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Shared genetic correlations between kidney diseases and sepsis.

Tianlong Zhang1, Ying Cui1, Siyi Jiang1

  • 1Department of Critical Care Medicine, The Fourth Affiliated Hospital of School of Medicine, and International School of Medicine, International Institutes of Medicine, Zhejiang University, Yiwu, China.

Frontiers in Endocrinology
|August 1, 2024
PubMed
Summary

This study reveals shared genetic factors between kidney diseases and sepsis, identifying specific genes and pathways. These findings enhance understanding of the complex relationship and inform potential interventions for these conditions.

Keywords:
blood urea nitrogencreatininegenetic correlationkidneykidney stonessepsisurateurinary albumin-to-creatinine ratio

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Area of Science:

  • Genetics
  • Nephrology
  • Infectious Diseases

Background:

  • Clinical observations suggest a comorbidity between sepsis and kidney diseases.
  • Genetic predispositions to kidney conditions increase sepsis risk, and vice versa, indicating potential shared genetic underpinnings.
  • The precise genetic etiology linking these conditions remains largely unelucidated.

Purpose of the Study:

  • To investigate the shared genetic etiology between kidney diseases and sepsis.
  • To identify pleiotropic loci, genes, and pathways common to both conditions.
  • To explore the causal relationships and immune cell involvement in the comorbidity.

Main Methods:

  • Genome-wide association meta-analysis summary statistics were used for genetic correlation and pleiotropy analysis (PLACO).
  • Pathway and gene-level analyses were performed using MAGMA (Gene-Set Analysis and Gene-Test).
  • Stratified LD score regression and Mendelian Randomization (MR) were employed to assess SNP heritability enrichment and causality.

Main Results:

  • Significant genetic correlations were found between kidney function markers (BUN, creatinine, UACR), kidney stones, and sepsis.
  • 24 pleiotropic loci and 50 enriched pathways were identified. Key shared risk genes (PPP2R3A, VAMP8, DOCK7, HIBADH) were pinpointed.
  • Pleiotropy was enriched in kidney tissue, and 37 immune cell types showed enrichment, though MR analysis found no causal links.

Conclusions:

  • This research establishes a foundation for understanding shared etiological factors between kidney diseases and sepsis.
  • Identified pleiotropic loci, shared genes, pathways, and immune cells deepen insights into their complex relationship.
  • Findings offer potential avenues for early disease intervention and treatment strategies.