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.
Copyright © 2018. Published by Elsevier Inc.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Acute Kidney Injury / complications
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Acute Kidney Injury / physiopathology*
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Acute Kidney Injury / therapy
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Animals
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Fibroblast Growth Factor-23
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Fibroblast Growth Factors / metabolism
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Humans
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Hyperparathyroidism / blood
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Hyperparathyroidism / etiology
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Hyperphosphatemia / etiology
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Hyperphosphatemia / therapy
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Hypocalcemia / etiology
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Hypocalcemia / physiopathology*
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Klotho Proteins
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Membrane Proteins / metabolism
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Minerals / metabolism*
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Parathyroid Hormone / blood
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Renal Replacement Therapy / adverse effects
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Vitamin D / analogs & derivatives
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Vitamin D / blood
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Vitamin D / therapeutic use
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Vitamin D Deficiency / blood
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Vitamin D Deficiency / drug therapy*
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Vitamin D Deficiency / etiology
Substances
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FGF23 protein, human
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KLB protein, human
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Membrane Proteins
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Minerals
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Parathyroid Hormone
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Vitamin D
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Fibroblast Growth Factors
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1,25-dihydroxyvitamin D
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Fibroblast Growth Factor-23
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25-hydroxyvitamin D
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Klotho Proteins