Mechanisms of Bee Venom-Induced Acute Renal Failure
Toxicon, Volume 48, Issue 1, July 2006, Pages 44-54
The spread of Africanized bees in the American continent has increased the number of severe envenomation after swarm attacks. Acute renal failure (ARF) is one of the major hazards in surviving patients.
To assess the mechanisms of bee venom-induced ARF, rats were evaluated before, up to 70 min and 24 h after 0.5 mg/kg of venom injection. Control rats received saline. Bee venom caused an early and significant reduction in glomerular filtration rate (GFR, inulin clearance, 0.84±0.05 to 0.40±0.08 ml/min/100 g, p<0.0001) and renal blood flow (RBF, laser Doppler flowmetry), which was more severe in the cortical (−72%) than in the medullary area (−48%), without systemic blood pressure decrease. Creatine phosphokinase, lactic dehydrogenase (LDH) and serum glutamic oxaloacetic transaminase increased significantly, pointing to rhabdomyolysis, whereas serum glutamic pyruvic transaminase and hematocrit remained stable.
Twenty-four hours after venom, RBF recovered but GFR remained significantly impaired. Renal histology showed acute tubular injury and a massive tubular deposition of myoglobin. Venom was added to isolated rat proximal tubules (PT) suspension subjected to normoxia and hypoxia/reoxygenation (H/R) for direct nephrotoxicity evaluation. After 60 min of incubation, 0.1, 2 and 10 μg of venom induced significant increases in LDH release: 47%, 64% and 86%, respectively, vs. 21% in control PT while 2 μg of venom enhanced H/R injury (85% vs. 55%, p<0.01).
These results indicate that vasoconstriction, direct nephrotoxicity and rhabdomyolysis are important mechanisms in the installation of bee venom-induced ARF that may occur even without hemolysis or hypotension.