SUN-781 - Milk-Alkali Syndrome-Induced Hypercalcemia in A 75-Year-Old Patient with End-Stage Renal Disease: A Diagnostic and Therapeutic Challenge

Background: Milk-alkali syndrome (MAS), historically associated with excessive calcium and absorbable alkali intake, remains a rare but important cause of non–PTH-mediated hypercalcemia, particularly in patients with chronic kidney disease. Early recognition is critical to avoid misdiagnosis and inappropriate therapy.

Case: A 75-year-old woman with ESRD secondary to IgA nephropathy on peritoneal dialysis, cardiomyopathy (EF 25%), osteopenia, and multiple squamous cell carcinomas presented with recent-onset hypercalcemia. She reported taking Tums four times daily for one month prior to admission. Laboratory evaluation revealed:
• Calcium 11.8 mg/dL (ref: 8.5–10.5 mg/dL)
• Creatinine 4.6 mg/dL (ref: 0.6–1.3 mg/dL)
• Magnesium 2.5 mg/dL (ref: 1.7–2.3 mg/dL)
• PTH 17.2 pg/mL (ref: 15–65 pg/mL)
• 25-OH Vitamin D 19 ng/mL (ref: 30–100 ng/mL)
• 1,25-(OH)₂ Vitamin D < 8 pg/mL (ref: 18–72 pg/mL)
• TSH 1.43 µIU/mL (ref: 0.4–4.0 µIU/mL)
• PTHrP 3.2 pmol/L (ref: < 4.0 pmol/L)
• ACE 43 U/L (ref: 8–52 U/L)
• Serum protein electrophoresis: no monoclonality detected
Management: She was treated with IV fluids, four doses of calcitonin, and a single 120 mg dose of denosumab, resulting in calcium normalization to 9.8 mg/dL prior to discharge.

Discussion: MAS is underrecognized in ESRD, where hypercalcemia may be multifactorial. Key diagnostic clues included suppressed PTH, low 1,25-(OH)₂ vitamin D, and absence of malignancy-related markers. Dialysis limits renal calcium excretion, yet acute hypercalcemia can be effectively managed with judicious antiresorptive therapy and supportive measures. Supplement and medication history remains critical.

Conclusion: MAS should be considered in ESRD patients with non–PTH-mediated hypercalcemia. Early identification allows targeted management and safe use of therapies such as denosumab.

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