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Bidirectional two-sample Mendelian randomization analysis reveals a causal effect of chronic pain on chronic kidney
Insights
Multisite chronic pain (MCP) is linked to increased chronic kidney disease (CKD) risk and declining kidney function. This study used Mendelian randomization to explore the causal relationship between chronic pain and CKD, finding a significant association for MCP.
Area of Science:
- Nephrology
- Genetics
- Epidemiology
Background:
- Chronic pain and chronic kidney disease (CKD) are prevalent conditions with established correlations.
- The causal relationship between CKD and chronic pain remains incompletely understood.
- Investigating genetic links can elucidate potential causal pathways.
Purpose of the Study:
- To investigate the potential causal link between chronic kidney disease (CKD) or renal function and chronic pain.
- To differentiate the impact of various chronic pain phenotypes on kidney health.
Main Methods:
- Bidirectional two-sample Mendelian randomization (MR) analyses were performed.
- Genome-wide association study (GWAS) datasets were utilized for chronic pain phenotypes and kidney function markers.
- Data included chronic widespread musculoskeletal pain (CWP), multisite chronic pain (MCP), estimated glomerular filtration rate (eGFRcrea), and eGFRcys.
Main Results:
- Multisite chronic pain (MCP) showed a significant association with an increased risk of CKD (OR = 1.52) and decline in cystatin C-based GFR (eGFRcys) (OR = 0.97).
- No significant association was found between chronic widespread musculoskeletal pain (CWP) and CKD or renal function decline.
- The study did not identify a causal link between renal function decline or CKD and chronic pain in the reverse direction.
Conclusions:
- Multisite chronic pain (MCP) is associated with a higher risk of developing chronic kidney disease (CKD) and experiencing renal function deterioration.
- The findings highlight the importance of considering pain status in the management of kidney disease.
Objective:
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.
Materials And Methods:
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).
Results:
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.
Conclusion:
Our research revealed a substantial correlation between MCP and a higher risk of CKD and renal function deterioration.
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