A 22-year-old homosexual male presented to hospital with progressive dyspnea, productive cough, generalized malaise and fever. He had a known history of intravenous cocaine abuse and recent serology in prior 3 months was negative for human immunodeficiency virus (HIV). Results of a physical examination showed signs of tachypnea, tachycardia, accessory muscle use and left lung base crackles. Tympanic temperature was 34.7°C. The remainder of the examination was unremarkable except for urethral meatus stenosis. Initial laboratory investigations are presented in Table. Arterial blood gases showed pH of 6.95, PaCO2 10 mmHg, PaO2 109 mmHg, HCO3 2 mmol/L, and lactate 0.6 mmol/L consistent with high anion gap metabolic acidosis with respiratory compensation. Serum creatinine and blood urea nitrogen were 587 μmol/L and 46.7 mmol/L, respectively. Toxicology and drug screen was negative. The metabolic acidosis was partially accounted for by acute renal failure with retained unmeasured anions and ketonemia. Urinalysis showed pyuria. Electrocardiogram (ECG) showed normal sinus rhythm. Chest radiograph revealed right middle lobe and lingular patchy opacification. An abdomino-pelvic CT scan demonstrated moderate to severe bilateral hydronephrosis, bladder wall thickening with multiple diverticuli, and retroperitoneal streaking consistent with acute infection. A provisional diagnosis of severe sepsis was made with multiple potential foci of infection. The patient was given empiric ceftriaxone, metronidazole and vancomycin. Sputum specimen cultured heavy methicillin-sensitive Staphylococcus aureus, blood cultures were positive for S. aureus, Escherichia coli, and Group B Streptococcus. Urine cultured greater than 108 CFU/L of multiple gram positive and negative organisms. The patient was admitted to the intensive care unit (ICU). The metabolic acidosis persisted (pH 7.00) a despite 100 mEq of 8.4% sodium bicarbonate bolus and infusion of three liters of normal bicarbonate solution (150 mEq of 8.4% sodium bicarbonate in 1000 mL D5W). The patient had a suprapubic bladder catheter inserted by angiography. However, due to concern the patient remained oliguric following 4 L crystalloid resuscitation, hemodialysis was organized. Hemodialysis parameters included: F160 membrane (surface area 1.5 m2 and KUf 50 mL/hr/mmHg), dialysate sodium 136 mmol/L, potassium 3 mmol/L, calcium 1.25 mmol/L, bicarbonate 40 mmol/L, and QD 500 mL/min, QB 250–300 mL/min via a 25 cm left femoral double-lumen Uldall catheter. The patient had 71.5 L of blood processed over four hours with no fluid removal. Although the patient was alert and appropriate (Glasgow Coma Scale 15) with tachycardia and stable normal range blood pressure before the initiation of dialysis, he was demonstrating an increased work of breathing and oxygen requirements suggestive of worsening sepsis syndrome. Approximately 2.5 hrs after start of dialysis the patient became rapidly unresponsive prompting intubation for airway protection. At completion of HD and over the subsequent 4 hours the patient's neurologic status deteriorated with evidence of loss of all brainstem reflexes. Head CT-scan is shown in Figure. Repeat laboratory investigations immediately following hemodialysis revealed a pH 7.36, HCO3 19 mmol/L, sodium 132 mmol/L, potassium 1.8 mmol/L, and urea 13.7 mmol/L (urea-reduction-ratio was 71%). The patient rapidly progressed to refractory shock and multi-organ dysfunction Diagnosis of brain death was declared independently by an intensivist and a neurologist. At autopsy, the brain showed evidence of diffuse cerebral edema. Cardiac assessment showed left ventricular enlargement consistent with systemic hypertension likely as a result of chronic kidney disease. Both lungs showed patchy acute bronchopneumonia with edema and congestion. Both kidneys appeared grossly pyonephrotic with dilated, thickened ureters and suggested the presence of acute on chronic pyelonephritis. The meatal aperture was scarred and stenosed.