Abstract: SA-PO0593
Electrolyte and Acid-Base Abnormalities in Severe Cholestatic Liver Disease: A Case of Distal Renal Tubular Acidosis
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 2
October 24, 2026 | Location: Exhibit Hall A, 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
- Matheu, Stephanie Marie, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States
- Kanduri, Swetha Rani, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States
- Ryan, Eric, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States
Introduction
Distal renal tubular acidosis (dRTA) results from impaired proton secretion by α-intercalated cells in the distal nephron, leading to non-anion gap metabolic acidosis, hypokalemia and inappropriately alkaline urine. Although autoimmune and hereditary causes are most common, dRTA associated with severe cholestatic liver disease is rare. We present a case of renal involvement manifesting as distal renal tubular acidosis in a patient with severe cholestatic jaundice.
Case Description
A 26-year-old male developed cholestatic liver disease a few months prior to the admission, attributed to drug-induced liver injury versus small duct primary sclerosing cholangitis. Colonoscopy incidentally revealed ulcerative colitis. During liver transplant evaluation, cervical lymphadenopathy was identified, and biopsy confirmed classical Hodgkin lymphoma. He was admitted for dose-reduced ABVD (Adriamycin, Bleomycin, Vinblastine, and Dacarbazine) chemotherapy. During this admission, nephrology was consulted for refractory hypokalemia, and persistent non-anion gap metabolic acidosis. Serum bicarbonate ranged 13–15 mmol/L. Urinalysis showed urine pH 6.5 with 4+ bilirubinuria; total bilirubin 23.1 mg/dL, direct 16.4 mg/dL. Urine electrolytes demonstrated Na 36, K 95.6, Cl 111 mmol/L, with a urine anion gap of +20.6 mEq/L, consistent with impaired ammonium excretion. Renal functions remained stable. Persistently alkaline urine despite systemic acidemia, positive urine anion gap, and refractory hypokalemia established dRTA.
Discussion
Severe cholestatic jaundice can lead to bile cast nephropathy in which conjugated bilirubin and bile acids exert direct tubular toxicity and promote intratubular cast formation, resulting in tubular dysfunction. Bile acid–mediated injury and cellular energy depletion may also impair distal tubular acidification leading to dRTA. Rare reports describe Hodgkin lymphoma associated proximal and distal tubular injury, though this remains uncommon entity. Clinicians should be vigilant for electrolyte and acid–base abnormalities in patients with cholestatic liver disease, along with consideration of hepatorenal syndrome and other causes of acute kidney injury.