Abstract
Cardiovascular diseases are the main cause of death in chronic kidney disease (CKD) patients. In dialysis patients, sudden cardiac death accounts for 40% of all deaths. In these patients, sudden cardiac death is usually secondary to an underlying cardiomyopathy, which is clinically identified by the high prevalence of left ventricular hypertrophy and the resultant mechanical and electrical dysfunction. CKD-related cardiomyopathy has a multifactorial pathophysiology. Recent evidence has highlighted the central pathophysiological role of chronic kidney disease-mineral and bone disorder (CKD-MBD) with hyperphosphatemia and high fibroblast growth factor 23 (FGF23) levels in these patients. Further, since CKD is known to be an αKlotho deficiency state, experimental studies have demonstrated that the deleterious effects of FGF23 can be minimized by reestablishing adequate soluble Klotho levels. Herein, we present a review that addresses not only the development of the understanding of CKD-related cardiomyopathy pathophysiology, but also explores the recent data that identify the triad of hyperphosphatemia, high FGF23 levels and αKlotho deficiency as playing a central role on it. Taken together, the data suggest that the uremic cardiomyopathy can be considered a new piece in the CKD-DMO puzzle.
Highlights
Cardiovascular disease is the leading cause of morbidity and mortality in chronic kidney disease (CKD) [1]
It was demonstrated in vivo that injection of fibroblast growth factor 23 (FGF23) resulted in Left ventricular hypertrophy (LVH). These findings revealed a causal role for FGF23 in the pathogenesis of LVH in CKD and suggest that chronic and extremely high FGF23 levels in dialysis patients may contribute to the development of LVH and mortality in this population [13]
There is no data demonstrating an increased cardiovascular risk or a higher prevalence of LVH in patients with FGF23-related hypophosphatemic diseases, but this is not expected since there is no hyperphosphatemia and CKD
Summary
Cardiovascular diseases are the main cause of death in chronic kidney disease (CKD) patients. Sudden cardiac death accounts for 40% of all deaths In these patients, sudden cardiac death is usually secondary to an underlying cardiomyopathy, which is clinically identified by the high prevalence of left ventricular hypertrophy and the resultant mechanical and electrical dysfunction. Recent evidence has highlighted the central pathophysiological role of chronic kidney disease-mineral and bone disorder (CKD-MBD) with hyperphosphatemia and high fibroblast growth factor 23 (FGF23) levels in these patients. We present a review that addresses the development of the understanding of CKD-related cardiomyopathy pathophysiology, and explores the recent data that identify the triad of hyperphosphatemia, high FGF23 levels and αKlotho deficiency as playing a central role on it.
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