Sources of calcium and alkali include dietary supplements taken for the prevention of osteoporosis or hyperparathyroidism and antacids taken for peptic ulcer disease.

[5] Common acute symptoms of milk-alkali syndrome include nausea and vomiting, dry mouth, confusion, lethargy, and distaste for milk.

[5][7] The signs and symptoms of milk-alkali syndrome can develop after only a few days and up to several months following the initial ingestion of absorbable calcium and alkali.

[3] However, the severity of signs and symptoms of milk-alkali syndrome is largely dependent upon the duration and quantity of calcium and alkali ingested.

[3] If ingestion of calcium and alkali is continued, neurologic symptoms such as memory loss, personality changes, lethargy, stupor, and coma will persistently develop over time, as a result of the extreme hypercalcemia and electrolyte imbalances.

[4][6] Histologically, the kidneys of individuals with milk-alkali syndrome have been shown to have "complete glomerulus hyalinization, thickening of the Bowman's capsule, tubular atrophy, vascular changes, and diffuse lymphocytic infiltration.

"[3] Other laboratory tests, such as measuring serum bicarbonate, pH, 1,25-OH vitamin D, and parathyroid hormone (PTH) can show signs of milk-alkali syndrome.

[3][5] Other drugs reported to be associated with the development of MAS include thiazide diuretics, which cause increased reabsorption of calcium in the kidneys; resulting hypovolemia can lead to contraction alkalosis.

[5][10] Prolonged hypercalcemia can decrease glomerular filtration rate (GFR) via vasoconstriction, reduce creatinine clearance, and eventually cause renal insufficiency.

[5] Additionally, hypercalcemia can decrease the reabsorption of water in the kidney's collecting ducts by suppressing antidiuretic hormone (ADH) receptors, contributing to more hypovolemia.

[5][10] Hypovolemia then leads to metabolic alkalosis (increase in blood pH) by stimulating bicarbonate reabsorption in order to maintain extracellular volume.

[5][10] In summary, the symptoms of alkalosis is the net result of over-consumption of absorbable alkali, hypercalcemia-induced hypovolemia, and impaired glomerular filtration rate.

[3] Over recent years, people have become more aware of the benefits of calcium and how to access it, leading to a consequential rise in cases of milk-alkali syndrome.

[citation needed] In mild cases of milk-alkali syndrome, full recovery is expected and reduction to renal function is reversible.

[3] Long term consumption of large amounts of calcium supplementation associated with milk-alkali syndrome has also been linked to adverse cardiovascular outcomes.

[16] In the early years after the discovery of milk-alkali syndrome, the prevalence of the disease among people treated with Sippy's treatment varied from 2% to 18%.

[3] The use of milk and alkali to treat gastric ulcers greatly contributed to the development of milk-alkali syndrome in people but the incidence of milk-alkali syndrome greatly diminished when the true cause of most gastric ulcers was identified and drugs other than antacids were developed to treat heartburn, such as acid-reducing drugs like H2-receptor antagonists or proton pump inhibitors.

[17] This syndrome was discovered in the early 1900s when people began experiencing adverse effects from Bertrand Sippy's gastric ulcer treatment consisting of milk and alkali.

[4] However, both the acute and chronic form of this illness involve renal impairment which is a key contributor to the hypercalcemia seen in people with MAS.