Campos Isaac, Faul Christian
Division of Nephrology and Section of Mineral Metabolism, Department of Medicine, Heersink School of Medicine, The University of Alabama at Birmingham, Birmingham, AL, USA.
Nephrol Dial Transplant. 2025 Jun 30;40(7):1294-1309. doi: 10.1093/ndt/gfaf001.
Elevations in systemic phosphate levels, also called hyperphosphatemia, occur in chronic kidney disease (CKD) and during the normal aging process, and are associated with various pathologies, such as cardiovascular injury. Experimental studies suggest that at high serum concentrations, phosphate can induce osteogenic differentiation of vascular smooth muscle cells and contribute to vascular calcification. However, the precise underlying mechanism leading to cardiovascular injury is not well understood. Here we discuss how elevations in extracellular phosphate levels could potentially affect cells and intracellular reactions and functions in general. We then zoom in on the heart to discuss whether hyperphosphatemia can have direct pathologic actions beyond inducing vascular calcification. Furthermore, we discuss myocardial calcification as a pathologic event that has not been described and studied in greater detail, but that seems to occur in the context of hyperphosphatemia-induced pathologic cardiac remodeling, as observed in dialysis patients.
全身磷酸盐水平升高,也称为高磷血症,发生于慢性肾脏病(CKD)及正常衰老过程中,且与多种病理状况相关,如心血管损伤。实验研究表明,在高血清浓度下,磷酸盐可诱导血管平滑肌细胞发生成骨分化并促成血管钙化。然而,导致心血管损伤的确切潜在机制尚未完全明确。在此,我们讨论细胞外磷酸盐水平升高如何可能影响细胞以及一般的细胞内反应和功能。然后我们聚焦于心脏,讨论高磷血症是否除了诱导血管钙化之外还能产生直接的病理作用。此外,我们讨论心肌钙化这一尚未得到更详细描述和研究,但似乎在高磷血症诱导的病理性心脏重塑背景下发生的病理事件,如在透析患者中所观察到的。