Abstract: SA-PO0531
Persistent Hypokalemia: A Manifestation of Long COVID Syndrome?
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 3
November 08, 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
Author
- Albashash, Hazem, Henry Ford Health System, Detroit, Michigan, United States
Introduction
Long COVID syndrome is increasingly recognized as a significant sequela of SARS-CoV-2 infection, affecting various organ systems. Renal involvement in acute COVID-19 infection is well-documented, primarily linked to SARS-CoV-2-mediated dysregulation of the renin-angiotensin-aldosterone system (RAAS) via ACE2 degradation, leading to increased renal potassium excretion and subsequent hypokalemia. Experimental data also suggest a direct impact of SARS-CoV-2 proteins on epithelial sodium channel (ENaC) activity, which can upregulate these channels and exacerbate potassium loss. While acute COVID-19 is known for renal involvement and electrolyte derangements, persistent electrolyte abnormalities as a feature of Long COVID are less understood, with only one prior case report. Here, we present a case of persistent hypokalemia following acute SARS-CoV-2 infection.
Case Description
A 43-year-old female, with no prior kidney disease, presented with new onset symptomatic hypokalemia six months after mild COVID-19 hospitalization. Workup confirmed Renal potassium wasting: 24-hour urine showed potassium 92 mmol/24 hours (low for serum potassium 2.8 mmol/L), calcium 73 mg/24 hours (low), chloride 116 mmol/24 hours (low normal), and sodium 84 mmol/L (normal). Metabolic alkalosis (pH 7.51, bicarbonate 27 mmol/L) was noted, with normal magnesium and calcium. Diuretic screen and Gitelman genetic testing were negative; a FAM111A gene variant of uncertain significance was found. Renin was elevated (71 pg/mL); aldosterone was normal (13 ng/dL). Blood pressure remained normal to low. Initial oral potassium/Amiloride therapy improved potassium but caused intolerance, leading to weekly intravenous potassium chloride infusions, maintaining serum potassium around 3 mmol/L.
Discussion
This case suggests Persistent hypokalemia from renal potassium wasting can be a Long COVID manifestation, even without common causes like diuretic use or Gitelman syndrome. The temporal link to COVID-19 and evidence of renal potassium wasting point to a potential long-term viral effect on renal tubular function, possibly via ENaC activation (as mouse studies suggest). This case adds to limited evidence that persistent electrolyte abnormalities can feature in Long COVID. Clinicians should consider Long COVID in new-onset persistent hypokalemia. Further research into prevalence and mechanisms is warranted.