The neutrophil-to-monocyte ratio: a superior inflammatory marker predicting poor prognosis in IgA nephropathy

Immunoglobulin A nephropathy (IgAN) is a chronic immune-mediated inflammatory disorder, and a substantial body of research indicates that the activation of inflammatory responses plays a pivotal role in its onset and progression. We conducted a comprehensive assessment of the influence of systemic inflammatory markers, specifically the neutrophil-to-monocyte ratio (NMR), lymphocyte-to-monocyte ratio (LMR), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), platelet-to-albumin ratio (PAR), and the systemic immune-inflammation (SII), on the phenotypic manifestations and disease progression of IgAN. A retrospective cohort study was conducted, involving 559 patients who underwent regular follow-up evaluations spanning a minimum of one year. The utility of these inflammatory indicators in predicting IgAN progression was quantified using the area under the receiver operating characteristic curve (AUROC). The kidney progression event was defined as a 30% estimated glomerular filtration rate (eGFR) decline or end-stage kidney disease or death. A prognostic model was developed using Cox proportional hazards regression. Circulating levels of galactose-deficient IgA1 (Gd-IgA1), factor B, and mannose-binding lectin (MBL) were quantitatively determined through enzyme-linked immunosorbent assay (ELISA). Among the investigated markers, NLR demonstrated the highest prognostic utility, with an AUROC of 0.622 (p < 0.001) at a cutoff value of 2.11. NMR and SII followed closely, exhibiting AUROCs of 0.611 (p < 0.001) and 0.581 (p = 0.006) respectively, at their respective cutoff points of 8.25 and 560.11. Conversely, LMR, PLR, and PAR yielded AUROCs below the statistical significance threshold (0.473, 0.532, and 0.556, respectively; all p > 0.05). Univariate Cox regression analysis revealed that elevated neutrophil counts, NMR, NLR, SII, urinary leukocyte levels, and severe Oxford C score were predictive of IgAN progression. Notably, NMR emerged as an independent risk factor for adverse renal outcomes in IgAN patients, even after adjusting for established risk factors, whereas NLR and SII lost statistical significance. Patients with high NMR displayed more pronounced clinical-pathological features and elevated Gd-IgA1 and factor B levels compared to those with low NMR, whereas no such correlation was observed between Gd-IgA1 and either NLR or SII. Our findings highlight the crucial role of NMR as an independent predictor of disease progression in IgAN, underscoring its utility in risk stratification for patients.