Abstract: PUB112
Dissociation of Urine Sodium (UNa) and Urine Chloride (UCl) in Surreptitious Diuretic Use Presenting as Recurrent Hypokalemia
Session Information
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Batool, Izza, West Virginia University, Morgantown, West Virginia, United States
- Kaushal, Amit, West Virginia University, Morgantown, West Virginia, United States
- Shahzad, Sheikh Raza, West Virginia University, Morgantown, West Virginia, United States
Introduction
Hypokalemia with renal K wasting and metabolic alkalosis (MA) has broad differentials including hyperaldosteronism, diuretics, and salt wasting tubulopathies. Distinguishing these etiologies can be challenging when clinical history is unreliable or urine electrolyte findings appear discordant.
Case Description
50-year-old female with CKD 3, gastric bypass presented with recurrent severe hypokalemia for 6 years, requiring multiple hospitalizations with K as low as 2.1 mEq/L. Mg normal. She had been taking loop and thiazide diuretics in the past for self-reported lower extremity edema, not noted on exam. Diuretics had reportedly been discontinued several weeks prior to evaluation, and the patient denied vomiting, diarrhea, or laxative abuse. BP was normotensive. Na 135 mEq/L, K 2.7 mEq/L, Cl 91 mEq/L, CO2 31 mEq/L, Cr 2.2 mg/dL, Ca 9.9 mg/dL, and albumin 4.4 g/dL. PRA was elevated at 12 ng/mL/h with aldosterone 18 ng/dL and ARR <15 obtained while K normal. Urine K/Cr ratio was 48 mEq/g, consistent with renal K wasting. UCl was elevated at 54 mEq/L, suggesting a Cl-resistant MA; however, UNa was low at <20 mEq/L. Genetic testing for Bartter and Gitelman syndromes was negative. The patient was treated with amiloride and K-Cl supplementation. Urine diuretic screening was positive for furosemide. Despite this finding, the patient continued to deny diuretic use and was lost to follow-up.
Discussion
This case highlights a diagnostically challenging presentation of recurrent hypokalemic MA due to covert diuretic exposure. Intermittent diuretic use may produce variable urine electrolyte patterns depending on timing of ingestion and degree of volume contraction. During active natriuresis, both UNa and UCl are elevated. However, after diuretic effect wanes, secondary hyperreninemia and Na avidity may lower UNa excretion while UCl remains elevated. MA increases proximal Na absorption via Na-H exchange. If Na is avidly reabsorbed distally under aldosterone influence, H+ and K+ are secreted in urine with Cl. In K wasting tubulopathies, both UNa and UCl are elevated. Persistently elevated UCl in the setting of MA should raise suspicion for surreptitious diuretic use even when UNa is low. This case underscores the diagnostic utility of UCl over UNa in evaluating hypokalemic MA and emphasizes the importance of thorough evaluation despite an initially misleading history.