# Atherogenic index of plasma and lower estimated glomerular filtration rate in IgA nephropathy

**Authors:** Ricong Xu, Abdul Rashid Qureshi, Mohamed E. Suliman, Nanbo Zhu, Hong Xu, Yuna Chen, Anni Zhong, Qijun Wan, Bengt Lindholm

PMC · DOI: 10.1186/s12944-026-02896-4 · Lipids in Health and Disease · 2026-02-18

## TL;DR

Higher atherogenic index of plasma is linked to worse kidney function in IgA nephropathy patients, especially in certain metabolic subgroups.

## Contribution

This study identifies AIP as a novel metabolic risk factor associated with renal function decline in IgA nephropathy.

## Key findings

- Each standard deviation increase in AIP was associated with a 2.08 mL/min/1.73 m² lower eGFR.
- Patients with the highest AIP tertile had 76% higher odds of eGFR < 60 mL/min/1.73 m².
- AIP was linked to higher proteinuria in patients with eGFR ≥ 60 mL/min/1.73 m².

## Abstract

IgA nephropathy (IgAN) demonstrates substantial progression to end-stage kidney disease, yet metabolic risk factors remain underexplored. The atherogenic index of plasma (AIP), calculated as log(triglycerides/HDL-cholesterol), integrates pro-atherogenic and anti-atherogenic lipid components, but its association with renal function in IgAN is unclear.

This cross-sectional study analyzed 1186 Chinese patients with biopsy-proven primary IgAN. AIP was standardized as Z-scores for analysis. Primary outcome was estimated glomerular filtration rate (eGFR). Secondary outcomes included eGFR < 60 mL/min/1.73 m² and proteinuria. Multivariable linear and logistic regression models assessed associations with progressive adjustments. Subgroup analyses evaluated effect modification.

Median age was 34 years with 48% males. Each standard deviation increase in AIP was associated with 2.08 mL/min/1.73 m² lower eGFR (95% CI: -3.48, -0.68; p = 0.004) and 33% higher odds of eGFR < 60 mL/min/1.73 m² (OR: 1.33; 95% CI: 1.07, 1.67; p = 0.012) in fully adjusted models. Patients in the highest versus lowest AIP tertile had 4.73 mL/min/1.73 m² lower eGFR (p = 0.005) and 76% higher odds of eGFR < 60 mL/min/1.73 m² (p = 0.034). AIP was associated with higher proteinuria in patients with eGFR ≥ 60 mL/min/1.73 m² (β: 141.63 mg/24 h per SD; 95% CI: 33.75, 249.51; p = 0.01). Significant effect modification occurred by BMI (p-interaction = 0.032) and hyperuricemia (p-interaction = 0.030), with stronger associations in patients with BMI < 23 kg/m² and without hyperuricemia.

Higher AIP independently associates with lower eGFR and higher proteinuria at diagnosis in IgAN patients, particularly in specific metabolic subgroups. Longitudinal studies are needed to determine whether AIP has prognostic value for renal outcomes.

The online version contains supplementary material available at 10.1186/s12944-026-02896-4.

## Linked entities

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

## Full-text entities

- **Genes:** REN (renin) [NCBI Gene 5972] {aka ADTKD4, HNFJ2, RTD}, IGHA1 (immunoglobulin heavy constant alpha 1) [NCBI Gene 3493] {aka IgA1}, CD79A (CD79a molecule) [NCBI Gene 973] {aka IGA, IGAlpha, MB-1, MB1}, AIP (AHR interacting HSP90 co-chaperone) [NCBI Gene 9049] {aka ARA9, FKBP16, FKBP37, PITA1, SMTPHN, XAP-2}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}
- **Diseases:** metabolic abnormalities (MESH:D008659), IgA nephropathy (MESH:D005922), proteinuria (MESH:D011507), hypertensive nephropathy (MESH:C563161), obese (MESH:D009765), MES (MESH:C536133), renal function (MESH:D058186), overweight (MESH:D050177), reduced renal function (MESH:D001523), minimal change disease (MESH:D009402), diabetes (MESH:D003920), anti-neutrophil cytoplasmic antibody-associated vasculitis (MESH:D056648), tubular (MESH:D000230), hepatitis B virus-associated (MESH:D006509), CKD (MESH:D051436), atrophy (MESH:D001284), lipotoxic injury (MESH:D014947), inflammatory (MESH:D007249), fibrosis (MESH:D005355), dyslipidemia (MESH:D050171), mitochondrial dysfunction (MESH:D028361), Castleman's disease (MESH:D005871), diabetic kidney disease (MESH:D003928), hyperuricemia (MESH:D033461), RCS (MESH:D002313), thin basement membrane nephropathy (MESH:C562476), hypertriglyceridemia (MESH:D015228), membranous nephropathy (MESH:D015433), underweight (MESH:D013851), adiposity (MESH:D018205), glomerular diseases (MESH:D007674), thrombotic microangiopathy (MESH:D057049), interstitial (MESH:D065167), ESRD (MESH:D007676), advanced glomerulosclerosis (MESH:D020178), glomerulonephritis (MESH:D005921), glomerular and tubular injury (MESH:D015499), albuminuria (MESH:D000419), hypertension (MESH:D006973), atherogenic (MESH:D050197)
- **Chemicals:** cholesterol (MESH:D002784), uric acid (MESH:D014527), TG (MESH:D014280), glucose (MESH:D005947), creatinine (MESH:D003404), Lipid (MESH:D008055), fatty-acid (MESH:D005227), TC (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

1 references — full list in the complete paper: https://tomesphere.com/paper/PMC12934030/full.md

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Source: https://tomesphere.com/paper/PMC12934030