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Kidney Week

Abstract: FR-PO601

A Rare Case of Hypoparathyroidism Complicating Pregnancy

Session Information

  • Trainee Case Reports - III
    October 26, 2018 | Location: Exhibit Hall, San Diego Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Reports

  • 402 Bone and Mineral Metabolism: Clinical


  • Antman, Elliott, University of Colorado School of Medicine, Denver, Colorado, United States
  • Bansal, Anip, University of Colorado School of Medicine, Denver, Colorado, United States
  • Carson, John M., NYU Winthrop Hospital, Mineola, New York, United States

Heterozygous activating mutations in the calcium sensing receptor (CaSR) which increase CaSR sensitivity to extracellular Ca cause autosomal dominant hypocalcemia (ADH). ADH results in hypocalcemia with low-normal parathyroid hormone (PTH) levels and is often diagnosed as hypoparathyroidism. This case describes the complicated course of a pregnant woman with ADH.

Case Description

A 31 year old female was diagnosed with autoimmune hypoparathyroidism at age 22 when she presented with paresthesias and cramping in both hands with a serum Ca of 5.5mg/dL, phosphate of 6.1mg/dL and PTH of 10pg/mL. Genetic testing for DiGeorge syndrome was negative. She had no family history of calcium or other electrolyte disorders.
Her symptoms improved with oral Ca supplementation and calcitriol. Three years later a renal sonogram demonstrated medullary nephrocalcinosis. Her 24 hour urine Ca ranged 300 to 700mg and a thiazide (HCTZ) was added. Due to persistent hyperphosphatemia, the calcitriol was replaced by recombinant PTH.
After starting HCTZ and recombinant PTH she developed symptomatic hypomagnesemia which persisted after stopping HCTZ. A 24hr urine magnesium (Mg) was 204mg. Her 24hr urine potassium was 140mEq while hypokalemic and off HCTZ.
At age 29 she had a pregnancy complicated by exacerbation of hypomagnesemia and unexpected intrauterine fetal demise (IUFD) at 35 weeks. At the time, her serum Mg level was 1.3mg/dL. Other electrolyte levels were normal. A fetal ultrasound 10 days prior showed mild polyhydramnios and otherwise normal fetus. The cause of IUFD was uncertain but attributed to the hypomagnesemia.
A year later she became pregnant again with exacerbation of hypomagnesemia. ADH was suspected and genetic testing was sent midterm. At 34 weeks she developed polyhydramnios, was induced, and delivered uneventfully. Two days post-partum, her newborn became bradycardic and seized with a serum Ca of 5.9mg/dL. PTH was 12pg/mL. Soon after, the mother's genetic testing confirmed a CaSR activating mutation consistent with ADH type 1.


ADH should be considered in the differential for hypoparathyroidism as its diagnosis has significant genetic/family planning implications. Treatment of ADH (thiazides, recombinant PTH) may exacerbate renal Mg wasting associated with this disease, as does pregnancy.
Calcilytics, allosteric antagonists of the CaSR, are an emerging therapy that may benefit patients with ADH.