A. Muthukumar et R. Selvam, RENAL INJURY MEDIATED CALCIUM-OXALATE NEPHROLITHIASIS - ROLE OF LIPID-PEROXIDATION, Renal failure, 19(3), 1997, pp. 401-408
The role of lipid peroxidation (LPO) in renal tubular damage mediated
calcium oxalate retention was investigated in a rat model. Hyperoxalur
ia, without deposition of oxalate in kidney, was induced by administra
tion of ethylene glycol (EG), a precursor of oxalate. Oxidative stress
condition was produced by administration of buthionine sulfoximine (B
SO), an inhibitor of glutathione biosynthesis. BSO-treated rats showed
a significant (p < 0.001) increase in LPO over EG-treated rats and it
was almost doubled in BSO + EG treated rats. LPO was accompanied by s
ignificant urinary excretion of renal damage marker enzymes such as ga
mma-glutamyl transpeptidase (gamma-GT), alkaline phosphatase (ALP) and
cathepsin D, mucoproteins, and glycosaminoglycans (GACs) in the BSO a
nd BSO + EG groups but nor in the EG group. Urinary excretion of gamma
-GT (r = +0.90) (p < 0.001) and deposition of oxalate (r = +0.78) (p <
0.001) in kidney positively correlated with LPO. These results sugges
t that LPO initiates renal damage, thereby leading to calcium oxalate
retention and stone formation.