provide a basis for better strategies in the control of bone abnormalities in uremic patients.
|Number of pages||6|
|Journal||Current Opinion in Nephrology and Hypertension|
|State||Published - 1997|
ASJC Scopus subject areas
- Internal Medicine