8472 A Little Too Much Of Tums: A Unique Presentation Of Milk Alkali Syndrome

Abstract Disclosure: Z. Al-Hiti: None. A. Misbah: None. Milk-Alkali Syndrome is characterized by a triad of hypercalcemia, metabolic alkalosis, and renal dysfunction. Historically associated with the excessive consumption of milk and alkali-containing antacids, it has re-emerged in recent years due to the widespread use of calcium and vitamin D supplements. It primarily results from an imbalance between calcium intake and renal excretion, leading to elevated calcium levels in the bloodstream. We present a case of milk-alkali syndrome with persistent renal dysfunction after normalizing calcium levels. We present the case of a 65-year-old male who presented to the emergency department with generalized weakness, poor oral intake, and confusion for 3 days. He was noted to have been more adherent with taking his prescribed medications over the last 2 weeks, which include calcitriol 0.5 mcg BID, calcium acetate 667 mg TID, and calcium carbonate 800 mg TID. On admission, he was afebrile and hemodynamically stable. . On examination, he had dry mucous membranes. He had no focal neurological deficits but he was confused and lethargic, and was only oriented to self. Other examination was noncontributory. Complete blood count and urinalysis were largely unremarkable. Chemistry demonstrated an elevated calcium level of 16.0 (8.3-10.6 mg/dL), ionized calcium of 7.3 (4.6-5.3 mg/dL), sodium of 134 (135-145 mmol/L), potassium of 5.4 (3.5-5.1 mmol/L), high phosphorus of 5.3 (2.4-5.1 mg/dL), and bicarbonate of 36 (20-31 mEq/L). Creatinine was elevated at 2.9 (0.6-1.1 mg/dL) from baseline of 1.3 to 1.4 mg/dL, and he had a BUN of 40(9-23 mg/dL). Venous blood gas showed a pH of 7.54( 7.32-7.42), pCO2 of 56 (40-52 mm Hg), and bicarbonate of 38 (23-28 mEq/L), indicating metabolic alkalosis. TSH was elevated at 36.15 (0.55- 4.78 uIU/mL) with a level of 140 two weeks back. Chest X-ray, renal ultrasound and CT head all showed no acute disease. Further work-up revealed a low PTH level of 6.3 (18.4-80 pg/mL), normal PTHrP level and 25-OH Vitamin D. There was no monoclonal gammopathy. Management included aggressive IV fluid resuscitation and IV calcitonin. However, no zoledronic acid was given due to a history of parathyroidectomy and risk of hypocalcemia. His serum calcium improved and eventually normalized. His confusion resolved. However, his creatinine and BUN increased to 3.4 mg/dL and 77, respectively, and did not improve to his baseline. This case highlights the importance of recognizing Milk-Alkali Syndrome as a potential consequence of over-the-counter calcium supplementation and highlights the potential for acute kidney injury which could be irreversible. Healthcare providers should be vigilant in identifying patients at risk, which includes older patients and patients with chronic kidney disease. Early recognition and appropriate management are crucial to prevent further renal deterioration and improve outcomes in individuals with Milk-Alkali Syndrome. Presentation: 6/2/2024