LIPID-PEROXIDATION AND RENAL TUBULAR DAMAGE IN CHRONIC PANCREATIC DISEASES - IS THERE ANY RELATIONSHIP

Lipid peroxidation is one of the most important expressions of oxidati ve stress induced by oxygen-derived free radicals. Here we evaluate th e behavior of malondialdehyde (MDA) in the serum and urine from patien ts with chronic pancreatic diseases, with respect to patients with ext ra-pancreatic digestive diseases and glomerulonephritis. Serum and uri nary phospholipase A2 (PLA2) activity was also determined, since this enzyme contributes to damage of plasma membranes. MDA and PLA2 levels increased in the sera from most of the patients with pancreatic and ex tra-pancreatic digestive diseases. In glomerulonephritis, pathological MDA levels (36%), but not PLA2 levels, were found. Serum MDA correlat ed with gamma-glutamyl transpeptidase (GGT), while PLA2 correlated wit h alanine-phosphodiesterase (ALP), GGT, alanine-aminotransferase (ALT) and creatinine. In urine, MDA and PLA2 behaved differently from the c orresponding serum values. MDA increased in some patients with pancrea tic cancer, extra-pancreatic diseases and glomerulonephritis. PLA2 lev els did not significantly vary between groups. Urinary MDA correlated with some indicators of renal tubular damage [urinary ribonuclease, be ta-2-microglobulin (B-2-M) and N-acetyl-glucosaminidase (NAG)] and wit h serum bilirubin. Urinary PLA2 correlated only with ribonuclease (RNa se). We conclude that serum MDA increases aspecifically in pancreatic and extra-pancreatic diseases, probably reflecting an aspecific phlogi stic phenomenon; PLA2, although sharing a similar pattern with MDA, se ems mainly related to hepato-biliary damage. Urinary MDA reflects the presence of renal tubular damage, which may be the cause or a conseque nce of lipid peroxidation; little variations in PLA2 are recorded in u rine, and mainly reflect the presence of impaired tubular function.