# Prognostic Significance of Lactate Dehydrogenase-to-Albumin Ratio and Neutrophil Percentage-to-Albumin Ratio in IgA Nephropathy

**Authors:** Balázs Sági, Tibor Vas, Sadra Salehi, Tibor József Kovács

PMC · DOI: 10.3390/biomedicines14020318 · Biomedicines · 2026-01-30

## TL;DR

This study shows that high LAR and NPAR levels are linked to worse kidney and heart outcomes in IgA nephropathy patients.

## Contribution

The study identifies LAR and NPAR as novel prognostic markers for IgA nephropathy outcomes.

## Key findings

- High LAR is independently associated with worse composite renal and cardiovascular outcomes.
- High NPAR is linked to poorer primary and separate renal and cardiovascular outcomes.
- LAR and NPAR reflect inflammation and nutritional status in IgAN patients.

## Abstract

Background: Inflammation plays a key role in the development of immunoglobulin A nephropathy (IgAN). The lactate dehydrogenase-to-albumin ratio (LAR) and neutrophil percentage-to-albumin ratio (NPAR) have emerged as markers reflecting inflammation and nutritional status. This study evaluated the prognostic significance of LAR and NPAR for predicting renal and cardiovascular (CV) outcomes in patients with IgAN. Methods: This study included 121 patients with biopsy-proven IgAN. The mean age was 43.6 ± 12.9 years, and 66% were male. Average follow-up time was 98.7 ± 63.3 months. The primary composite endpoints were total mortality, major CV events, and end-stage renal disease. Secondary endpoints, cardiovascular, or renal endpoints were also examined separately. Cox proportional hazards analyses were performed to evaluate these markers in predicting renal and CV prognosis. Results: Patients were divided into high and low groups for both LAR and NPAR based on ROC curve analysis. High LAR was linked to poorer outcomes for the primary composite endpoint (p = 0.03) and for separate renal (p = 0.018) and cardiovascular (p = 0.009) endpoints. Similarly, high NPAR was associated with worse primary (p = 0.02), renal (p = 0.039), and CV (p = 0.042) outcomes. In multivariate Cox regression analysis, high LAR remained an independent risk factor for the primary composite endpoint (HR = 4.165, 95% CI = 1.45–11.959, and p = 0.008) but not for renal or CV endpoints individually. Conclusions: High LAR and NPAR, as markers of inflammation and altered nutritional status, are associated with poorer renal and cardiovascular outcomes in IgAN and may serve as useful prognostic indicators.

## Linked entities

- **Diseases:** IgA nephropathy (MONDO:0005342), end-stage renal disease (MONDO:0004375)

## Full-text entities

- **Genes:** IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, PTPRF (protein tyrosine phosphatase receptor type F) [NCBI Gene 5792] {aka BNAH2, LAR}, IGHA1 (immunoglobulin heavy constant alpha 1) [NCBI Gene 3493] {aka IgA1}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}
- **Diseases:** hypoxic (MESH:D002534), Renal Injury (MESH:D007674), heart failure (MESH:D006333), LVMI (MESH:D018487), S (MESH:D018455), systemic (MESH:D015619), Hypoalbuminemia (MESH:D034141), AKI (MESH:D058186), stroke (MESH:D020521), NPAR (OMIM:194470), IgA Nephropathy (MESH:D005922), proteinuria (MESH:D011507), coronary (MESH:D003323), hypoxia (MESH:D000860), systemic disease (MESH:D034721), sepsis (MESH:D018805), concentric remodeling (MESH:C567712), segmental glomerulosclerosis (MESH:C538457), tissue damage (MESH:D017695), damage (MESH:D020263), albuminuria (MESH:D000419), MetS (MESH:D024821), fibrosis (MESH:D005355), Chronic inflammation (MESH:D007249), glomerulosclerosis (MESH:D005921), injury to (MESH:D014947), disease (MESH:D004194), hypoproteinemia (MESH:D007019), atherosclerosis (MESH:D050197), deaths (MESH:D003643), malnutrition (MESH:D044342), DD (MESH:C536170), LVH (MESH:D017379), HT (MESH:D006973), stiffness (MESH:C566112), MEST-C (OMIM:211750), cancer (MESH:D009369), Diabetes (MESH:D003920), concentric hypertrophy (MESH:D006984), ESKD (MESH:D007676), cardiogenic shock (MESH:D012770), CV (MESH:D002318), myocardial infarction (MESH:D009203), protein loss (MESH:D011488), acute pancreatitis (MESH:D010195), atrophy (MESH:D001284), CKD (MESH:D051436), DM (MESH:D009223), LDH (MESH:C538133), galactose-deficient (MESH:D005693), vascular dysfunction (MESH:D002561)
- **Chemicals:** ATP (MESH:D000255), acetyl-CoA (MESH:D000105), Cholesterol (MESH:D002784), glucose (MESH:D005947), pyruvate (MESH:D019289), uric acid (MESH:D014527), lactate (MESH:D019344), TCA (MESH:D014233), TG (MESH:D014280)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12938721/full.md

## References

41 references — full list in the complete paper: https://tomesphere.com/paper/PMC12938721/full.md

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Source: https://tomesphere.com/paper/PMC12938721