RENAL INJURY MEDIATED CALCIUM-OXALATE NEPHROLITHIASIS - ROLE OF LIPID-PEROXIDATION

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.