Fibroblast growth factor 23—Klotho and hypertension: experimental and clinical mechanisms

Michael Freundlich, Gerardo Gamba, Bernardo Rodriguez-Iturbe

Research output: Contribution to journalReview articlepeer-review

Abstract

Hypertension (HTN) and chronic kidney disease (CKD) are increasingly recognized in pediatric patients and represent risk factors for cardiovascular morbidity and mortality later in life. In CKD, enhanced tubular sodium reabsorption is a leading cause of HTN due to augmented extracellular fluid volume expansion. The renin-angiotensin-aldosterone system (RAAS) upregulates various tubular sodium cotransporters that are also targets of the hormone fibroblast growth factor 23 (FGF23) and its co-receptor Klotho. FGF23 inhibits the activation of 1,25-dihydroxyvitamin D that is a potent suppressor of renin biosynthesis. Here we review the complex interactions and disturbances of the FGF23–Klotho axis, vitamin D, and the RAAS relevant to blood pressure regulation and discuss the therapeutic strategies aimed at mitigating their pathophysiologic contributions to HTN.

Original languageEnglish (US)
JournalPediatric Nephrology
DOIs
StateAccepted/In press - 2020

Keywords

  • Angiotensin
  • Blood pressure
  • FGF23
  • Tubular sodium handling
  • Vitamin D

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Nephrology

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