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Compensatory renal growth and mitochondrial function: the influence of warm ischemia and reperfusion
Silvio Tucci1, Carlos Augusto Fernandes Molina, Adauto José Cologna
1Division of Urology, Department of Surgery and Anatomy, Ribeirão Preto Faculty of Medicine, University of São Paulo, SP, Brazil. stucci@convex.com.br
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 1st (6 rats) and 7th (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 7th 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.
