Oxalate-induced damage to renal tubular cells.
Our own studies and those of others have shown that the incidence of calcium oxalate stones and plaques is markedly increased by nephrotoxins. The possible role of oxalate as a nephrotoxin has not been fully appreciated. However, recent studies in experimental animals and in cultured cells support this possibility. The results of these studies led us to hypothesize that hyperoxaluria promotes stone formation in several ways: by providing a substrate for the formation of the most common form of renal stones, calcium oxalate stones, and by inducing damage to renal epithelial cells. Damaged cells in turn would produce an environment favorable for crystal retention and provide membranous debris that promotes crystal nucleation, aggregation and adherence. The present report summarizes evidence for oxalate nephrotoxicity and discusses the potential importance of oxalate toxicity in the pathogenesis of stone disease.
Scheid
C R
CR
Department of Physiology, University of Massachusetts Medical School, Worcester 01655-0127, USA. C Scheid@bangate.ummed.edu
Koul
H K
HK
Kennington
L
L
Hill
W A
WA
Luber-Narod
J
J
Jonassen
J
J
Honeyman
T
T
Menon
M
M
D000818:Animals; D002463:Cell Membrane Permeability / Q000187:drug effects; D002478:Cells, Cultured; D003460:Crystallization; D004848:Epithelium / Q000187:drug effects; D005609:Free Radicals; D007684:Kidney Tubules / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D010070:Oxalates / Q000633:toxicity*; D013552:Swine; D014545:Urinary Calculi / Q000209:etiology
D005609:Free Radicals; D010070:Oxalates