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Background <p>Obstructive sleep apnea (OSA) has been increasingly associated with chronic kidney disease (CKD). NLRP3, a central component of the inflammasome, is involved in hypoxia- and inflammation-related pathways. We therefore investigated whether circulating NLRP3 was associated with prevalent CKD and incident CKD risk in patients with OSA.</p> Methods <p>This single-center observational study included 648 OSA patients. Multivariable linear and logistic regression models were used to evaluate the associations of circulating NLRP3 with renal function indices and prevalent CKD. Cox proportional hazards models and Kaplan–Meier analysis were used to assess the relationship between baseline NLRP3 and incident CKD.</p> Results <p>Compared with the non-CKD group, the CKD group showed a greater nocturnal hypoxic burden, including a higher apnea-hypopnea index (37.53 ± 18.80 vs. 29.74 ± 17.95 events/h) and higher T90 (18.37% [7.26–31.94] vs. 10.84% [4.12–21.63]) (all <i>P</i> &lt; 0.01). Circulating NLRP3 was independently associated with lower estimated glomerular filtration rate (eGFR) (β = −4.18, 95% CI − 5.69 to − 2.67; <i>P</i> &lt; 0.001) and higher logarithmically transformed urinary albumin-to-creatinine ratio [ln(UACR)] (β = 0.14, 95% CI 0.08 to 0.21; <i>P</i> &lt; 0.001). In fully adjusted logistic models, each 1-standard deviation increase in NLRP3 was associated with higher odds of prevalent CKD (OR = 1.49, 95% CI 1.16–1.92; <i>P</i> = 0.002), and the highest quartile showed a greater likelihood of CKD than the lowest quartile (OR = 2.68, 95% CI 1.57–4.58; <i>P</i> &lt; 0.001; P for trend &lt; 0.001). In the prospective cohort, higher baseline NLRP3 remained associated with incident CKD after full adjustment (HR = 1.46, 95% CI 1.10–1.94; <i>P</i> = 0.009), and Kaplan–Meier analysis showed lower CKD-free survival in the high-NLRP3 group (log-rank <i>P</i> = 0.011).</p> Conclusions <p>In patients with OSA, elevated circulating NLRP3 was associated with prevalent CKD, and an increased risk of incident CKD during follow-up. These findings suggest that NLRP3 may serve as a potential inflammatory marker for renal risk stratification in OSA.</p>

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Association of peripheral NLRP3 inflammasome activation with prevalent and incident chronic kidney disease in patients with obstructive sleep apnea: a prospective study

  • 期刊论文

  • 发表日期：

    2026年6月30日

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  • Panpan Cai,
  • Boke Li,
  • Yunxia Li,
  • Liping Duan

摘要

Background

Obstructive sleep apnea (OSA) has been increasingly associated with chronic kidney disease (CKD). NLRP3, a central component of the inflammasome, is involved in hypoxia- and inflammation-related pathways. We therefore investigated whether circulating NLRP3 was associated with prevalent CKD and incident CKD risk in patients with OSA.

Methods

This single-center observational study included 648 OSA patients. Multivariable linear and logistic regression models were used to evaluate the associations of circulating NLRP3 with renal function indices and prevalent CKD. Cox proportional hazards models and Kaplan–Meier analysis were used to assess the relationship between baseline NLRP3 and incident CKD.

Results

Compared with the non-CKD group, the CKD group showed a greater nocturnal hypoxic burden, including a higher apnea-hypopnea index (37.53 ± 18.80 vs. 29.74 ± 17.95 events/h) and higher T90 (18.37% [7.26–31.94] vs. 10.84% [4.12–21.63]) (all P < 0.01). Circulating NLRP3 was independently associated with lower estimated glomerular filtration rate (eGFR) (β = −4.18, 95% CI − 5.69 to − 2.67; P < 0.001) and higher logarithmically transformed urinary albumin-to-creatinine ratio [ln(UACR)] (β = 0.14, 95% CI 0.08 to 0.21; P < 0.001). In fully adjusted logistic models, each 1-standard deviation increase in NLRP3 was associated with higher odds of prevalent CKD (OR = 1.49, 95% CI 1.16–1.92; P = 0.002), and the highest quartile showed a greater likelihood of CKD than the lowest quartile (OR = 2.68, 95% CI 1.57–4.58; P < 0.001; P for trend < 0.001). In the prospective cohort, higher baseline NLRP3 remained associated with incident CKD after full adjustment (HR = 1.46, 95% CI 1.10–1.94; P = 0.009), and Kaplan–Meier analysis showed lower CKD-free survival in the high-NLRP3 group (log-rank P = 0.011).

Conclusions

In patients with OSA, elevated circulating NLRP3 was associated with prevalent CKD, and an increased risk of incident CKD during follow-up. These findings suggest that NLRP3 may serve as a potential inflammatory marker for renal risk stratification in OSA.