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. 2024 Jan 15;25(1):21.
doi: 10.1186/s12882-023-03443-4.

The causal relationship between COVID-19 and estimated glomerular filtration rate: a bidirectional Mendelian randomization study

Qiuling Li  1 , Mengjiao Lin  2 , Yinghui Deng  3 , Haozhang Huang  4   5   6
Affiliations

The causal relationship between COVID-19 and estimated glomerular filtration rate: a bidirectional Mendelian randomization study

Qiuling Li et al. BMC Nephrol. .

Abstract

Background: Previous Mendelian studies identified a causal relationship between renal function, as assessed by estimated glomerular filtration rate (eGFR), and severe infection with coronavirus disease 2019 (COVID-19). However, much is still unknown because of the limited number of associated single nucleotide polymorphisms (SNPs) of COVID-19 and the lack of cystatin C testing. Therefore, in the present study, we aimed to determine the genetic mechanisms responsible for the association between eGFR and COVID-19 in a European population.

Methods: We performed bidirectional Mendelian randomization (MR) analysis on large-scale genome-wide association study (GWAS) data; log-eGFR was calculated from the serum levels of creatinine or cystatin C by applying the Chronic Kidney Disease Genetics (CKDGen) Meta-analysis Dataset combined with the UK Biobank (N = 1,004,040) and on COVID-19 phenotypes (122,616 COVID-19 cases and 2,475,240 controls) from COVID19-hg GWAS meta-analyses round 7. The inverse-variance weighted method was used as the main method for estimation.

Results: Analyses showed that the genetically instrumented reduced log-eGFR, as calculated from the serum levels of creatinine, was associated with a significantly higher risk of severe COVID-19 (odds ratio [OR]: 2.73, 95% confidence interval [CI]: 1.38-5.41, P < 0.05) and significantly related to COVID-19 hospitalization (OR: 2.36, 95% CI: 1.39-4.00, P < 0.05) or infection (OR: 1.24, 95% CI: 1.01-1.53, P < 0.05). The significance of these associations remained when using log-eGFR based on the serum levels of cystatin C as genetically instrumented. However, genetically instrumented COVID-19, regardless of phenotype, was not related to log-eGFR, as calculated by either the serum levels of creatinine or cystatin C.

Conclusions: Our findings suggest that genetical predisposition to reduced kidney function may represent a risk factor for COVID-19. However, a consistent and significant effect of COVID-19 on kidney function was not identified in this study.

Keywords: Coronavirus Disease 2019; Estimated glomerular filtration rate; Kidney function; Mendelian randomization; Single nucleotide polymorphism.

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Conflict of interest statement

Competing interests. The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
Overall design of the MR analysis in the present study
Fig. 2
Fig. 2
IVW estimates for per 1 unit of log transformed eGFR lower on COVID-19
Fig. 3
Fig. 3
IVW estimates of the effect of COVID-19 on kidney function
See this image and copyright information in PMC

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