Kidney Week

Abstract: SA-PO0597

A Rare Cause of Persistent Hypokalemic Metabolic Alkalosis: Suspected Gitelman Syndrome in an Asymptomatic Adult

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

• Akbar, Zain J., The University of Texas Medical Branch John Sealy School of Medicine, Galveston, Texas, United States

Zain J. Akbar

• Tipo, Jerricho, The University of Texas Medical Branch John Sealy School of Medicine, Galveston, Texas, United States

Jerricho Tipo

• Yakubu, Aliu Opeyemi, The University of Texas Medical Branch John Sealy School of Medicine, Galveston, Texas, United States

Aliu Opeyemi Yakubu, MD

• Wong, Mike, The University of Texas Medical Branch John Sealy School of Medicine, Galveston, Texas, United States

Mike Wong, MD

• Dabech, Abdulaziz, The University of Texas Medical Branch John Sealy School of Medicine, Galveston, Texas, United States

Abdulaziz Dabech, MD

• Shenawi, Ibrahim S., The University of Texas Medical Branch John Sealy School of Medicine, Galveston, Texas, United States

Ibrahim S. Shenawi, MD, MBA

Introduction

Gitelman syndrome is a rare autosomal recessive salt-losing tubulopathy caused by mutations in SLC12A3, encoding the thiazide-sensitive sodium-chloride cotransporter in the distal convoluted tubule. Impaired sodium reabsorption leads to secondary hyperaldosteronism, resulting in hypokalemic metabolic alkalosis, hypomagnesemia, and hypocalciuria. We present a case of newly suspected Gitelman syndrome identified during evaluation of severe hypokalemia.

Case Description

A 34-year-old incarcerated man with no significant past medical history was referred for severe hypokalemia after outpatient testing showed potassium of 2.5 mmol/L. He was asymptomatic, denying chest pain, dyspnea, nausea, vomiting, diarrhea, or diuretic use, though he reported intermittent dizziness occurring once to twice weekly. Family history was negative for renal disease.
On admission, blood pressure was low-normal (97–110/57–70 mmHg), ECG showed normal sinus rhythm without acute abnormalities, and renal function was preserved (creatinine 0.69–0.82 mg/dL). Laboratory evaluation demonstrated persistent hypokalemia (nadir 2.5 mmol/L), hypomagnesemia (1.1 mg/dL), metabolic alkalosis (bicarbonate 31–33 mmol/L), and nondetectable urine calcium. TTKG was 9 during hypokalemia, consistent with inappropriate renal potassium wasting, while fractional excretion of magnesium was 4.4%, indicating renal magnesium wasting.
Given hypokalemic metabolic alkalosis, hypomagnesemia, hypocalciuria, low-normal blood pressure, and renal electrolyte wasting, Gitelman syndrome was suspected. The patient required aggressive potassium and magnesium repletion with persistent losses despite supplementation. Nephrology initiated amiloride, titrated to 10 mg daily, with oral potassium chloride and magnesium replacement. Potassium improved to 3.9 mmol/L prior to discharge. Genetic confirmation was not obtained during admission due to logistical barriers to specialty testing, and outpatient nephrology follow-up was arranged.

Discussion

Gitelman syndrome may present with minimal or nonspecific symptoms despite marked electrolyte abnormalities, making diagnosis challenging. Recognition of the characteristic biochemical pattern is essential for distinguishing it from other causes of renal potassium wasting and initiating appropriate long-term management to prevent recurrent electrolyte disturbances and cardiac complications.