ArticleLupus science & medicine2025
Neutrophil gelatinase-associated lipocalin (NGAL) in lupus nephritis and beyond.
Article in Lupus science & medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Transitioning from invasive to liquid biopsy techniques: a bibliometric analysis and prospective insights on biomarkers in lupus nephritis.Frontiers in medicine · 2026Pooled it
- Hyper-activated low-density neutrophil-derived NGAL predicts fatal SFTS: a multi-cohort and single-cell study.Infection · 2026Article
- Distinct Longitudinal Trajectories of SLEDAI-2K Scores Predict Prognosis in Systemic Lupus Erythematosus Based on Group-Based Trajectory Modeling.Journal of immunology research · 2026Article
- Breaking the cycle: immune complexes, complement activation, and novel immunotherapies in lupus nephritis.Frontiers in immunology · 2025Review
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Authors and funding
7 authors.
Funding
Abstract
objectivesTo study neutrophil gelatinase-associated lipocalin (NGAL) levels in peripheral blood in SLE, and to propose a mechanism by which neutrophils secrete NGAL on stimulation with immune complexes (IC).
methodsNGAL was measured by ELISA in two independent Swedish SLE cohorts acting as exploratory and validation cohort (n=124 and n=308, respectively), disease controls (n=38) and healthy controls (n=77). NGAL levels were measured in supernatant from IC-stimulated neutrophils in the presence or absence of a toll-like receptor 8 inhibitor (TLR8i).
resultsIn the exploratory cohort, serum levels of NGAL were increased in patients with SLE as compared with healthy controls (p=0.021), and associated with histological-proven membranoproliferative lupus nephritis (LN) (p=0.018). In the validation cohort, plasma levels of NGAL were elevated in patients with a history of LN (p=0.0048), as well as in patients with SLE with secondary antiphospholipid syndrome (APS) compared with those without (p=0.0022). In both cohorts, NGAL was able to discriminate patients with a creatinine clearance <60 mL/min (chronic kidney disease stage 3 or more) with high accuracy, with an area under the curve of 0.92 (p<0.0001) and 0.94 (p=0.0088), respectively. Neutrophils stimulated with IC secrete more NGAL, when compared with baseline, and this process was blocked by adding a TLR8i.
conclusionBlood levels of NGAL are increased in patients with SLE with decreased kidney function, and in those with secondary APS. The mechanism behind NGAL increase in SLE may be related to TLR8 pathway activation by circulating RNA-containing IC.
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