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Calcium-alkali syndrome; Cope syndrome; Burnett syndrome; Hypercalcemia; Calcium metabolism disorder DefinitionMilk-alkali syndrome is a condition in which there is a high level of calcium in the body (hypercalcemia). This causes a shift in the body's acid/base balance toward alkaline (metabolic alkalosis). As a result, there can be a loss of kidney function. CausesMilk-alkali syndrome is almost always caused by taking too many calcium supplements, usually in the form of calcium carbonate. Calcium carbonate is a common calcium supplement. It is often taken to prevent or treat bone loss (osteoporosis). Calcium carbonate is also an ingredient found in antacids (such as Tums). A high level of vitamin D in the body, such as from taking supplements, can worsen milk-alkali syndrome. Calcium deposits in the kidneys and in other tissues can occur in milk-alkali syndrome. SymptomsIn the beginning, the condition usually has no symptoms (asymptomatic). When symptoms do occur, they can include:
Exams and TestsCalcium deposits within the tissue of the kidney (nephrocalcinosis) may be seen on:
Other tests used to make a diagnosis may include:
TreatmentIn severe cases, treatment involves giving fluids through the vein (by IV). Otherwise, treatment involves drinking fluids along with reducing or stopping calcium supplements and antacids that contain calcium. Vitamin D supplements also need to be reduced or stopped. Outlook (Prognosis)This condition is often reversible if kidney function remains normal. Severe prolonged cases may lead to permanent kidney failure requiring dialysis. Possible ComplicationsThe most common complications include:
When to Contact a Medical ProfessionalContact your health care provider if:
PreventionIf you use calcium-containing antacids often, tell your provider about digestive problems. If you are trying to prevent osteoporosis, do not take more than 1.2 grams (1200 milligrams) of calcium per day unless instructed by your provider. ReferencesBringhurst FR, Demay MB, Kronenberg HM. Hormones and disorders of mineral metabolism. In: Melmed S, Auchus RJ, Goldfine AB, Koenig RJ, Rosen CJ, eds. Williams Textbook of Endocrinology. 14th ed. Philadelphia, PA: Elsevier; 2020:chap 29. DuBose TD, Rosner MH. Metabolic alkalosis. In: Gilbert S, ed. National Kidney Foundation Primer on Kidney Diseases. 8th ed. Philadelphia, PA: Elsevier; 2023:chap 14. Thakker RV. The parathyroid glands, hypercalcemia, and hypocalcemia. In: Goldman L, Cooney KA, eds. Goldman-Cecil Medicine. 27th ed. Philadelphia, PA: Elsevier; 2024:chap 227. | |
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Review Date: 12/31/2023 Reviewed By: Walead Latif, MD, Nephrologist and Clinical Associate Professor, Rutgers Medical School, Newark, NJ. Review provided by VeriMed Healthcare Network. Also reviewed by David C. Dugdale, MD, Medical Director, Brenda Conaway, Editorial Director, and the A.D.A.M. Editorial team. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed medical professional should be consulted for diagnosis and treatment of any and all medical conditions. Links to other sites are provided for information only -- they do not constitute endorsements of those other sites. No warranty of any kind, either expressed or implied, is made as to the accuracy, reliability, timeliness, or correctness of any translations made by a third-party service of the information provided herein into any other language. © 1997- A.D.A.M., a business unit of Ebix, Inc. Any duplication or distribution of the information contained herein is strictly prohibited. | |