Effects of russell's viper venom on renal histopathology in rats

Abstract

The histopathological changes of the kidney after Russill’s viper envenomation were studied. Highly inbred male Wistar rats, devided into 3 groups, were intramuscularly injectd with lypophylized Russell’s viper (RVV) dissolved in sterile physiologic saline. The dose of RVV was 1 mg./kg. in group A and 2 mg./kg. in group while 0.9% NaCl colution was injected in group C (control group). Nephrectomies were performed at the 2nd hour, 6th hour, 1st day, 3rd da, and 30th day after injection and renal tissue were processed for light and transmission electron microscopic examination. The renal histopathology revealed varying degrees of tubular degeneration, intratubular casts and microvascular congestion in patchy distribution. These changes were seen as early as 2 hours following envenomation but were more apparent after 24 hours. Tubular regeneration was demonstrated at the 3rd and 10th day. Most glomeruli appeared normal; however, congested glomerular tufts containing fibrin were demonstrable in some cases. The electron microscopic findings confirmed the results of light microscope. According to severity, tubular lesion and vascular congestion were score to grades 3 and 4 respectively. In this study, the renal pathology and its patchy distribution resembling the renal pathology in various ischemic conditions would indicate the role of renal ischemia as the pathogenetic mechanism. The role of direct nephrotoxicity, albeit not completely excluded, seems less significant because there was no correlation between dosages of the venom and the renal histological changes. The mechanisms of ischemic renal damage from RVV may be due to hemodynamic alteration or intravascular coagulation. The mean tubular lesion score of the group of animals with positive fibrin strain was higher at a p-value < 0.050. Since fibrin was found only 25% of cases which already showed renal histological changes, intravascular coagulation would not be the main pathogenetic factor. However, in the group of animals with positive fibrin stain, the mean tubular lesion score was significantly higher at a p-value < 0.05. Thus, it is concluded that hemodynamic alteration could play the primary role in the pathogenesis of renal lesions while intravascular coagulation plays an additive role in severe cases.