Abstract: TH-PO0413
COVID-19-Associated Hypokalemia and Metabolic Alkalosis Mimicking Gitelman Syndrome
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 1
November 06, 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
- Venkatesh, Harini Kayravini, Henry Ford Macomb Hospital, Charter Township of Clinton, Michigan, United States
- Atchison, Douglas Kyle, Henry Ford Hospital, Detroit, Michigan, United States
- Decker, Ilka, University of Michigan, Ann Arbor, Michigan, United States
Introduction
Acid-base & electrolyte derangements are common with COVID and usually settle with the resolution of the infection. Rarely, these imbalances last for unclear reasons. This report describes the first case of persistent hypokalemia & metabolic alkalosis giving rise to a Gitelman syndrome-like picture, possibly linked to COVID.
Case Description
A 44-year-old female visited the Nephrology clinic for 1 year of persistent hypokalemia requiring multiple hospitalizations after presenting with fatigue, numbness & tingling of her extremities. No vomiting, diarrhea, use of diuretics, laxatives, NSAIDs or herbal supplements. She denied a personal or family history of electrolyte disorders, kidney disease, hypertension, recurrent UTIs or gout. BP was low-normal. 1 year prior, she was found to have low potassium (K) while hospitalized for COVID. Since then, K remained between 2.8 & 3.4 with metabolic alkalosis, elevated renin & aldosterone and high urine K & Cl. Serum Mg & Ca were normal without supplementation. GI, endocrine & autoimmune workup was unremarkable; diuretic screen was negative. Eventually, aggressive K replacement, K-sparing diuretics & Na tablets were initiated. The patient declined a trial of steroids.
Discussion
In a Chinese cohort study, hypokalemia occurred in 55% of COVID patients, attributed to ACE2 degradation by SARS-CoV-2 leading to increased RAS activity, elevated aldosterone and increased renal K excretion. Other contributing factors include GI losses, acute respiratory acidosis causing intracellular K shift and administration of diuretics, β-agonists & steroids. In this case, there was no obvious cause of salt-wasting nephropathy. Hypokalemia and metabolic alkalosis with high urine Cl and low-normal BP were concerning for high mineralocorticoid activity. Renal K wasting was confirmed by high urine K despite low serum K & TTKG. However, low/normal BP is not a feature of primary hyperaldosteronism or Liddle syndrome. Although Gitelman syndrome can have adult onset, the temporal sequence following COVID, the abrupt onset of severe hypokalemia and negative genetic testing made it the more likely etiology. Only one similar case was reported, but without an acid-base disorder, ruling out Gitelman syndrome. More studies evaluating the mechanisms of post-COVID hypokalemia could provide greater insight and prevent its life-threatening consequences.