Animal toxins and the kidney

Abstract

Envenomation or poisoning by toxins from animals poses an important health hazard in the tropics. Animal toxins are complex mixtures of proteins, peptides, enzymes and chemicals. These toxins exert their effects through modulation of ion channels and receptors, and via direct enzyme action. Depolarization or hyperpolarization of ion channels--caused by most marine toxins, and some snake and insect venoms--results in neuromuscular symptoms that can be associated with hemodynamic changes. Toxin enzymes, especially proteases and phospholipase A2, initiate inflammatory processes that involve the generation of proinflammatory cytokines and vasoactive mediators, resulting in systemic and renal hemodynamic alterations. Toxin enzymes also have direct effects on erythrocytes, myocytes, blood coagulation factors, vascular endothelium and epithelial cells. As a result, disseminated intravascular coagulation, bleeding diathesis, intravascular hemolysis and rhabdomyolysis are common after exposure to animal toxins. The renal manifestations of animal toxin envenomation, which are usually acute, result mainly from these enzymatic effects. All renal structures can be affected by animal toxins, and tubular necrosis is common. Acute kidney injury is attributed to decreased renal blood flow (associated with intravascular hemolysis or rhabdomyolysis), disseminated intravascular coagulation or direct tubular toxicity. Immunologic mechanisms have a minor role in the pathophysiology of nephropathy caused by animal toxins.

Enzymatic and toxinological activities of Hypnale hypnale (hump-nosed pit viper) venom and its fractionation by ion exchange high performance liquid chromatography

“…Thus, a tentative explanation of nephropathy observed in some of the victims (11,66) is that the kidney damage is likely the result of complications from the venom's hematoxic effects mediated through its procoagulant and possibly fibrinolytic actions. This suggestion is in line with the view that the nephropathy was associated with disseminated intravascular coagulopathy (61).…”

“…The injury mechanisms can be either by direct effect of the toxins or secondary to hemostatic defect, intravascular hemolysis, shock, immune response or rhabdomyolysis. Hematoxic and myotoxic venoms from viperids or crotalids are a rich source of enzymes that include phospholipases, endopeptidases, L-amino acid oxidases and metalloproteases which can directly cause cellular damage and kidney injury (60,61). In the present study, D. russellii venom from Myanmar was administered to the positive control group (DV group) to produce acute kidney injury as the venom was known to be highly nephrotoxic (62)(63)(64)(65).…”

Symptom patterns in adult patients stung by scorpions with emphasis on coagulopathy and hemoglubinuria

“…Resolving this controversy is somewhat difficult and requires further research in other areas. Second, it was previously reported that kidney impairment or failure due to scorpion envenoming, especially in the case of H. lepturus is one of the early symptoms and the scorpion venom is toxic (6,(15)(16)(17). While in the present study, kidney problems were present only in patients with blood cell lysis and hemoglobinuria.…”

A Study of Acute Kidney Injury in Patients with Snakebite Envenomation

“…In cases of severe envenomation, snake venom can induce the release of auto pharmacological vasoactive substances, particularly bradykinin, resulting in vasodilatation and myocardial depression, and consequently reduce myocardial contractility [32] . Therefore, our findings support the pathophysiology of sAKI as multifactorial, including hemodynamic changes, direct toxicity of snake venom, immunologic reaction and pigmenturia [33] . This pathophysiology would explain pathological observation of tubular necrosis, mesangiolysis, cortical necrosis, vasculitis, glomerulonephritis, interstitial nephritis, and renal infarction after snakebite envenomation [33] .…”