Yen Cheng-Chieh, Hsu Po-Chao, Lin Chih-Ching, Chen Szu-Chia, Hsiao Chih-Yen, Hwang Shang-Jyh
Division of Nephrology, Department of Internal Medicine, Ditmanson Medical Foundation Chia-Yi Christian Hospital, Chia-Yi, Taiwan.
Division of Cardiology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan.
Front Med (Lausanne). 2023 Sep 8;10:1268212. doi: 10.3389/fmed.2023.1268212. eCollection 2023.
Hemostatic abnormality has contributed to vascular access thrombosis in patients with chronic kidney disease (CKD). Previous studies have demonstrated that far-infrared radiation (FIR) therapy can maintain the patency and maturity of arteriovenous fistulas of patients undergoing hemodialysis (HD). However, prolonged access bleeding is observed once FIR is conducted at the end of dialysis. FIR can block the binding of platelet and von Willebrand factor (vWF), a predictor of hemostatic abnormality and vascular access thrombosis. However, clinical studies exploring FIR and vWF are sparse.
We recruited 20 HD patients, 21 CKD patients, and 20 controls to examine the alteration of vWF and a disintegrin and metalloproteinase with thrombospondin type 1 repeats 13 (ADAMTS13) following a single 40-min session of FIR therapy. In addition, the alteration of these factors in the HD group was examined following a 40-min FIR session thrice a week for 3 months.
A decreasing trend in the vWF activity-antigen ratio of participants in all groups following a single FIR session was observed. In addition, the ratio in the HD group was significantly lower following 3 months of FIR therapy. The subgroup analysis revealed a consistent trend and multiple regression analysis showed that participants not taking hydroxymethylglutaryl-coenzyme A reductase inhibitor, diabetes mellitus, and higher hemoglobin levels were the significant factors. The alteration of the vWF activity-antigen ratio correlated moderately to that of ADAMTS13 antigen and activity.
FIR may alter the ratio of ultra-large vWF multimers through ADAMTS13, contributing to inhibiting platelet-endothelium interactions of CKD patients.
止血异常是导致慢性肾脏病(CKD)患者血管通路血栓形成的原因之一。既往研究表明,远红外辐射(FIR)疗法可维持接受血液透析(HD)患者动静脉内瘘的通畅和成熟。然而,在透析结束时进行FIR治疗后,会出现血管通路长时间出血的情况。FIR可阻断血小板与血管性血友病因子(vWF)的结合,vWF是止血异常和血管通路血栓形成的一个预测指标。然而,探索FIR与vWF关系的临床研究较少。
我们招募了20例HD患者、21例CKD患者和20名对照者,以检测单次40分钟FIR治疗后vWF及含Ⅰ型血小板反应蛋白基序的解聚素和金属蛋白酶13(ADAMTS13)的变化。此外,对HD组患者进行每周3次、每次40分钟、共3个月的FIR治疗,检测这些因子的变化。
单次FIR治疗后,所有组参与者的vWF活性-抗原比值均呈下降趋势。此外,FIR治疗3个月后,HD组的该比值显著降低。亚组分析显示出一致的趋势,多元回归分析表明,未服用羟甲基戊二酰辅酶A还原酶抑制剂、患有糖尿病以及血红蛋白水平较高的参与者是显著因素。vWF活性-抗原比值的变化与ADAMTS13抗原及活性的变化呈中度相关。
FIR可能通过ADAMTS13改变超大vWF多聚体的比例,有助于抑制CKD患者的血小板-内皮相互作用。