Abstract: FR-PO0595
Hyperammonemia and Encephalopathy in Ureterosigmoidostomy: A Nephrology Challenge Beyond the Liver
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 2
November 07, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Balakrishnan, Suryanarayanan, Mayo Clinic Minnesota, Rochester, Minnesota, United States
- Craici, Iasmina, Mayo Clinic Minnesota, Rochester, Minnesota, United States
- Cheungpasitporn, Wisit, Mayo Clinic Minnesota, Rochester, Minnesota, United States
Introduction
Hyperammonemia(HA) is a metabolic disturbance due to accumulation of ammonia(NH3) in the blood, a neurotoxin that can precipitate encephalopathy. Although classically associated with liver dysfunction, nonhepatic causes, including urinary diversions, must also be recognized.
Case Description
68M with a history of stage CKD IIIa with baseline creatinine about 1.3-1.5 mg/dL, non alcoholic steatohepatitis, bladder and prostate cancer managed with pelvic exenteration with bilateral (b/l) ureterosigmoidostomy(USS) in 2001, postoperatively, he developed progressive renal complications, including b/l ureteroenteric obstruction leading to functionally solitary right kidney. He was admitted to ICU in 12/24 for metabolic encephalopathy and severe acid-base disturbances, including HA at 236 umol/L, non anion gap metabolic acidosis attributed to ureteral diversion, AKI. Workup for cirrhosis including elastography was notable for steatosis, synthetic function on labs was intact. He was initiated on Lactulose, rifaximin, bicarbonate and fluid repletion. HA was attributed to USS and gut microbiota. Rectal tube was placed to facilitate urine drainage and clearance of NH3. The patient required hemodialysis followed by CRRT for persistent HA. A right nephrostomy tube was placed to divert urine and prevent urea from entering the colon. Broad-spectrum antibiotics with piperacillin-tazobactam and doxycycline were initiated for gut bacterial suppression, resulting in clinical improvement and resolution of HA. Following discharge, he was referred to Urology for alternative urinary diversion
Discussion
In patients with USS, recurrent HA results from diversion of urinary urea into colon, where colonic bacterial urease converts it into NH3 and carbon dioxide. NH3, being a diffusible gas, is rapidly absorbed across the colonic epithelium into the portal circulation. Under normal conditions, hepatic enzymes detoxify NH3 by converting it to urea for renal excretion. However, in the setting of CKD, increased colonic NH3 production, or impaired hepatic function, hepatic clearance is overwhelmed, resulting in systemic HA. Additionally, patients with USS lack a urinary route for NH3 excretion, predisposing them to HA and metabolic encephalopathy. This case highlights the need for awareness of this unique presentation; urinary diversion is necessary