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Electrolyte disturbances such as hypokalemia and hypomagnesemia are common in pregnancy and often attributed to vomiting, diet, or medication. However, pregnancy’s physiologic changes can unmask inherited tubulopathies. Gitelman syndrome (GS), caused by biallelic SLC12A3 variants affecting the thiazide-sensitive NaCl cotransporter in the distal convoluted tubule, typically presents with hypokalemia, hypomagnesemia, metabolic alkalosis, and hypocalciuria. Distinguishing GS from acquired causes (e.g., Tenofovir disoproxil fumarate (TDF)-associated proximal tubulopathy) is critical, as the diagnoses imply different maternal-fetal risks, genetic counseling considerations, and management strategies.
We present a unique case of a 29-year-old pregnant woman with chronic hepatitis B who was evaluated for persistent hypokalemia/hypomagnesemia initially attributed to poor intake and later to TDF use. Given electrolyte derangements that predated TDF and inconsistent medication adherence, a targeted work-up was pursued: serum/urine electrolytes, acid–base profile, and spot urine calcium and magnesium excretion. Genetic testing for renal tubulopathies was obtained.
At 25 weeks of gestation, the patient had refractory hypokalemia (2.7 mg/dL) and hypomagnesemia (1.0 mg/dL), metabolic alkalosis (HCO3- 30 mEq/L), hypocalciuria (urine Ca/Cr 0.036 mg/mg), and renal Mg and K wasting (Fe-Mg 23.7%; urine K > 20 mEq/L). These features were inconsistent with proximal tubular injury (which typically produces phosphaturia, glycosuria, uricosuria, and metabolic acidosis) and strongly suggestive of GS. Sequencing identified two pathogenic SLC12A3 variants, confirming the diagnosis. Management included aggressive electrolyte repletion and initiation of amiloride to limit renal potassium and magnesium losses, with a stable maternal–fetal course.
In pregnancy, persistent or longstanding electrolyte abnormalities warrant systematic evaluation for inherited tubulopathies. A pattern of hypocalciuria with metabolic alkalosis and renal potassium and magnesium wasting should prompt consideration of GS and genetic confirmation. Recognizing this distinction from drug- induced proximal tubulopathy changed management in this case and supports the careful use of potassium-sparing strategies such as amiloride in pregnancy (Figure 1).
