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Identifying Genetic Variants and Metabolites Associated with Rapid Estimated Glomerular Filtration Rate Decline in Korea Based on Genome-Metabolomic Integrative Analysis. | LitMetric

AI Article Synopsis

  • Identifying genetic variants linked to rapid kidney function decline is crucial for preventing chronic kidney disease progression, particularly in patients with diabetes and hypertension.
  • A genome-wide association study revealed a new genetic risk factor, MARCHF1 (located at 4q32.3), associated with a noticeable decline in eGFR among the study participants.
  • The study also found that specific metabolites related to MARCHF1 may worsen kidney disease by causing oxidative stress, indicating a potential pathway to target for treatment.

Article Abstract

Identifying the predisposing factors to chronic or end-stage kidney disease is essential to preventing or slowing kidney function decline. Therefore, here, we investigated the genetic variants related to a rapid decline in the estimated glomerular filtration rate (eGFR) (i.e., a loss of >5 mL/min/1.73 m2 per year) and verified the relationships between variant-related diseases and metabolic pathway signaling in patients with chronic kidney disease. We conducted a genome-wide association study that included participants with diabetes, hypertension, and rapid eGFR decline from two Korean data sources (N = 115 and 69 for the discovery and the validation cohorts, respectively). We identified a novel susceptibility locus: 4q32.3 (rs10009742 in the MARCHF1 gene, beta = −3.540, P = 4.11 × 10−8). Fine-mapping revealed 19 credible, causal single-nucleotide polymorphisms, including rs10009742. The pimelylcarnitine and octadecenoyl carnitine serum concentrations were associated with rs10009742 (beta = 0.030, P = 7.10 × 10−5, false discovery rate (FDR) = 0.01; beta = 0.167, P = 8.11 × 10−4, FDR = 0.08). Our results suggest that MARCHF1 is associated with a rapid eGFR decline in patients with hypertension and diabetes. Furthermore, MARCHF1 affects the pimelylcarnitine metabolite concentration, which may mediate chronic kidney disease progression by inducing oxidative stress in the endoplasmic reticulum.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9695695PMC
http://dx.doi.org/10.3390/metabo12111139DOI Listing

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