Changes in tissue-oxidative stress markers in an experimental model of laparoscopic donor nephrectomy.

Abstract

Laparoscopic donor nephrectomy (LDN) is associated with prolonged warm ischemia, which could potentially increase oxidative stress in the graft. Because pneumoperitoneum (Pp) used to facilitate LDN impairs renal perfusion, it could augment the effects of warm ischemia. Our experimental, randomized, controlled study with blind outcome assessment is the first to address this possibility. Wistar-Albino rats were randomized to 4 groups. Controls were subjected to a sham operation; the remainder were subjected to Pp with or without warm ischemia of differing durations. The kidneys were removed at the end of each experiment. The concentrations of malondialdehyde (MDA), protein carbonyl, and sulfhydryl groups and the activities of superoxide dismutase (SOD) and catalase were measured in renal samples as markers of oxidative stress. Renal samples were also evaluated histopathologically using light microscopy. Pp promoted oxidative stress in renal tissues, with an increase of MDA and protein carbonyls and a decrease in protein sulfhydryls and SOD activity. Warm ischemia exerted an additive effect on Pp-associated oxidative stress only when sustained for 10 minutes. These changes occurred in the absence of light-microscopic evidence of overt tissue damage. In an experimental model resembling LDN, Pp and 10 minutes of warm ischemia emerged as additive factors with respect to causing increased oxidative stress in the kidney. Because these effects imply subtle injury not only in the harvested kidneys of live donors but also in the kidneys the donors retain, avoiding Pp and warm ischemia above 5 minutes during LDN appears advisable.