机构:
Drexel Univ, Div Nephrol & Hypertens, Coll Med, Philadelphia, PA 19102 USADrexel Univ, Div Nephrol & Hypertens, Coll Med, Philadelphia, PA 19102 USA
Patel, Ami M.
[1
]
Adeseun, Gbemisola A.
论文数: 0引用数: 0
h-index: 0
机构:
Univ So Calif, Keck Sch Med, Div Nephrol, Los Angeles, CA 90033 USADrexel Univ, Div Nephrol & Hypertens, Coll Med, Philadelphia, PA 19102 USA
Adeseun, Gbemisola A.
[2
]
Goldfarb, Stanley
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机构:
Univ Penn, Div Renal Electrolyte & Hypertens, Perelman Sch Med, Philadelphia, PA 19104 USADrexel Univ, Div Nephrol & Hypertens, Coll Med, Philadelphia, PA 19102 USA
Goldfarb, Stanley
[3
]
机构:
[1] Drexel Univ, Div Nephrol & Hypertens, Coll Med, Philadelphia, PA 19102 USA
[2] Univ So Calif, Keck Sch Med, Div Nephrol, Los Angeles, CA 90033 USA
[3] Univ Penn, Div Renal Electrolyte & Hypertens, Perelman Sch Med, Philadelphia, PA 19104 USA
The ingestion of calcium, along with alkali, results in a well-described triad of hypercalcemia, metabolic alkalosis, and renal insufficiency. Over time, the epidemiology and root cause of the syndrome have shifted, such that the disorder, originally called the milk-alkali syndrome, is now better described as the calcium-alkali syndrome. The calcium-alkali syndrome is an important cause of morbidity that may be on the rise, an unintended consequence of shifts in calcium and vitamin D intake in segments of the population. We review the pathophysiology of the calcium-alkali syndrome.