# Lupus nephritis and its association with subclinical myocardial alterations in systemic lupus erythematosus assessed by cardiovascular magnetic resonance

**Authors:** Zhi Yang, Ling-li Wang, Tian-yue Zhang, Miao Wen, Hao Zou, Yong Zhu, Xue Meng, Liang-chao Gao, Bing Fu, Shu-yue Pan

PMC · DOI: 10.3389/fimmu.2026.1749478 · Frontiers in Immunology · 2026-02-06

## TL;DR

This study shows that lupus nephritis in SLE patients is linked to hidden heart changes detected by advanced imaging.

## Contribution

The study identifies subclinical myocardial alterations in SLE patients with lupus nephritis using cardiovascular magnetic resonance.

## Key findings

- SLE patients with LN had worse global longitudinal strain compared to those without LN and healthy controls.
- Higher native T1, ECV, and native T2 values were observed in SLE patients with LN, indicating myocardial abnormalities.
- LN status was independently associated with increased native T1 and ECV values in SLE patients.

## Abstract

Lupus nephritis (LN) is the most common and severe complication in patients with systemic lupus erythematosus (SLE) and is associated with cardiac disease. The purpose of this study was to assess the cardiac phenotype of SLE patients with LN using cardiovascular magnetic resonance (CMR), and to investigate whether comorbid LN is associated with left ventricular (LV) remodeling.

Clinical assessment and CMR were performed in 66 SLE patients without LN, 36 SLE patients with LN, and 20 age- and sex-matched healthy subjects.

SLE patients with LN had a more impaired global longitudinal strain (-12.37 ± 5.15% vs. -14.40 ± 2.80% vs. -14.92 ± 3.04%; P = 0.045) than SLE patients without LN and control group. Moreover, native T1 (1330 ± 54 vs. 1286 ± 81 vs. 1256 ± 41; P<0.001), extracellular volume (ECV) (30.53 ± 4.57% vs. 28.34 ± 3.59% vs. 26.20 ± 3.03; P<0.001), and native T2 (43.69 ± 4.32 vs. 41.98 ± 3.66 vs. 39.60 ± 2.94; P<0.001) were higher in SLE patients with LN, intermediate in SLE patients without LN and lowest in control group. However, LV-LGE did not differ significantly between the SLE patients with or without LN (P > 0.05). In multivariable linear regression, LN status was associated with higher native T1 (β=0.244, P<0.05) and ECV values (β=0.224, P<0.05).

SLE patients with LN showed more pronounced subclinical myocardial abnormalities on CMR. LN was an independent risk factor for cardiac impairment in patients with SLE.

## Linked entities

- **Diseases:** Lupus nephritis (MONDO:0005556), systemic lupus erythematosus (MONDO:0007915), cardiac disease (MONDO:0005267)

## Full-text entities

- **Genes:** CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, BTG3 (BTG anti-proliferation factor 3) [NCBI Gene 10950] {aka ANA, ANA/BTG3, APRO4, TOB5, TOB55, TOFA}
- **Diseases:** left ventricular (LV) remodeling (MESH:D020257), coronary artery disease (MESH:D003324), cardiac damage (MESH:D006331), cardiac amyloidosis (MESH:D000686), LV myocardium (MESH:D056830), heart failure (MESH:D006333), impaired renal indices (MESH:D007674), myocardial mechanical injury (MESH:D041781), immune dysregulation (OMIM:614878), ventricular (MESH:D014693), CMR abnormalities (MESH:D018376), hypertension (MESH:D006973), death (MESH:D003643), atherosclerosis (MESH:D050197), myocardial microvascular dysfunction (MESH:D017566), myocardial involvement (MESH:C564676), congenital heart disease (MESH:D006330), renal involvement (MESH:C565423), myocardial infarction (MESH:D009203), myocardial oedema (MESH:C536897), CMR (MESH:D002318), cardiac sarcoidosis (MESH:D012507), cardiomyopathy (MESH:D009202), ventricular stroke (MESH:D020521), GLS impairment (MESH:D013180), LV systolic dysfunction (MESH:D018487), autoimmune disease (MESH:D001327), SLE (MESH:D008180), fat (MESH:D004620), proteinuria (MESH:D011507), myocardial remodeling (MESH:D064752), myocardial alterations (MESH:D004408), hematuria (MESH:D006417), inflammation (MESH:D007249), fibrosis (MESH:D005355), edema (MESH:D004487), LGE (MESH:C564835), valvular disease (MESH:D006349), LN (MESH:D008181)
- **Chemicals:** lipid (MESH:D008055), urea nitrogen (MESH:C530477), gadolinium (MESH:D005682), prednisone (MESH:D011241), creatinine (MESH:D003404), calcium (MESH:D002118), Gd-DTPA (MESH:D019786), sodium (MESH:D012964), triglyceride (MESH:D014280)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

37 references — full list in the complete paper: https://tomesphere.com/paper/PMC12920543/full.md

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Source: https://tomesphere.com/paper/PMC12920543