Snakebite envenomation-associated acute kidney injury: a South-Asian perspective

Snakebite is a neglected public health problem in tropical countries. Snakebite envenomation-associated acute kidney injury (SBE-AKI) is a major complication accounting for significant morbidity and mortality. The pathogenesis of SBE-AKI may be multifactorial, including prerenal AKI secondary to hemodynamic alterations, intrinsic renal injury, immune-related mechanisms, venom-induced consumptive coagulopathy and capillary leak syndrome. Epidemiological factors include snake species, duration and severity of snakebite, traditional healers and native medication and accessibility to modern healthcare and antisnake venom. Renal histopathology observed consist of acute tubular necrosis, interstitial nephritis, cortical necrosis, disseminated intravascular coagulation, rhabdomyolysis and thrombotic microangiopathy. Glomerular involvement is rare. Proteinuria can be present rarely, hematuria is more common, most often due to venom-induced coagulopathy or hemolysis; it is only rarely due to renal injury. Management includes supportive care and renal replacement therapy when indicated. Progression to chronic kidney disease remains one of the biggest concerns of SBE-AKI. Hence the role and timing of renal biopsy remain controversial, given the risk involved and the benefit obtained in cases of interstitial nephritis. Various biomarkers, including cystatin C, neutrophil gelatinase-associated lipocalin, clusterin and beta-2-glycoprotein, have shown a tendency to predict AKI and also predict progression to chronic kidney disease.