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Angiotensin II receptor 1 antibodies associate with post-transplant focal segmental glomerulosclerosis and proteinuria.
BMC Nephrology ( IF 2.3 ) Pub Date : 2020-07-02 , DOI: 10.1186/s12882-020-01910-w
Mohammad Abuzeineh 1 , Amtul Aala 2 , Sami Alasfar 1 , Nada Alachkar 1
Affiliation  

Angiotensin II type 1 receptors (AT1Rs) are expressed on podocytes, endothelial and other cells, and play an essential role in the maintenance of podocyte function and vascular homeostasis. The presence of AT1R antibodies (AT1R-Abs) leads to activation of these receptors resulting in podocyte injury and endothelial cell dysfunction. We assessed the correlation between AT1R-Abs and the risk of post-transplant FSGS. This is a retrospective study, which included all kidney transplant recipients with positive AT1R-Abs (≥ 9 units/ml), who were transplanted and followed at our center between 2006 and 2016. We assessed the development of biopsy proven FSGS and proteinuria by urine protein to creatinine ratio of ≥1 g/g and reviewed short and long term outcomes. We identified 100 patients with positive AT1R-Abs at the time of kidney transplant biopsy or proteinuria. 49% recipients (FSGS group) had biopsy-proven FSGS and/or proteinuria and 51% did not (non-FSGS group). Pre-transplant hypertension was present in 89% of the FSGS group compared to 72% in the non-FSGS group, p = 0.027. Of the FSGS group, 43% were on angiotensin converting enzyme inhibitors or angiotensin receptor blockers prior to transplantation, compared to 25.5% in the non-FSGS group, p = 0.06. Primary idiopathic FSGS was the cause of ESRD in 20% of the FSGS group, compared to 6% in the non-FSGS group, p = 0.03. The allograft loss was significantly higher in the FSGS group 63% compared to 39% in non-FSGS. Odds ratio and 95% confidence interval were 2.66 (1.18–5.99), p = 0.017. Our data suggest a potential association between AT1R-Abs and post-transplant FSGS leading to worse allograft outcome. Therefore, AT1R-Abs may be considered biomarkers for post-transplant FSGS.

中文翻译:

血管紧张素 II 受体 1 抗体与移植后局灶节段性肾小球硬化和蛋白尿有关。

血管紧张素 II 1 型受体 (AT1R) 在足细胞、内皮细胞和其他细胞上表达,在维持足细胞功能和血管稳态中发挥重要作用。AT1R 抗体 (AT1R-Abs) 的存在导致这些受体的激活,导致足细胞损伤和内皮细胞功能障碍。我们评估了 AT1R-Abs 与移植后 FSGS 风险之间的相关性。这是一项回顾性研究,其中包括 2006 年至 2016 年期间在我们中心接受移植和随访的所有 AT1R-Ab 阳性(≥ 9 个单位/毫升)的肾移植受者。我们评估了活检证实的 FSGS 和尿蛋白尿的发展蛋白质与肌酐的比率≥1 g/g 并回顾了短期和长期结果。我们确定了 100 名在肾移植活检或蛋白尿时具有阳性 AT1R-Ab 的患者。49% 的受者(FSGS 组)有活检证实的 FSGS 和/或蛋白尿,51% 没有(非 FSGS 组)。FSGS 组中有 89% 存在移植前高血压,而非 FSGS 组为 72%,p = 0.027。在 FSGS 组中,43% 的患者在移植前使用血管紧张素转换酶抑制剂或血管紧张素受体阻滞剂,而非 FSGS 组为 25.5%,p = 0.06。FSGS 组 20% 的原发性特发性 FSGS 是 ESRD 的原因,而非 FSGS 组为 6%,p = 0.03。与非 FSGS 组的 39% 相比,FSGS 组的同种异体移植物丢失显着更高,为 63%。优势比和 95% 置信区间为 2.66 (1.18–5.99),p = 0.017。我们的数据表明 AT1R-Ab 与移植后 FSGS 之间存在潜在关联,导致同种异体移植结果较差。因此,AT1R-Abs 可能被认为是移植后 FSGS 的生物标志物。
更新日期:2020-07-02
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