Blood:血凝素缺乏促进镰状细胞病患者发生急性肾损伤!

2020-08-11 MedSci原创 MedSci原创

急性肾损伤(AKI)是镰状细胞病(SCD)的主要临床表现之一。临床证据表明,红血球白蛋白可引起SCD的AKI,但其无菌炎症过程至今未明确。

中心点:

在镰状细胞病(SCD)中,血浆α-1微球蛋白与血凝蛋白浓度的比值与AKI生物标志物相关。

在转基因SCD小鼠中,循环血红素对肾脏的清除增强可触发AKI。

摘要:

急性肾损伤(AKI)是镰状细胞病(SCD)的主要临床表现之一。临床证据表明,红血球白蛋白可引起SCD的AKI,但其无菌炎症过程至今未明确。

近期,研究人员发现,与健康对照组相比,SCD患者的血凝素缺陷与α-1微球蛋白(A1M)的代偿性增加相关,从而导致SCD患者的A1M/血凝素的比值增加高达10倍。A1M/血凝素比值与患有SCD的人和小鼠的溶血和AKI标志物相关。

小鼠实验表明在SCD小鼠中,过量的血红素被导向肾脏,在该过程中,A1M可导致AKI,而对照组中过量的血红素则如预期的那样被输送到肝脏。利用遗传和骨髓嵌合技术,研究人员证实,在溶血性应激刺激下,血凝蛋白缺乏可促进镰状小鼠发生AKI。但在诱导溶血应激之前,用纯化的血凝蛋白进行纠正镰状小鼠的血凝蛋白缺乏时,AKI则被阻断。

本研究明确了获得性血凝素缺乏是SCD患者发生AKI的危险因素,血凝素替代疗法是一种潜在的治疗选择。

原始出处:

Solomon Ofori-Acquah, et al.Hemopexin deficiency promotes acute kidney injury in sickle cell disease.Blood. Feburary 10, 2020.

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