Calcium alkali syndrome, a resurging entity: a case report and historical overview
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Abstract
Background: Calcium-alkali syndrome (CAS), previously termed milk-alkali syndrome, is characterized by hypercalcemia, metabolic alkalosis, and acute kidney injury due to excessive intake of calcium and absorbable alkali. Initially associated with the Sippy diet for peptic ulcer treatment, its prevalence declined with modern gastrointestinal therapies but has resurged due to widespread Calcium Carbonate supplementation. Early recognition of CAS is essential to prevent hypercalcemic crises and renal dysfunction.
Case Presentation: A 60-year-old male with a history of hypertension and type 2 diabetes mellitus presented with palpitations, generalized weakness, muscle aches, polyuria, nausea, and a single episode of non-bloody vomiting. Examination revealed tachycardia (117 beats per minute) and severe hypertension (193/126 mmHg). Electrocardiography showed sinus tachycardia with premature ventricular complexes. Laboratory findings included severe hypercalcemia (18.9 mg/dL), acute kidney injury (creatinine rise from 0.8 to 2.9 mg/dL), and elevated BUN, bilirubin, total protein, white blood cell count, and CRP. Imaging ruled out alternative causes, and suppressed parathyroid hormone levels excluded hyperparathyroidism. A detailed history revealed chronic ingestion of 3–6 Calcium Carbonate (TUMS) tablets daily for acid reflux. Management included intravenous hydration, Zoledronic Acid, Furosemide, and antihypertensives, resulting in calcium normalization and renal function recovery.
Conclusion: This case highlights the resurgence of CAS due to excessive over-the-counter Calcium use. Early diagnosis and management, including cessation of calcium supplements, aggressive hydration, and electrolyte monitoring, are crucial in preventing complications. Long-term follow-up is essential to ensure renal function recovery and prevent recurrence.
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