Compensatory renal growth and mitochondrial function: the influence of warm ischemia and reperfusion Hipertrofia renal compensatória e função mitocondrial: influência da isquemia quente e reperfusão

Purpose: To evaluate the influence of ischemia/reperfusion injury on renal compensatory growth (CGR) and mitochondrial function. Methods: Forty five Wistar rats were divided in 3 groups: Control Group (GC) – 21 rats were submitted to a sham laparotomy and sacrificed at 1 (6 rats) and 7 (15 rats) postoperative days to evaluate the dry weight of both kidneys and their growth during 1 week (6 rats) and to quantify mitochondrial respiration (9 rats); Group 1 (G1) 12 rats underwent right nephrectomy and were sacrificed 7 days later for analysis of renal mitochondrial function (6 rats) and dry weight (6 rats). Group 2 (G2) – renal warm ischemia for 60 minutes followed by right nephrectomy was performed in 12 rats; they were sacrificed 7 days later to evaluate renal mitochondrial function (6 rats) and dry weight (6 rats). Results: Dry weight (mg) of left kidneys at 7 day: GC 219±18, G1 281±23 and G2 338±39 (GCxG1 p<0.01; GCxG2 p<0.001; G1xG2 p<0.01). State 4 mitochondrial respiration rate and respiratory control ratio (RCR) were similar in all groups (p>0.05). State 3 respirations (mM/min/mg) in GC, G1 and G2 was respectively: 99±23, 132±22 and 82±44 (p<0.02; the only statistical difference noted was between groups G1xG2 – p<0.05). Conclusions: Following unilateral nephrectomy CRG is associated with an increase in state 3 of mitochondrial respiration. Renal ischemia/reperfusion injury enhances the CRG provoked by unilateral nephrectomy but such enhancement seems independent on mitochondrial respiration.