Abstract: PUB157
Chronic Milk-Alkali Syndrome
Session Information
Category: Fluid, Electrolyte, and Acid-Base Disorders
- 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Saggese, Samantha M., Northwestern Memorial Hospital, Chicago, Illinois, United States
- Alotaibi, Manal, Northwestern Memorial Hospital, Chicago, Illinois, United States
Introduction
Milk-alkali syndrome is a common cause of hypercalcemia. Excessive calcium carbonate (antacid) consumption is a classic cause. We present a case of a 41 year old female with AKI, hypercalcemia and metabolic alkalosis due to dairy and supplemental vitamin D consumption.
Case Description
Our patient presented with abnormal labs (Table 1). She had no urinary frequency, abdominal pain, nausea, vomiting, constipation, or confusion on admission. She had mild pruritus and bilateral plantar foot pain and elbow pain. Her EKG was unremarkable. She received 2 liters of 0.9% saline and was started on continuous 0.9% saline intravenous fluids at 150 mL/hour upon admission.
She drank a half-gallon of milk per day for the last two years. She consumed a Premier protein shake each morning with breakfast, which contains 50% of the daily value (DV) of calcium and 25% of the DV of Vitamin D. She rarely took antacids. She had a multivitamin containing 100% of the DV of Vitamin D and an additional Vitamin D supplement. Review of systems was positive for episodes of polyuria, urinary frequency, and dry mouth, for which she compensated with large volume fluid intake.
Discussion
Our patient was diagnosed with chronic milk-alkali syndrome.
This syndrome is characterized by hypercalcemia, hyperphosphatemia, metabolic alkalosis, AKI and metastatic calcification. Hypercalcemia causes vasoconstriction, which decreases the glomerular filtration rate (GFR). It suppresses PTH secretion and leads to renal retention of phosphate. It activates the calcium-sensing receptor (CaSR) at the basolateral surface of Loop of Henle cells, inhibiting the Na-K-2Cl co-transporter, enhancing natriuresis and inducing volume depletion, which augments proximal reabsorption of calcium and bicarbonate. Alkalosis activates the pH-sensitive calcium channel, TRPV5, in the distal nephron, thereby contributing to calcium retention and hypercalcemia.
Standard treatment is withdrawal of exogenous calcium and administration of intravenous normal saline. Furosemide is sometimes used in severe cases.
Lab Results
| Calcium (mg/dL) | Creatinine (mg/dL) | Bicarbonate (mEq/L) | Phosphorous (mg/dL) | iPTH (pg/mL) | |
| 2.5 years prior | 9.7 | 1.08 | 29 | ||
| 1.5 years prior | 10.4 | 1.4 | 46 | ||
| 2 weeks prior | 12.2 | 4.57 | 38 | ||
| Admission | 13.2 | 4.94 | 38 | 5.8 | 25 |
| Discharge | 10.7 | 4.34 | 32 | 4 | |
| 1 month post | 10.6 | 3.38 | 27 | 3 | 27 |