Respiratory medicine case reports · 2026
Acute tubular necrosis with secondary acute respiratory distress syndrome after organophosphate poisoning: A rare clinical case.
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Bereda Gudisa
Аннотация
BACKGROUND: Organophosphate (OP) poisoning is a potentially life-threatening condition that predominantly affects the nervous system. Acute kidney injury (AKI), particularly intrinsic acute tubular necrosis (ATN), is a rare but serious complication. Acute respiratory distress syndrome (ARDS) may further complicate severe intoxication.
CASE PRESENTATION: A 41-year-old female intentionally ingested 48 % soluble chlorpyrifos. She developed vomiting, abdominal pain, decreased level of consciousness, oliguria, and generalized edema. On examination, she was hypotensive, tachycardic, tachypneic, and hypoxic. Laboratory investigations revealed metabolic acidosis, elevated serum creatinine (4.1 mg/dL), blood urea nitrogen (47 mg/dL), electrolyte imbalances, reduced serum cholinesterase level, and a fractional excretion of sodium (FENa) of 3 %, consistent with intrinsic renal injury. Imaging demonstrated pulmonary edema and bilaterally enlarged kidneys. She was treated with intravenous fluids, atropine infusion (0.02 mg/kg/h), pralidoxime (30 mg/kg bolus followed by 8 mg/kg/h infusion), intermittent hemodialysis for AKI, supplemental oxygen, and mechanical ventilation for ARDS. Over 84 hours, urine output improved, renal function recovered, and respiratory distress resolved. She was discharged after one week with plan for psychiatric evaluation and monthly ambulatory nephrology follow-up.
CONCLUSION: This case highlighted a rare presentation of intrinsic ATN complicated by ARDS following OP poisoning. Early recognition and intensive supportive management of renal and respiratory complications are essential. Clinicians should consider direct OP-induced nephrotoxicity in severe poisoning to optimize outcomes.
CASE PRESENTATION: A 41-year-old female intentionally ingested 48 % soluble chlorpyrifos. She developed vomiting, abdominal pain, decreased level of consciousness, oliguria, and generalized edema. On examination, she was hypotensive, tachycardic, tachypneic, and hypoxic. Laboratory investigations revealed metabolic acidosis, elevated serum creatinine (4.1 mg/dL), blood urea nitrogen (47 mg/dL), electrolyte imbalances, reduced serum cholinesterase level, and a fractional excretion of sodium (FENa) of 3 %, consistent with intrinsic renal injury. Imaging demonstrated pulmonary edema and bilaterally enlarged kidneys. She was treated with intravenous fluids, atropine infusion (0.02 mg/kg/h), pralidoxime (30 mg/kg bolus followed by 8 mg/kg/h infusion), intermittent hemodialysis for AKI, supplemental oxygen, and mechanical ventilation for ARDS. Over 84 hours, urine output improved, renal function recovered, and respiratory distress resolved. She was discharged after one week with plan for psychiatric evaluation and monthly ambulatory nephrology follow-up.
CONCLUSION: This case highlighted a rare presentation of intrinsic ATN complicated by ARDS following OP poisoning. Early recognition and intensive supportive management of renal and respiratory complications are essential. Clinicians should consider direct OP-induced nephrotoxicity in severe poisoning to optimize outcomes.