Renal control of calcium, phosphate, and magnesium homeostasis.

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Abstract

Calcium, phosphate, and magnesium are multivalent cations that are important for many biologic and cellular functions. The kidneys play a central role in the homeostasis of these ions. Gastrointestinal absorption is balanced by renal excretion. When body stores of these ions decline significantly, gastrointestinal absorption, bone resorption, and renal tubular reabsorption increase to normalize their levels. Renal regulation of these ions occurs through glomerular filtration and tubular reabsorption and/or secretion and is therefore an important determinant of plasma ion concentration. Under physiologic conditions, the whole body balance of calcium, phosphate, and magnesium is maintained by fine adjustments of urinary excretion to equal the net intake. This review discusses how calcium, phosphate, and magnesium are handled by the kidneys.

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Most cited references 102

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Claudins and the modulation of tight junction permeability.

Dorothee Günzel, Alan Yu (2013)

Claudins are tight junction membrane proteins that are expressed in epithelia and endothelia and form paracellular barriers and pores that determine tight junction permeability. This review summarizes our current knowledge of this large protein family and discusses recent advances in our understanding of their structure and physiological functions.

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The parathyroid is a target organ for FGF23 in rats.

Iddo Z. Ben-Dov, Hillel Galitzer, Vardit Lavi-Moshayoff … (2007)

Phosphate homeostasis is maintained by a counterbalance between efflux from the kidney and influx from intestine and bone. FGF23 is a bone-derived phosphaturic hormone that acts on the kidney to increase phosphate excretion and suppress biosynthesis of vitamin D. FGF23 signals with highest efficacy through several FGF receptors (FGFRs) bound by the transmembrane protein Klotho as a coreceptor. Since most tissues express FGFR, expression of Klotho determines FGF23 target organs. Here we identify the parathyroid as a target organ for FGF23 in rats. We show that the parathyroid gland expressed Klotho and 2 FGFRs. The administration of recombinant FGF23 led to an increase in parathyroid Klotho levels. In addition, FGF23 activated the MAPK pathway in the parathyroid through ERK1/2 phosphorylation and increased early growth response 1 mRNA levels. Using both rats and in vitro rat parathyroid cultures, we show that FGF23 suppressed both parathyroid hormone (PTH) secretion and PTH gene expression. The FGF23-induced decrease in PTH secretion was prevented by a MAPK inhibitor. These data indicate that FGF23 acts directly on the parathyroid through the MAPK pathway to decrease serum PTH. This bone-parathyroid endocrine axis adds a new dimension to the understanding of mineral homeostasis.

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Physiology and function of the tight junction.

Wayne F. Anderson, Henriëtte E. van der Horst (2009)

Understanding of tight junctions has evolved from their historical perception as inert solute barriers to recognition of their physiological and biochemical complexity. Many proteins are specifically localized to tight junctions, including cytoplasmic actin-binding proteins and adhesive transmembrane proteins. Among the latter are claudins, which are critical barrier proteins. Current information suggests that the paracellular barrier is most usefully modeled as having two physiologic components: a system of charge-selective small pores, 4 A in radius, and a second pathway created by larger discontinuities in the barrier, lacking charge or size discrimination. The first pathway is influenced by claudin expression patterns and the second is likely controlled by different proteins and signals. Recent information on claudin function and disease-causing mutations have led to a more complete understanding of their role in barrier formation, but progress is impeded by lack of high resolution structural information.

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Author and article information

Journal

Journal ID (iso-abbrev): Clin J Am Soc Nephrol

Title: Clinical journal of the American Society of Nephrology : CJASN

ISSN (Electronic): 1555-905X

ISSN (Print): 1555-9041

Publication date (Electronic): Jul 7 2015

Volume: 10

Issue: 7

Affiliations

[1 ] Division of Renal Diseases and Hypertension, Department of Medicine, University of Colorado Denver, Aurora, Colorado Judith.Blaine@ucdenver.edu.

[2 ] Division of Renal Diseases and Hypertension, Department of Medicine, University of Colorado Denver, Aurora, Colorado.

Article

Publisher Item ID: CJN.09750913

DOI: 10.2215/CJN.09750913

PubMed ID: 25287933

SO-VID: c06e2649-97de-4380-8242-432adfd115b5

History

Keywords: calcium,cell and transport physiology,channel,electrolytes,ion,renal physiology

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Keywords: calcium, cell and transport physiology, channel, electrolytes, ion, renal physiology

Renal control of calcium, phosphate, and magnesium homeostasis.

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Abstract

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Neuronal Signaling

Most cited references 102

Claudins and the modulation of tight junction permeability.

The parathyroid is a target organ for FGF23 in rats.

Physiology and function of the tight junction.

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