Methylglyoxal increase in uremia with special reference to snakebite-mediated acute renal failure

Abstract

BackgroundAdvanced glycation and lipoxidation endproducts (AGEs and ALEs) due to oxidative and carbonyl stress are involved in pathogenesis of several diseases including uremia. Methylglyoxal, a dicarbonyl compound is a metabolic hazard and potent glycating agent in the body, which is an important precursor of AGE and ALE. Methylglyoxal has been reported to be increased in uremia, but there is no report of MG status in snake venom mediated acute renal failure cases (SARF). We investigated the carbonyl and oxidative stress as well as the methylglyoxal concentration in SARF where renal clearance is rapidly shut down. MethodsWe studied serum carbonyl compounds, methylglyoxal, total antioxidant status, GSH and cellular damage marker thiobarbituric acid reacting substances (TBARS) and intracellular erythrocytic GSH concentration following standard methods of 45 SARF and 56 normoglycemic chronic renal failure cases (CRF) and compared with 81 normal controls. ResultMethylglyoxal concentration has been found to be significantly increased in SARF associated with decreased concentration of serum as well as erythrocytic GSH and other antioxidant markers , in comparison with CRF and normal control. The cellular damage (TBARS concentration), is also found increased in SARF. ConclusionMG increase as well as accumulation due to GSH depletion may play a pivotal role in their rapid pathophysiological complicacies in SARF.