The following is a summary of “Causal relationship between COVID-19 and estimated glomerular filtration rate: a bidirectional Mendelian randomization study,” published in the January 2024 issue of Nephrology by Li et al.
While past Mendelian studies linked estimated glomerular filtration rate (eGFR) to severe COVID-19, limited single nucleotide polymorphisms (SNPs) and lack of cystatin C tests left gaps in understanding this link.
Researchers conducted a retrospective study investigating the genetic underpinnings of the eGFR-COVID-19 link in Europeans.
They conducted bidirectional Mendelian randomization (MR) analysis using extensive genome-wide association study (GWAS) data. The log-eGFR was derived from serum creatinine or cystatin C levels, utilizing the Chronic Kidney Disease Genetics (CKDGen) Meta-analysis Dataset with the UK Biobank (N = 1,004,040). Examining COVID-19 phenotypes, the analysis included 122,616 COVID-19 cases and 2,475,240 controls from COVID-19 GWAS meta-analyses round 7. The primary estimation method employed was the inverse-variance weighted method.
The results showed genetically instrumented reduction in log-eGFR, derived from serum creatinine levels, exhibited a significantly elevated risk of severe COVID-19 (OR: 2.73, 95% CI: 1.38–5.41, P<0.05) and was notably linked 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). These associations retained significance when log-eGFR was genetically instrumented based on cystatin C levels. However, genetically instrumented COVID-19, irrespective of phenotype, did not correlate with log-eGFR calculated from either serum creatinine or cystatin C levels.
They concluded that reduced kidney function genes were linked to COVID-19 risk, but no apparent effect of COVID-19 on kidney function was found.
Source: bmcnephrol.biomedcentral.com/articles/10.1186/s12882-023-03443-4