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Semin Nephrol. 2019 Jan;39(1):41-56. doi: 10.1016/j.semnephrol.2018.10.004.

Dysregulated Mineral Metabolism in AKI.

Author information

1
Division of Renal Medicine, Brigham and Women's Hospital, Boston, MA. Electronic address: deleaf@bwh.harvard.edu.
2
Division of Nephrology, Department of Medcine, New York Medical College, Valhalla, NY.

Abstract

Dysregulated mineral metabolism is a nearly universal sequalae of acute kidney injury (AKI). Abnormalities in circulating mineral metabolites observed in patients with AKI include hypocalcemia, hyperparathyroidism, hyperphosphatemia, decreased vitamin D metabolite levels, and increased fibroblast growth factor 23 levels. We review the pathophysiology of dysregulated mineral metabolism in AKI with a focus on calcium, phosphate, parathyroid hormone, and vitamin D metabolites. We discuss how mineral metabolite levels can serve as novel prognostic markers for incident AKI and other related outcomes in various clinical settings. Finally, we discuss how vitamin D metabolites potentially could be used as novel therapeutic agents for AKI prevention and treatment.

KEYWORDS:

AKI; FGF23; PTH; acute kidney injury; calcium; mineral metabolism; phosphate; vitamin D

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