Why the study?
Elevated FGF23 induces LVH and cardiac fibrosis in CKD, but whether it also stimulates the local cardiac RAAS to promote these pathologies remained unclear.
Population
5/6 nephrectomized rats and isolated neonatal rat ventricular myocytes and fibroblasts
Comparison
5/6 nephrectomy vs sham operation, and FGF23 stimulation vs controls in vitro
Design
In vivo and in vitro animal and cell experimental study
Authors
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Preclinical data link FGF23 to cardiac remodeling via local RAAS; hypothesis-generating and requires human validation before clinical consideration.
FGF23 promotes cardiac hypertrophy and fibrosis by activating the local renin-angiotensin-aldosterone system, providing a mechanistic link between CKD and uremic cardiomyopathy that can be attenuated by RAAS inhibitors.
Böckmann et al. (2019) studied this question.
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