Key result
Genetically predicted obstructive sleep apnea shows no causal link to CKD but correlates with higher BUN.
Why the study?
The causal relationship between obstructive sleep apnea, chronic kidney disease, and renal function remains unclear.
Does genetically predicted obstructive sleep apnea cause chronic kidney disease or altered kidney function, and vice versa?
Observational
Mendelian Randomization
Yes
Does genetically predicted obstructive sleep apnea cause chronic kidney disease or altered kidney function, and vice versa?
Effect estimate: OR 1.075 (95% CI 0.916-1.263)
p-value: p=0.375
Mendelian randomization suggests that while kidney function markers (BUN, eGFRcys) may causally influence the risk of obstructive sleep apnea, OSA does not appear to causally increase the risk of chronic kidney disease.
This is the authors' abstract. We don't add key points for this paper.
Purpose: It remains unclear about the causal association between obstructive sleep apnea (OSA) and chronic kidney disease (CKD) and renal function. This study aimed to explore the bidirectional causal relationship between OSA and CKD and renal function. Methods: We used a 2-sample bidirectional Mendelian randomization (MR) method to evaluate the causal relationship between OSA and estimated glomerular filtration rate from creatinine (eGFRcrea), eGFR from cystatin C (eGFRcys), urine albumin to creatinine ratio (UACR), blood urea nitrogen (BUN), and chronic kidney disease (CKD). Inverse variance weighted (IVW), MR-Egger, weighted median, MR-Egger, and pleiotropy residual sum and outlier test (MR-PRESSO) were used to calculate the β or odds ratio [OR] and their 95% CIs. Results: Genetically predicted OSA was found to be associated with BUN (β=0.040, 95% CI: 0.013-0.067, p = 0.003), but not associated with CKD (OR = 1.075, 95% CI: 0.916-1.263, p = 0.375), eGFRcrea (β=0.007, 95% CI: -0.004-0.017, p = 0.203), eGFRcys (β=-0.012, 95% CI: -0.026-0.002, p = 0.102), or UACR (β=-0.025, 95% CI: -0.058-0.007, p = 0.122). In the reverse analysis, genetically predicted eGFRcys (OR, 0.687; 95% CI, 0.497-0.950, p = 0.023) and BUN (OR, 1.686; 95% CI, 1.299-2.073, p = 0.008) was associated with an increased risk of OSA. The Cochrane's Q test reveals significant heterogeneity between various single nucleotide polymorphisms. MR-Egger indicated no evidence of genetic pleiotropy. Results were robust using other MR methods in sensitivity analyses. Conclusion: Through the two-sample MR analysis, we identified kidney function may have a causal relationship with OSA, but a causal relationship between OSA and CKD and kidney function remains uncertain. More studies are required to better understand the relationship between OSA and CKD and kidney function.
Mendelian randomization finds no causal OSA-CKD link; leaves open reverse effects of kidney markers on OSA risk.
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Liu et al. (2025) conducted an observational in Obstructive Sleep Apnea and Chronic Kidney Disease. Genetically predicted Obstructive Sleep Apnea vs. Genetically predicted absence of Obstructive Sleep Apnea was evaluated on Chronic Kidney Disease (CKD) (OR 1.075, 95% CI 0.916-1.263, p=0.375). Genetically predicted obstructive sleep apnea was not causally associated with chronic kidney disease (OR 1.075), but was associated with increased blood urea nitrogen levels (β=0.040).
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