Abstract: SA-PO0592
Hypocitraturia and Nephrolithiasis as Manifestations of Lithium-Induced Incomplete 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
- Jalloul, Youssef, Albany Medical College Division of Nephrology & Hypertension, Albany, New York, United States
- Monrroy, Mauricio, Albany Medical College Division of Nephrology & Hypertension, Albany, New York, United States
Introduction
Lithium is a cornerstone treatment for bipolar disorder, but long-term use is associated with nephrotoxicity, including distal renal tubular acidosis (dRTA). Lithium accumulates in collecting duct cells via the epithelial sodium channel and inhibits H-ATPase function in alpha-intercalated cells, impairing urinary acidification. In incomplete dRTA, systemic bicarbonate remains normal while tubular defects persist, reducing urinary citrate excretion (an important inhibitor of calcium stone formation) and predisposing to nephrolithiasis.
Case Description
A 75-year-old man on chronic lithium therapy presented with a 7 mm right midpole calyceal stone and CKD stage 3a (creatinine 1.38 mg/dL, eGFR 53). History included resolved obstructive uropathy and prior chronic NSAID use. Serum bicarbonate was 25 mEq/L, anion gap 7, potassium 4.1, calcium 9.6, and phosphorus 3.0 mg/dL. 24-hour urine showed severe hypocitraturia (<42 mg/day) and low ammonium excretion (25 mEq/day), consistent with impaired distal acidification. All supersaturation indices were below 1.0. Urine volume (2,820 mL), calcium (35 mg/day), oxalate (20 mg/day), and uric acid (477 mg/day) were normal. Urine Sodium (103 mmol/day) was borderline.
Discussion
The combination of severe hypocitraturia, low urine ammonium, and preserved serum bicarbonate is consistent with incomplete dRTA. Impaired H secretion in the collecting duct drives intracellular acidosis in the proximal tubule, upregulating citrate reabsorption and dramatically reducing urinary citrate (an important inhibitor of calcium stone formation). This patient's undetectable urine citrate explains his stone formation despite his low supersaturation indices.
Lithium is the most likely etiology, given its well-known mechanism of inhibiting the collecting duct H-ATPase. Resolved obstructive uropathy and prior NSAID use may have contributed to CKD, but they are unlikely to be the drivers of the ongoing acidification defect.
Potassium citrate 45 mEq/day was initiated to replenish urinary citrate and restore stone inhibition. Close monitoring of serum potassium is essential due to his CKD. Psychiatric consultation regarding lithium dose reduction or transition to an alternative mood stabilizer was recommended to address the underlying nephrotoxic exposure.
Acknowledgment
OpenEvidence (OpenEvidence, Inc.), an AI-powered medical knowledge assistant, was used to assist with literature review, data interpretation, and manuscript drafting. All content was reviewed, verified, and edited by the authors, who take full responsibility for the accuracy and integrity of the work.