EFFECT OF CHRONIC IMMOBILIZATION STRESS ON KIDNEY FUNCTION IN RENAL ISCHEMIA/REPERFUSION RAT MODEL

Abstract

Background: Renal ischemia/reperfusion (I/R) injury, a common and important cause of acute kidney injury (AKI), is considered a major socioeconomic health problem. Stress, a state of disrupted normal homeostasis is known to trigger the progression of many illnesses. Objectives: This study was designed to determine changes in renal function and structure induced by renal I/R in rats subjected to chronic immobilization stress and to elucidate the possible underlying mechanism(s). Materials and Methods: Forty seven adult male albino rats were allocated into 3 groups: Group I: Sham-Operated Control, Group II: Renal I/R in which rats were subjected to 45 minutes ischemia followed by 24 hours of reperfusion, and Group III: Stressed Renal I/R in which rats were separately subjected to immobilization stress, 2 hours/day for 4 weeks, and then exposed to renal I/R procedure. All rats were subjected to determination of body weight (BW) and kidney weight (KW), plasma levels of creatinine, urea and tumor necrosis factor-α (TNF-α), as well as renal tissue levels of malondialdehyde (MDA), nitrite and catalase activity. Kidney tissues were also examined histopathologically. Results: Stressed renal I/R group showed significant decrease in final BW, BW % change, KW and KW/BW, and significant increase in plasma levels of creatinine, urea, TNF-α, renal tissue MDA, and nitrite levels as compared to both renal I/R and sham-operated groups. Renal catalase significantly increased as compared to renal I/R group, but significantly decreased compared to sham-operated group. Stress provoked significant augmentation in renal histomorphological damage scores compared to renal I/R and sham groups, evidenced in the form of glomerular capsular thickening and tuft retraction, tubular cells necrosis with loss of brush borders and cast formation, interstitial cell necrosis and hemorrhage, and endothelial cell disruption. Conclusion: Chronic immobilization stress aggravated renal dysfunction and morphological disturbance induced by renal I /R injury. Accentuation of oxidative stress, inflammation and nitric oxide may contribute to such effect.