SAT-765 - Diagnostic Complexity of Postpartum Hypercalcemia in the Setting of Chronic Kidney Disease

Background
Hypercalcemia in the postpartum period is rare, with a broad differential diagnosis including primary hyperparathyroidism, malignancy, vitamin D–mediated etiologies, medication or supplement use, and less commonly, lactation-associated mechanisms. During lactation, mammary production of parathyroid hormone–related peptide (PTHrP) increases to support calcium mobilization for milk production. Excessive PTHrP secretion can lead to clinically significant hypercalcemia, particularly in the setting of high milk demand. Lactation-induced hypercalcemia remains an underrecognized cause of severe hypercalcemia and acute kidney injury in postpartum women. We report a case of hypercalcemia in a lactating woman with biochemical evidence of PTHrP-mediated hypercalcemia.

Case presentation
A 42-year-old lactating woman presented one month postpartum with polyuria, polydipsia, and insomnia, and was found to have severe hypercalcemia (15 mg/dL) and acute kidney injury (eGFR < 10 mL/min/1.73 m²). Initial labs showed an inappropriately normal PTH (26 pg/mL), normal 25-hydroxyvitamin D (66 ng/mL), elevated phosphorus (5.6 mg/dL), elevated PTHrP (35 pg/mL), and suppressed 1,25-dihydroxyvitamin D ( < 8 pg/mL).Hypercalcemia normalized and renal function improved partially (eGFR 33 mL/min/1.73 m²) with intravenous fluids, three doses of calcitonin, and cessation of breastfeeding. The patient had a normal age-appropriate cancer screening and serum protein electrophoresis. A low 24-hour urine calcium-to-creatinine ratio and lack of family history made familial hypocalciuric hypercalcemia unlikely. The etiology of hypercalcemia was attributed to lactation-induced mammary PTHrP production. At follow up appointments, labs showed normalization of PTHrP, serum calcium, and improvement of renal function (eGFR 50 mL/min/1.73 m²).

Conclusion
This case illustrates lactation-associated PTHrP overproduction as a rare but reversible cause of severe postpartum hypercalcemia. Early recognition and management with cessation of breastfeeding and supportive therapy led to biochemical improvement. Awareness of lactation-induced hypercalcemia may help prevent extensive and invasive diagnostic workup. This diagnosis should be considered in postpartum patients with hypercalcemia, particularly when PTH is suppressed in the setting of elevated PTHrP.

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