C51-05 Profound Uremia, Encephalopathy, and Coagulopathy: From Critical Illness to Full Recovery

Abstract Introduction Acute kidney injury requiring dialysis (AKI-D) is characterized by a sudden impairment in kidney function that cannot be managed by medical therapy alone. This case highlights multiple life-threatening complications of AKI-D and the measures taken to achieve clinical recovery. Case A 49-year-old male with unknown medical history presented with progressive abdominal pain, back pain, and fatigue/weakness for one week, as well as oral bleeding for one day. In the ED, his initial blood pressure was 199/133. On exam, he was confused and had white flakes across his forehead. Initial labwork included creatinine 51.7, BUN 269, K + 10.0, HCO3- 13, and anion gap 35, all confirmed on repeat BMP. His EKG revealed peaked T waves. He was given calcium gluconate, insulin/dextrose, and IV furosemide. An indwelling urinary catheter was placed by Urology and subsequently drained 7 liters of bloody urine. Nephrology was consulted for emergent dialysis and DDAVP ordered for presumed uremic platelet dysfunction. He was admitted to the MICU where a non-tunneled dialysis catheter was placed and urgent CRRT initiated. Despite dialysis, he briefly required bicarbonate infusion for refractory hyperkalemia and high anion gap metabolic acidosis. CT abdomen/pelvis and CT urogram both revealed bilateral hydroureteronephrosis to the bladder and an enlarged prostate without any other clear source of obstruction. Over the subsequent four days, his encephalopathy improved and his electrolytes normalized. His circuit was discontinued and he was transferred to the floor, where his hematuria resolved and his serum creatinine improved to 1.2 with full renal recovery. Discussion This case highlights a striking example of acute renal failure complicated by profound hyperkalemia and uremia. Significant uremia contributed to this patient’s encephalopathy and bleeding. Severe uremia 200 mg/dl may be accompanied by uremic frost, seen on this patient’s forehead, in which crystallized urea deposits on the skin. This patient’s acute kidney injury was likely multifactorial, with a pre-renal component due to hypovolemia and a post-renal component due to obstruction, perhaps at the prostate, causing bilateral hydroureteronephrosis. Prompt initiation of dialysis can lead to rapid clinical improvement and, in this patient’s case, renal recovery. This abstract is funded by: None