Format

Send to:

Choose Destination
See comment in PubMed Commons below
Adv Ren Replace Ther. 1995 Jan;2(1):40-51.

The role of metabolic acidosis in the pathogenesis of renal osteodystrophy.

Author information

  • 1Division of Nephrology, Veterans Administration Medical Center, West Los Angeles, CA 90073, USA.

Abstract

Renal osteodystrophy is thought to be the result of abnormalities in the serum levels of parathyroid hormone, vitamin D, calcium, and phosphorus, and excess exposure to certain substances such as aluminum and iron. However, a significant amount of data suggest that the metabolic acidosis that develops in the course of chronic renal failure may also play a contributory role. Metabolic acidosis may effect changes in bone by directly inducing dissolution of bone, stimulating osteoclast-mediated bone resorption, inhibiting osteoblast-mediated bone formation, and altering the serum concentrations or the biological actions of parathyroid hormone and vitamin D. As a consequence, in some patients with normal renal function, osteoporosis and osteomalacia have been reported that are linked in part to metabolic acidosis. Also, in patients with chronic renal failure before and after initiation of dialysis, the severity of the metabolic acidosis appears to have a bearing on the presence and degree of hyperparathyroidism, osteitis fibrosa, and osteomalacia. Taken as a whole, these data suggest that correction of the metabolic acidosis of chronic renal failure may have a beneficial effect on the bone disease observed in these patients. This article reviews (1) the data indicating the mechanisms by which metabolic acidosis causes alterations in bone; (2) the types of bone lesions observed in animals and humans with metabolic acidosis in the presence of normal and abnormal renal function; (3) the impact of correction of the acidosis on the bone lesions; and (4) specific recommendations for treatment in patients with chronic renal failure both before and after initiation of maintenance dialysis.

PMID:
7614335
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Loading ...
    Write to the Help Desk