Massry S G, Fadda G Z
Division of Nephrology, University of Southern California, School of Medicine, Los Angeles 90033.
Am J Kidney Dis. 1993 Jan;21(1):81-6. doi: 10.1016/s0272-6386(12)80727-x.
Studies on the metabolic profile of many cells have shown that chronic renal failure (CRF) is associated with a significant elevation in the basal levels of cytosolic calcium ([Ca2+]i). This latter abnormality is, in major part, responsible for the organ dysfunction in CRF. The initial step leading to the eventual increase in the basal level of [Ca2+]i is parathyroid hormone (PTH)-mediated increased calcium influx into cells. This is followed by decreased extrusion of calcium out of cells due to reduced activity of the enzymes responsible for pumping calcium out of the cells. The combination of increased entry and decreased exit of calcium results in elevation of [Ca2+]i. Prevention of secondary hyperparathyroidism in CRF or blocking of the effect of PTH by a calcium channel blocker results in normalization of [Ca2+]i and restoration of cell function. Thus, the available data are consistent with the notion that CRF is a state of cellular calcium toxicity, which underlies many of the metabolic and functional derangements in CRF.
对许多细胞代谢特征的研究表明，慢性肾衰竭（CRF）与胞质钙（[Ca2+]i）基础水平的显著升高有关。后一种异常在很大程度上是CRF器官功能障碍的原因。导致[Ca2+]i基础水平最终升高的第一步是甲状旁腺激素（PTH）介导的钙流入细胞增加。随后，由于负责将钙泵出细胞的酶活性降低，细胞内钙的排出减少。钙进入增加和排出减少的共同作用导致[Ca2+]i升高。预防CRF中的继发性甲状旁腺功能亢进或用钙通道阻滞剂阻断PTH的作用可使[Ca2+]i恢复正常并恢复细胞功能。因此，现有数据与CRF是一种细胞钙中毒状态的观点一致，这是CRF中许多代谢和功能紊乱的基础。
