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Hypercalcemia, Acute Kidney Injury, and Metabolic Alkalosis.

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Citation: Case Reports in Nephrology Print. 2022:1320259, 2022.PMID: 35433065Institution: MedStar Union Memorial HospitalDepartment: Internal Medicine ResidencyForm of publication: Journal ArticleMedline article type(s): Case ReportsSubject headings: IN PROCESS -- NOT YET INDEXEDYear: 2022 ISSN:

2090-665X

Name of journal: Case reports in nephrologyAbstract: Calcium regulation is tightly controlled in the body. Multiple causes of hypercalcemia have been studied including primary hyperparathyroidism, hypercalcemia of malignancy, and chronic granulomatous disorders. Among the less studied causes is calcium-alkali syndrome. Here, we discuss a case of hypercalcemia secondary to calcium-alkali syndrome, presenting with hypercalcemia, metabolic alkalosis, and acute kidney injury as a result of ingestion of a large amount of calcium supplements. Hypercalcemia can result in impaired collecting duct system sensitivity to antidiuretic hormone, afferent arteriole constriction, and activation of calcium sensor receptors in multiple tissues. The net effect is an increase in calcium reabsorption with a salt and water diuresis which leads to volume depletion, acute kidney injury, and metabolic alkalosis. Copyright © 2022 Faten Aqeel et al.All authors: Aqeel F, Del Castillo J, Hanouneh M, Jaar BGFiscal year: FY2022Digital Object Identifier:

https://dx.doi.org/10.1155/2022/1320259

Date added to catalog: 2022-05-11

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Item type	Current library	Collection	Call number	Status	Date due	Barcode
Journal Article	MedStar Authors Catalog	Article	35433065	Available		35433065

Calcium regulation is tightly controlled in the body. Multiple causes of hypercalcemia have been studied including primary hyperparathyroidism, hypercalcemia of malignancy, and chronic granulomatous disorders. Among the less studied causes is calcium-alkali syndrome. Here, we discuss a case of hypercalcemia secondary to calcium-alkali syndrome, presenting with hypercalcemia, metabolic alkalosis, and acute kidney injury as a result of ingestion of a large amount of calcium supplements. Hypercalcemia can result in impaired collecting duct system sensitivity to antidiuretic hormone, afferent arteriole constriction, and activation of calcium sensor receptors in multiple tissues. The net effect is an increase in calcium reabsorption with a salt and water diuresis which leads to volume depletion, acute kidney injury, and metabolic alkalosis. Copyright © 2022 Faten Aqeel et al.

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