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+A 20-year-old previously healthy Bengali man presented to our hospital with anuria and features of uremic encephalopathy.
+Ten days prior to this presentation, he had experienced severe upper abdominal pain and vomiting, and he had been treated in a primary care facility for having a case of acute pancreatitis.
+His initial symptoms improved; however, he gradually became anuric and disoriented.
+Then he was transferred to our hospital for further management.
+At presentation to our hospital, he was severely agitated, restless, and disoriented.
+He was tachypneic with acidotic breath.
+Mild pedal edema was present; however, his jugular venous pressure was not raised.
+His pulse was 112 beats/minute, his blood pressure was 140/90 mmHg, and his body temperature was 98 °F.
+Signs of meningeal irritation were absent, and his plantar response was bilaterally extensor.
+His fundus could not be evaluated, and examination of his other systems was unremarkable.
+His laboratory parameters showed features of renal dysfunction (serum creatinine 13 mg/dl, serum urea 293 mg/dl), raised pancreatic enzymes (serum amylase 249 U/L [reference up to 100 U/L], serum lipase 227 U/L [reference 13–60 U/L), normal liver function tests (serum bilirubin 0.9 mg/dl, alanine aminotransferase 38 U/L, aspartate aminotransferase 35 U/L, alkaline phosphatase 122 U/L, serum albumin 37 g/L), normal potassium (5.1 mmol/L), normal bicarbonate (19 mmol/L), and normal triglycerides (173 mg/dl).
+His serological markers, including antinuclear antibodies, cytoplasmic antineutrophil cytoplasmic antibodies, perinuclear antineutrophil cytoplasmic antibodies, C3, and C4, were within normal limits.
+An ultrasonogram of his whole abdomen was unremarkable, but non-contrast-enhanced computed tomography (CT) findings were suggestive of acute pancreatitis (Fig.1).
+His kidneys were unremarkable, however.
+The patient was managed as having a case of AKI and acute pancreatitis.
+Urgent hemodialysis was initiated.
+After he had received two sessions of hemodialysis, his level of consciousness improved, but he complained of profound visual loss.
+An assessment revealed only perception of light.
+A funduscopic examination showed retinal whitening and extensive cotton wool exudates as well as Purtscher’s flecken (Fig.2) compatible with Purtscher’s retinopathy.
+High-dose parenteral methylprednisolone (1 g intravenously once daily for 3 days) was administered.
+For evaluation of renal dysfunction, a renal biopsy was done; the histopathological findings were compatible with renal cortical necrosis (Fig.3).
+The patient denied substance abuse or alcohol ingestion.
+He did not consume any nephrotoxic drugs or herbal products in the recent past.
+No history suggesting connective tissue diseases was available, nor did he have a history of hypotension throughout the course of his current illness.
+The patient was finally diagnosed with acute pancreatitis complicated with renal cortical necrosis leading to AKI and Purtscher’s retinopathy leading to complete bilateral blindness.
+He died 16 months after his initial presentation as a result of a recurrent attack of acute pancreatitis.
+Before that, he had been undergoing maintenance hemodialysis; however, his renal function did not recover, though his vision was improved to finger-counting at 2 feet.