Low molecular weight heparin protection against oxalate-induced oxidative renal insult.

BACKGROUND

Oxidative stress has emerged as an invariable feature of calculogenesis, the process of stone formation. The cytoprotective action of low molecular weight heparin (LMWH) in calcium oxalate-induced oxidative renal injury in experimental calculogenesis was studied.

METHODS

A renal membrane injury model involving gentamicin (40 mg/kg body weight) and 2% ammonium oxalate was used. Rats induced with gentamicin and ammonium oxalate were investigated for any impairment of cellular redox status as revealed by renal superoxide dismutase, catalase, glutathione peroxidase, xanthine oxidase activities and glutathione, ascorbate levels. In renal membrane protein activities such as aminotransferases in kidney and lactate dehydrogenase, total protein in urine of rats rendered lithogenic were assessed and compared with healthy vehicle-treated controls. The biochemical index of tissue lipid peroxidation was assessed in terms of malondialdehyde formation. LMWH was co-administered (250 microg/kg body weight) to gentamicin- and ammonium oxalate-dosed rats.

RESULTS

The extent of oxidative damage was indicated by the increased lipid peroxidation in the renal tissues of gentamicin- and ammonium oxalate-administered groups. The decline in the antioxidative status of the stone forming kidneys further confirmed the oxidative stress to renal cells. The extensive nephritic damage in the form of proteinuria was quite evident and the injured status of the tissue was reflected in the significant alterations of the few membrane associated enzyme levels in urine and the kidney. LMWH restricted all the cyto-oxidative ill effects of ammonium oxalate and gentamicin.

CONCLUSION

Low molecular weight heparin has antioxidant potential in countering the oxalate/calcium oxalate-mediated oxidative challenge in the experimental lithogenic model.