Beyond the Cholinergic Crisis: Non-Oliguric Acute Kidney Injury in Organophosphate Poisoning

Abstract

Organophosphate (OP) poisoning is a common toxicological emergency, primarily presenting with cholinergic manifestations. Acute kidney injury (AKI) is an uncommon but clinically important complication of OP poisoning, usually attributed to secondary factors such as hypotension, dehydration, rhabdomyolysis, or sepsis. However, intrinsic renal injury may occur even in the absence of these classical risk factors. We report a case of a 24-year-old male who developed non-oliguric acute kidney injury following intentional ingestion of an organophosphate compound containing chlorpyrifos 50.0% and cypermethrin 5.0%. The patient presented with features of cholinergic excess and markedly reduced plasma cholinesterase levels. He remained hemodynamically stable during hospitalization without persistent hypotension or need for renal replacement therapy. Laboratory investigations showed a transient rise in serum creatinine, peaking on the second day and returning to baseline with supportive management. Serum creatine kinase levels were normal, and urine output was preserved throughout the hospital stay. This case suggests the possibility of intrinsic tubular injury as a mechanism of AKI in organophosphate poisoning. Routine monitoring of renal function may help in early detection of renal involvement even in clinically stable patients. Awareness of non-oliguric AKI as a potential complication of organophosphate toxicity is important for timely supportive management.