Clinical Case Scenario
A 38-year-old previously healthy man was admitted following a snakebite to his lower limb. At presentation, he had progressive local swelling with evidence of systemic envenomation. His initial serum creatinine was 0.9 mg/dL, platelet count and hemoglobin were within acceptable limits, and urinalysis showed no significant proteinuria or hematuria.
He received polyvalent anti-snake venom (ASV) as per the clinical indication, along with supportive care. His clinical condition improved over the next 48–72 hours, with resolution of the acute manifestations of envenomation. Renal function remained stable, and he was subsequently discharged.
Ten days after receiving ASV, he returned with fever, generalized fatigue, intense pruritus and a widespread erythematous rash. He also complained of pain involving both knees, ankles and wrists, without significant morning stiffness. Examination revealed mild periorbital and pedal edema. He was hemodynamically stable, with no wheeze, stridor, hypotension or features of recurrent envenomation.
Investigations showed:
There was no recent hypotension, nephrotoxic drug exposure, recurrent hemolysis or rhabdomyolysis.
Right Answer: ✅ A. Delayed serum sickness secondary to anti-snake venom with immune-complex renal involvement Diagnostic Clues Hidden in the Case The important clue is the biphasic course: the patient recovers from the acute envenomation and has preserved renal function, followed by a new systemic illness 10 days after ASV exposure. The combination of: ASV exposure → symptom-free interval → fever + pruritic rash + polyarthralgia + edema + low C3/C4 + glomerular hematuria/proteinuria + AKI strongly suggests a type III immune-complex hypersensitivity reaction (serum sickness) with renal involvement. 💎NephroCC Pearl 💥Not every AKI occurring after a snakebite is venom-induced AKI. 💥When kidney dysfunction develops after an initial period of recovery, reconstruct the timeline. A delayed combination of rash, fever, polyarthralgia, hypocomplementemia and an active glomerular urinary sediment should prompt consideration of ASV-induced serum sickness with immune-complex glomerular involvement.
Wrong Answer: ❌ B. Snakebite-associated thrombotic microangiopathy Snakebite-associated TMA typically presents with AKI together with microangiopathic hemolytic anemia and thrombocytopenia. Schistocytes, elevated LDH and other evidence of hemolysis may be present. In this case, the normal platelet count, absence of schistocytes and lack of significant hemolysis argue against TMA. The delayed fever-rash-arthralgia syndrome with low complement instead points toward an immune-complex process.
Wrong Answer: ❌ C. Delayed venom-associated acute tubular injury Venom-related AKI generally occurs during the acute phase of envenomation and can result from hemodynamic instability, hemolysis, rhabdomyolysis, coagulopathy or direct nephrotoxicity. Acute tubular injury would not adequately explain the delayed systemic hypersensitivity features, low complement, dysmorphic hematuria and RBC casts after an interval of clinical recovery.
Wrong Answer: ❌ D. Acute interstitial nephritis secondary to supportive medications Drug-induced acute interstitial nephritis can cause AKI with fever and rash, making it a relevant differential. However, the urinary picture is usually tubulointerstitial rather than distinctly glomerular. Dysmorphic RBCs, RBC casts, significant proteinuria and hypocomplementemia favor immune-complex glomerular involvement. The temporal relationship to heterologous ASV exposure and associated polyarthralgia further supports serum sickness.
