Kidney Injury and Animal Toxins

Abstract

Animal toxins are complex mixtures of peptides, enzymes, proteins, and chemical compounds. The kidney as a highly vascularized organ is vulnerable to toxin injury. Hemodynamic changes resulting in decreased renal blood flow are the basic finding in severe envenoming and represent the net result of the effect of vasoactive substances from toxins, the effect of toxins on vascular or autonomic neuronal ion channels, and the effect of proinflammatory cytokines and vasoactive mediators from the host. Several enzymes in toxins including phospholipase A2, metalloprotease, and sphingomyelinase are cytotoxic and potentially nephrotoxic. They are also responsible for intravascular coagulation, intravascular hemolysis, and rhabdomyolysis which further enhance renal ischemia. In general, renal injury is attributed to the interaction of inflammatory reaction and renal ischemia. Direct nephrotoxicity is responsible for acute renal injury in some animal envenoming. Immunologic mechanism plays a minor role in renal injury. Clinically, manifestations of animal toxin injury vary from mild urinary sediment changes to nephritic or nephritis syndrome and acute renal failure. Renal pathological changes involve all renal structures which include mesangiolysis, glomerulonephritis, vasculitis, tubular necrosis, interstitial nephritis, thrombotic microangiopathy, and cortical necrosis. Serum electrolyte changes due to effects of toxins on ion transport in renal tubules and cell membranes open a new dimension in animal toxin injury.