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Abstract: SA-PO485

Hypokalemia in Pregnancy Concerning for a Masked Renal Tubulopathy

Session Information

Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders

  • 1002 Fluid‚ Electrolyte‚ and Acid-Base Disorders: Clinical


  • Rajendren, Soumya V., Columbia University Irving Medical Center, New York, New York, United States
  • Ahn, Wooin, Columbia University Irving Medical Center, New York, New York, United States

Pregnancy causes many physiologic alterations in fluid and electrolyte balance. Increased progesterone-mediated systemic vasodilation results in hypotension. RAAS upregulation increases renal K secretion. K loss is counteracted by progesterone’s inhibition of kaliuresis, protecting the pregnant woman against hypokalemia. GFR rises, increasing proximal tubular K resorption. All of these maintain normokalemia in pregnancy. Hypokalemia in pregnancy therefore may be the first clue to an underlying renal tubulopathy in an otherwise healthy patient.

Case Description

A 37 year old asymptomatic G5P4 at 28 weeks gestation with no significant history was referred for hypokalemia to 3.0-3.2 mmol/L. She was mildly hypotensive (93/58). A pre-pregnancy BMP showed serum Na 144 mmol/L, K 3.3 mmol/L, Cl 113 mmol/L, bicarbonate 17 mmol/L and Ca 8.7 mg/dL. During this pregnancy, serum Cl 103-107 mmol/L, bicarbonate 17-22 mmol/L, Ca 8.1-8.7 mg/dL with ionized Ca 1.16 mmol/L and Mg 1.8-2.0 mg/dL. All blood gases were drawn during pregnancy with pH 7.31-7.39 and pCO2 32-39 mmHg. Urine pH ranged 5.5-7.0 during this pregnancy and was 6.0-7.0 prior. Urine AG during this pregnancy was 38 mmol/L and TTKG 7 evidenced renal K wasting.There was no nephrocalcinosis, although calcium oxalate crystals were seen on a prior UA. She was given 10 mEq KCl daily with improvement and referred for genetic testing.


This case demonstrates the challenges in diagnosing renal tubulopathies in pregnancy, as the classic abnormalities may masquerade as normal pregnancy physiology. Scant pre-pregnancy data in these otherwise healthy patients makes accurate diagnoses even harder. Here, the challenge is differentiating a primary NAGMA with respiratory compensation from a physiologic progesterone-mediated respiratory alkalosis with metabolic compensation. Borderline hypocalcemia and questionable hypercalciuria could suggest a type 1 RTA or Bartter Syndrome. Hypotension could be physiologic or suggestive of a tubulopathy like Gitelman or Bartter. And while the absence of an obvious metabolic alkalosis argues against these, the very mild acidosis and correction with a just 10 mEq KCl daily is atypical of a pure type 1 RTA, raising concern for a mixed acid-base disorder. Accurate diagnosis in this population is essential for the prevention of adverse maternal and fetal outcomes, and renal genetic testing may play a key diagnostic role.