Generally, the daily intake of less than 2 grams of calcium is considered to be safe. Prior to starting any calcium supplementation, it is recommended to discuss the individualized calcium requirements of the person. If a person begins a calcium supplementation regimen, they should be educated on the common signs and symptoms of hypercalcemia and milk-alkali syndrome, as well as how to reverse the syndrome by discontinuing the offending agent and seeking medical attention. Treatment
For mild cases of MAS, the only intervention needed is to withdraw the offending agent. By having the person stop taking any calcium supplements and any other alkali agents they have been taking rapidly corrects hypercalcemia and alkalosis in MAS.In severe cases, hospitalization may be required to manage this syndrome. Withholding calcium and initiating IV fluids such as saline to correct hypovolemia. The initial rate of infusion is generally around 200-300 mL/h in people not experiencing edema then it is adjusted to maintain urine output of 100 - 150 mL/h. However, the rate is variable depending on the individuals age, renal status, comorbidities, and the severity of hypercalcemia.Furosemide can be used to treat hypercalcemia as it induces caliuresis (excreting calcium in the urine). Standard practice of adequate rehydration and electrolyte monitoring should be used to avoid alkalosis and renal insufficiency.If kidney failure is advanced then treatment for that is required, namely chronic dialysis.Calcimimetic agents may be necessary, e.g. Cinacalcet. Outcomes
In mild cases of milk-alkali syndrome, full recovery is expected and reduction to renal function is reversible.
However, it is well known that MAS is usually associated with a triad of symptoms that include hypercalcemia, alkalosis, and acute kidney injury. In general, milk-alkali syndrome starts with excess calcium levels in the body (hypercalcemia), which causes the bodys pH to increase (become more alkaline) resulting in metabolic alkalosis and ultimately contributes to a decrease in renal function.Factors involved in the development of hypercalcemia include excess intestinal absorption of calcium, saturation of the bones buffering capacity for calcium, decreased renal excretion, and abnormal vitamin D metabolism. Underlying kidney disease is a risk factor for MAS, but even people with healthy kidneys can develop the syndrome.For a healthy individual, if calcium levels are high, the kidneys will decrease its production of calcitriol (active vitamin D) by reducing the hydroxylation of calcidiol (inactive vitamin D); lower calcitriol levels means a lower rate of calcium absorption in the small intestine, which eventually offsets the elevated calcium levels. However, excessive ingestion of calcium of more than 10-15 g per day has been reported to cause calcium levels too high for renal calcitriol suppression to control, resulting in net calcium absorption that ultimately causes hypercalcemia.Hypercalcemia affects the kidneys in multiple ways that altogether contributes to hypovolemia. Prolonged hypercalcemia can decrease glomerular filtration rate (GFR) via vasoconstriction, reduce creatinine clearance, and eventually cause renal insufficiency. Hypercalcemia also causes natriuresis by blocking the Na-K-Cl cotransporter (NKCC) in the medullary thick ascending limb of the loop of Henle, leading increased sodium excretion followed by water excretion that leads to hypovolemia.