Bidirectional two-sample Mendelian randomization analysis reveals a causal effect of chronic pain on chronic kidney diseases and renal function.

A growing body of research has shown a connection between chronic pain and chronic kidney disease (CKD). However, it is unclear if these correlations point to a cause-and-effect link. Our goal is to investigate the causal link between renal function or CKD and chronic pain. Using genome-wide association study (GWAS) datasets on these traits, we performed bidirectional two-sample Mendelian randomization (MR) analyses in this work to evaluate genetic linkages and possible causal links between chronic pain and CKD or renal function. The CKD Genetics Consortium provided the GWAS data for CKD symptoms, estimated creatinine-based glomerular filtration rate (eGFRcrea) and cystatin C-based GFR (eGFRcys). A sizable biomedical database of GWAS provided summary statistics for both chronic widespread musculoskeletal pain (CWP) and multisite chronic pain (MCP). MR analysis revealed that MCP was significantly associated with an increased risk of CKD (OR = 1.52; 95% CI: 0.97 - 2.40; p = 0.037) and eGFRcys decline (OR = 0.97; 95% CI: 0.95 - 0.99; p = 0.014). The reliability of the MR analysis was demonstrated by sensitivity analysis. However, MR analysis did not find a significant association between CWP and CKD or renal function decline. Additionally, this study did not discover a link between renal function decline or CKD and chronic pain. Our research revealed a substantial correlation between MCP and a higher risk of CKD and renal function deterioration.