APOL1 High-Risk Genotype is Not Associated With New or Worsening of Proteinuria or Kidney Function Decline Following COVID-19 Vaccination

IF 8.3 2区材料科学 Q1 MATERIALS SCIENCE, MULTIDISCIPLINARY

ACS Applied Materials & Interfaces Pub Date : 2024-09-01 DOI:10.1016/j.ekir.2024.06.023

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Abstract

Introduction

SARS-CoV-2 infection increases systemic inflammatory cytokines which act as a second-hit driver of Apolipoprotein L1 (APOL1)-mediated collapsing glomerulopathy. SARS-CoV-2 vaccination also increases cytokines. Recent reports of new glomerular disease in individuals with APOL1 high-risk genotype (HRG) following SARS-CoV-2 vaccination raised the concern SARS-CoV-2 vaccination may also act as a second-hit driver of APOL1-mediated glomerulopathy.

Methods

We screened 1507 adults in the Duke’s Measurement to Understand Reclassification of Disease of Cabarrus and Kannapolis (MURDOCK) registry and enrolled 105 eligible participants with available SARS-CoV-2 vaccination data, prevaccination and postvaccination serum creatinine, and urine protein measurements. Paired data were stratified by number of APOL1 risk alleles (RAs) and compared within groups using Wilcoxon signed rank test and across groups by analysis of variance.

Results

Among 105 participants, 30 (28.6%) had 2, 39 (37.1%) had 1, and 36 (34.3%) had 0 APOL1 RA. Most of the participants (94%) received at least 2 doses of vaccine. Most (98%) received the BNT162B2 (Pfizer) or mRNA-1273 (Moderna) vaccine. On average, the prevaccine and postvaccine laboratory samples were drawn 648 days apart. There were no detectable differences between pre- and post-serum creatinine or pre- and post-urine albumin creatinine ratio irrespective of the participants’ APOL1 genotype. Finally, most participants with APOL1 RA had the most common haplotype (E150, I228, and K255) and lacked the recently described protective N264K haplotype.

Conclusion

In this observational study, APOL1 HRG is not associated with new or worsening of proteinuria or decline in kidney function following SARS-CoV-2 vaccination. Validation of this result in larger cohorts would further support the renal safety of SARS-CoV-2 vaccine in individuals with APOL1 HRG.

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接种COVID-19疫苗后，APOL1高风险基因型与蛋白尿或肾功能下降的新增或恶化无关

SARS-CoV-2 感染会增加全身炎症细胞因子，从而成为载脂蛋白 L1（APOL1）介导的塌陷性肾小球病的第二驱动力。接种 SARS-CoV-2 疫苗也会增加细胞因子。最近关于接种 SARS-CoV-2 疫苗后 APOL1 高危基因型 (HRG) 患者出现新的肾小球疾病的报道引起了人们的关注，SARS-CoV-2 疫苗接种也可能成为 APOL1 介导的肾小球病变的二次驱动因素。我们在杜克大学的 "卡巴鲁斯和坎纳波利斯疾病重新分类测量"（MURDOCK）登记处筛选了 1507 名成人，并招募了 105 名符合条件的参与者，这些参与者均有 SARS-CoV-2 疫苗接种数据、接种前和接种后血清肌酐及尿蛋白测量结果。根据 APOL1 风险等位基因（RA）的数量对配对数据进行分层，并通过 Wilcoxon 符号秩检验对组内数据进行比较，通过方差分析对组间数据进行比较。在 105 名参与者中，30 人（28.6%）有 2 个 APOL1 风险等位基因，39 人（37.1%）有 1 个，36 人（34.3%）没有。大多数参与者（94%）至少接种了 2 剂疫苗。大多数参与者（98%）接种了 BNT162B2（辉瑞）或 mRNA-1273（Moderna）疫苗。疫苗接种前和疫苗接种后实验室样本的采集时间平均相隔 648 天。无论参与者的 APOL1 基因型如何，接种前和接种后的血清肌酐或尿液白蛋白肌酐比值均无明显差异。最后，大多数 APOL1 RA 患者具有最常见的单倍型（E150、I228 和 K255），缺乏最近描述的保护性 N264K 单倍型。在这项观察性研究中，APOL1 HRG 与接种 SARS-CoV-2 疫苗后出现或加重蛋白尿或肾功能下降无关。在更大的群体中验证这一结果将进一步支持 SARS-CoV-2 疫苗对 APOL1 HRG 患者肾脏的安全性。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

ACS Applied Materials & Interfaces 工程技术-材料科学：综合

CiteScore

16.00

自引率

6.30%

发文量

4978

审稿时长

1.8 months

期刊介绍： ACS Applied Materials & Interfaces is a leading interdisciplinary journal that brings together chemists, engineers, physicists, and biologists to explore the development and utilization of newly-discovered materials and interfacial processes for specific applications. Our journal has experienced remarkable growth since its establishment in 2009, both in terms of the number of articles published and the impact of the research showcased. We are proud to foster a truly global community, with the majority of published articles originating from outside the United States, reflecting the rapid growth of applied research worldwide.