Abstract
Hyperphosphatemia or even serum phosphate levels within the “normal laboratory range” are highly associated with increased cardiovascular disease risk and mortality in the general population and patients suffering from chronic kidney disease (CKD). As the kidney function declines, serum phosphate levels rise and subsequently induce the development of hypertension, vascular calcification, cardiac valvular calcification, atherosclerosis, left ventricular hypertrophy and myocardial fibrosis by distinct mechanisms. Therefore, phosphate is considered as a promising therapeutic target to improve the cardiovascular outcome in CKD patients. The current therapeutic strategies are based on dietary and pharmacological reduction of serum phosphate levels to prevent hyperphosphatemia in CKD patients. Large randomized clinical trials with hard endpoints are urgently needed to establish a causal relationship between phosphate excess and cardiovascular disease (CVD) and to determine if lowering serum phosphate constitutes an effective intervention for the prevention and treatment of CVD.
Highlights
High serum phosphate concentrations associate with cardiovascular disease (CVD) risk in both the general population and chronic kidney disease (CKD) patients (Lim et al, 2015; Reiss et al, 2018)
Myocardial biopsy analysis on 24 patients who died of CKD indicated that 67% of them had Left Ventricular Hypertrophy (LVH), which was characterized by significantly expressed FGFR4, nuclear factor of activated T cells (NFAT), and klotho deficiency compared with the control group (Leifheit-Nestler et al, 2016)
Hyperphosphatemia participates in the occurrence and development of a variety of cardiovascular diseases, as an important risk factor for the excessively increased cardiovascular mortality, especially in CKD population
Summary
Reviewed by: Dongdong Sun, Xijing Hospital, Fourth Military Medical University, China. Hyperphosphatemia or even serum phosphate levels within the “normal laboratory range” are highly associated with increased cardiovascular disease risk and mortality in the general population and patients suffering from chronic kidney disease (CKD). As the kidney function declines, serum phosphate levels rise and subsequently induce the development of hypertension, vascular calcification, cardiac valvular calcification, atherosclerosis, left ventricular hypertrophy and myocardial fibrosis by distinct mechanisms. Phosphate is considered as a promising therapeutic target to improve the cardiovascular outcome in CKD patients. The current therapeutic strategies are based on dietary and pharmacological reduction of serum phosphate levels to prevent hyperphosphatemia in CKD patients. Large randomized clinical trials with hard endpoints are urgently needed to establish a causal relationship between phosphate excess and cardiovascular disease (CVD) and to determine if lowering serum phosphate constitutes an effective intervention for the prevention and treatment of CVD.
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