Background <p>Left ventricular hypertrophy (LVH) is a common cardiovascular complication in chronic kidney disease (CKD), associated with increased morbidity and mortality. Systemic inflammation may contribute to LVH, but evidence remains limited in non-dialysis CKD populations. The neutrophil-to-lymphocyte ratio (NLR), a readily accessible inflammatory marker, may serve as a predictor of LVH.</p> Methods <p>In this cross-sectional study, 514 hospitalized CKD patients were enrolled. LVH was defined by echocardiographic criteria based on left ventricular mass index. NLR was calculated from complete blood counts. Logistic regression models were used to evaluate the association between NLR and LVH after adjusting for potential confounders. Subgroup and restricted cubic spline (RCS) analyses were conducted to assess consistency and non-linear relationships. Mediation analysis was performed to explore whether NLR mediated the relationship between CKD and LVH.</p> Results <p>Patients with LVH had significantly higher NLR levels than those without (3.14 vs. 2.20, <i>p</i> &lt; 0.001). After full adjustment, standardized NLR remained independently associated with LVH (adjusted OR: 1.34, 95% CI: 1.05–1.72, <i>p</i> = 0.02). RCS showed a linear relationship between NLR and LVH risk (p for nonlinear = 0.229). Subgroup analyses confirmed this robust association across subgroups (p for interaction ≥ 0.05). Mediation analysis indicated that NLR partially mediated the relationship between CKD and LVH, accounting for 5.1% of the total effect.</p> Conclusion <p>Elevated NLR was independently associated with LVH and may reflect underlying inflammatory processes involved in cardiac remodeling among patients with CKD. Given its simplicity and accessibility, NLR may serve as a potential marker for identifying individuals at increased cardiovascular risk, although further validation in prospective studies is warranted.</p> Clinical trial number <p>Not applicable.</p>

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Association between Neutrophil-to-Lymphocyte ratio and left ventricular hypertrophy in chronic kidney disease patients: a cross-sectional study

  • Li Wang,
  • Wen Zhang,
  • Jun Ji,
  • Fangfang Xiang,
  • Lin Zhang,
  • Xiaotian Jiang,
  • Yi Fang,
  • Xiaoqiang Ding,
  • Wuhua Jiang

摘要

Background

Left ventricular hypertrophy (LVH) is a common cardiovascular complication in chronic kidney disease (CKD), associated with increased morbidity and mortality. Systemic inflammation may contribute to LVH, but evidence remains limited in non-dialysis CKD populations. The neutrophil-to-lymphocyte ratio (NLR), a readily accessible inflammatory marker, may serve as a predictor of LVH.

Methods

In this cross-sectional study, 514 hospitalized CKD patients were enrolled. LVH was defined by echocardiographic criteria based on left ventricular mass index. NLR was calculated from complete blood counts. Logistic regression models were used to evaluate the association between NLR and LVH after adjusting for potential confounders. Subgroup and restricted cubic spline (RCS) analyses were conducted to assess consistency and non-linear relationships. Mediation analysis was performed to explore whether NLR mediated the relationship between CKD and LVH.

Results

Patients with LVH had significantly higher NLR levels than those without (3.14 vs. 2.20, p < 0.001). After full adjustment, standardized NLR remained independently associated with LVH (adjusted OR: 1.34, 95% CI: 1.05–1.72, p = 0.02). RCS showed a linear relationship between NLR and LVH risk (p for nonlinear = 0.229). Subgroup analyses confirmed this robust association across subgroups (p for interaction ≥ 0.05). Mediation analysis indicated that NLR partially mediated the relationship between CKD and LVH, accounting for 5.1% of the total effect.

Conclusion

Elevated NLR was independently associated with LVH and may reflect underlying inflammatory processes involved in cardiac remodeling among patients with CKD. Given its simplicity and accessibility, NLR may serve as a potential marker for identifying individuals at increased cardiovascular risk, although further validation in prospective studies is warranted.

Clinical trial number

Not applicable.