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Kidney–Bone: Interaction

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Bone Toxicology

Abstract

Kidney–bone interaction is a key controlling mechanism for the physiologic electrolyte balance in the body important for many physiological functions from the intracellular cell signaling to the energy metabolism and skeletal mineralization. Kidney, as a primary avenue for the regulating extracellular fluid and electrolyte homeostasis, participates to the maintenance of the continuous bone turnover and mineralization. At the same time, bone is the permanent physiological mineral store which could be activated for the normalizing electrolyte shift in the blood. This functional co-regulation in the kidney–bone interaction axis is accomplished by the tight feedback regulation between both organs and requires the input from the nervous and endocrine systems. The impact on the mineral homeostasis is achieved through the action of the (1) kidney-derived factors like vitamin D, acid–base metabolites, as well as blood electrolyte status and (2) bone-derived factors including FGF23, MEPE, and osteocalcin. Dysfunction in any of these factors alone or in combination can disrupt a multitude of the mineral balance in the cross-organ communication between the kidneys, intestine, bones, and parathyroid gland. Indeed, two essential bone-acting hormones vitamin D and parathyroid hormone (PTH) influence mineral balances by affecting the rate of intestinal absorption, renal reabsorption, and bone resorption and closing the key endocrine regulatory loop in mineral homeostasis.

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Correspondence to Olena V. Andrukhova PhD .

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Andrukhova, O.V., Erben, R.G. (2017). Kidney–Bone: Interaction. In: Smith, S., Varela, A., Samadfam, R. (eds) Bone Toxicology. Molecular and Integrative Toxicology. Springer, Cham. https://doi.org/10.1007/978-3-319-56192-9_11

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