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Hypercalcemia, Acute Kidney Injury, and Metabolic Alkalosis
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 hyper...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9007678/ https://www.ncbi.nlm.nih.gov/pubmed/35433065 http://dx.doi.org/10.1155/2022/1320259 |
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author | Aqeel, Faten Del Castillo, Jennifer Jaar, Bernard G. Hanouneh, Mohamad |
author_facet | Aqeel, Faten Del Castillo, Jennifer Jaar, Bernard G. Hanouneh, Mohamad |
author_sort | Aqeel, Faten |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-9007678 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-90076782022-04-14 Hypercalcemia, Acute Kidney Injury, and Metabolic Alkalosis Aqeel, Faten Del Castillo, Jennifer Jaar, Bernard G. Hanouneh, Mohamad Case Rep Nephrol Case Report 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. Hindawi 2022-04-06 /pmc/articles/PMC9007678/ /pubmed/35433065 http://dx.doi.org/10.1155/2022/1320259 Text en Copyright © 2022 Faten Aqeel et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Case Report Aqeel, Faten Del Castillo, Jennifer Jaar, Bernard G. Hanouneh, Mohamad Hypercalcemia, Acute Kidney Injury, and Metabolic Alkalosis |
title | Hypercalcemia, Acute Kidney Injury, and Metabolic Alkalosis |
title_full | Hypercalcemia, Acute Kidney Injury, and Metabolic Alkalosis |
title_fullStr | Hypercalcemia, Acute Kidney Injury, and Metabolic Alkalosis |
title_full_unstemmed | Hypercalcemia, Acute Kidney Injury, and Metabolic Alkalosis |
title_short | Hypercalcemia, Acute Kidney Injury, and Metabolic Alkalosis |
title_sort | hypercalcemia, acute kidney injury, and metabolic alkalosis |
topic | Case Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9007678/ https://www.ncbi.nlm.nih.gov/pubmed/35433065 http://dx.doi.org/10.1155/2022/1320259 |
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