Abstract: SA-PO0625
When Milk-Alkali Syndrome Is Not the Whole Story
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 2
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Gopannagari, Sai Tharun Reddy, Garden City Hospital, Garden City, Michigan, United States
- Kadari, Monika, Garden City Hospital, Garden City, Michigan, United States
- Achuta, Kesava Manikanta, Garden City Hospital, Garden City, Michigan, United States
- Kunzler, Daniel, Garden City Hospital, Garden City, Michigan, United States
- Chowdhury, Towfiqul Abedin, Garden City Hospital, Garden City, Michigan, United States
Introduction
Milk-alkali syndrome, also termed calcium-alkali syndrome, is characterized by hypercalcemia, metabolic alkalosis, and acute kidney injury resulting from excessive intake of calcium and absorbable alkali. Severe presentations may be complicated by pancreatitis and can be diagnostically challenging when parathyroid hormone is not appropriately suppressed.
Case Description
A 50-year-old man with hypertension, obesity, and gastroesophageal reflux disease presented with vomiting, poor oral intake, and severe epigastric pain after taking 6–8 calcium carbonate tablets every night for several weeks. Home medications included hydrochlorothiazide and lisinopril. Initial labs showed calcium 19.5 mg/dL, ionized calcium 10.4 mg/dL, creatinine 4.2 mg/dL from baseline 1.1 mg/dL, bicarbonate 36 mmol/L, and lipase 1,069 U/L. CT abdomen showed acute pancreatitis.
Home medications were stopped. He received fluids, calcitonin, pamidronate 90 mg, then 60 mg the next day, and two hemodialysis sessions for severe symptomatic hypercalcemia with oliguric AKI. Calcium and creatinine trends are shown in Figure 1. Calcium normalized, creatinine improved to 1.39 mg/dL, and lipase normalized.
Initial PTH was 21.3 pg/mL during severe hypercalcemia, an inappropriately non-suppressed value. Repeat PTH increased to 105.1 pg/mL after calcium improved. Neck ultrasound showed a 7 × 6 × 11 mm nodule posterior to the right thyroid gland, concerning for parathyroid adenoma.
He then developed rebound hypocalcemia, with calcium 6.6–7.0 mg/dL and ionized calcium 4.3 mg/dL. He was discharged on calcium carbonate and calcitriol with follow-up plans for calcium monitoring, parathyroid imaging, and endocrine/surgical follow-up.
Discussion
This case highlights calcium carbonate–associated milk-alkali syndrome complicated by dialysis-requiring AKI and pancreatitis. Non-suppressed PTH should prompt evaluation for coexisting primary hyperparathyroidism. Bisphosphonate therapy may cause significant hypocalcemia once calcium intake is stopped and kidney function recovers.
Figure 1. Trend in total calcium and creatinine during hospitalization.