Sohail Azmat, Obereigner Jakob, Mitter Gregor, Schmid Thomas, Hofer Anna-Sofie, Schuster Gerhard, Hügl Astrid, Dorninger Angelika H, Mandl Markus, Pasch Andreas, Lackner Helmut K, Papousek Ilona, Dieplinger Benjamin, Suessner Susanne, Antlanger Marlies, Cejka Daniel, Alesutan Ioana, Voelkl Jakob
Institute for Physiology and Pathophysiology, Johannes Kepler University Linz, Linz, Austria.
AMD GmbH, Linz, Austria.
Clin Kidney J. 2024 Aug 20;17(9):sfae258. doi: 10.1093/ckj/sfae258. eCollection 2024 Sep.
The excessive cardiovascular mortality of patients with chronic kidney disease (CKD) could be linked to mineral stress, the biological consequence of calcium-phosphate nanoparticle exposure. This study investigated whether zinc is associated with mineral stress markers in CKD.
inc and T50 (serum calcification propensity) as well as hydrodynamic radius of secondary calciprotein particles (CPP2) were measured in blood donors and CKD patients with/out dialysis.
Serum zinc concentrations and T50 were reduced, while CPP2 radius was increased in CKD patients. Serum zinc levels positively correlated with T50 and inversely correlated with CPP2 radius. In a hierarchical linear regression model, T50 was associated with age, calcium, phosphate, magnesium and albumin. Addition of zinc significantly improved prediction of the model, confirming an additional contribution of zinc to T50. Similar observations were made for the association of zinc and CPP2 radius, but spiking experiments indicated that zinc may stronger modify T50 than CPP2 radius. Also, urinary zinc excretion was increased in patients with kidney disease and correlated to T50 and CPP2 radius. erum zinc further correlated with markers of arterial stiffness in blood donors and CKD patients, but these associations did not remain significant in a multivariate linear regression model.
Reduced serum zinc levels in CKD appear directly linked to lower T50 and associated with larger CPP2 radius. Further studies on the associations of zinc and mineral stress as well as putative therapeutic benefits of zinc supplementation are required.
慢性肾脏病(CKD)患者过高的心血管死亡率可能与矿物质应激有关,这是钙磷纳米颗粒暴露的生物学后果。本研究调查了锌是否与CKD中的矿物质应激标志物相关。
在献血者以及接受或未接受透析的CKD患者中测量了inc和T50(血清钙化倾向)以及次级钙蛋白颗粒(CPP2)的流体动力学半径。
CKD患者的血清锌浓度和T50降低,而CPP2半径增加。血清锌水平与T50呈正相关,与CPP2半径呈负相关。在分层线性回归模型中,T50与年龄、钙、磷、镁和白蛋白相关。加入锌显著改善了模型的预测,证实了锌对T50的额外贡献。对于锌与CPP2半径的关联也有类似观察结果,但加标实验表明锌对T50的修饰作用可能比对CPP2半径的修饰作用更强。此外,肾病患者的尿锌排泄增加,且与T50和CPP2半径相关。血清锌在献血者和CKD患者中还与动脉僵硬度标志物相关,但在多变量线性回归模型中这些关联不再显著。
CKD患者血清锌水平降低似乎与较低的T50直接相关,并与较大的CPP2半径相关。需要进一步研究锌与矿物质应激的关联以及补锌的假定治疗益处。