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Cohort study examines urinary soluble CD163 as a biomarker for renal disease activity in Egyptian patients, suggesting its clinical potential.
Background Lupus nephritis (LN) is a severe manifestation of systemic lupus erythematosus (SLE) that requires reliable, non-invasive biomarkers for disease monitoring. Urinary soluble CD163 (uCD163), shed from intrarenal M2c macrophages, may reflect active glomerular inflammation and treatment response.The study aimed to examine if uCD163 could serve as indicator of renal disease activity and to evaluate its capacity to predict treatment response in cohort of Egyptian SLE patients. Methods In this single-centre, a cohort study with a nested prospective longitudinal follow-up restricted to the active lupus nephritis subgroup, 90 SLE cases were categorized into four groups: active Lupus Nephritis (aLN, n = 30), active non-renal SLE (aNR, n = 20), inactive Lupus Nephritis (iLN, n = 20), and inactive non-renal SLE (iNR, n = 20), plus 20 healthy controls. Urinary soluble CD163 was measured by Enzyme-linked immunosorbent assay (ELISA) at baseline from all patients groups, as well as at 6 and 12 months follow-up visits from aLN cases. Activity of disease was detected by SLE Disease Activity Index 2000 (SLEDAI-2 K), renal biopsy, and standard laboratory parameters. Results uCD163 levels were markedly elevated in aLN (8.40 ± 1.09 ng/ml) versus all other groups (all p < 0.001), with no significant differences among aNR, iLN, iNR, and controls. uCD163 correlated strongly with SLEDAI ( r = 0.821), anti-double-stranded DNA (anti-dsDNA) antibodies ( r = 0.857), proteinuria ( r = 0.851), estimated Glomerular Filtration Rate (eGFR) ( r = − 0.873), and renal activity index ( r = 0.644), but not with chronicity index. Class IV LN showed the highest uCD163 levels. Longitudinal follow-up confirmed significant decline over 12 months of treatment ( p < 0.001), mirroring clinical and renal improvement. Conclusion In this single-centre cohort, urinary soluble CD163 was strongly associated with active lupus nephritis and was markedly higher in aLN than in non-renal or inactive SLE. It correlated with histopathological activity and was independently associated with treatment response on regression analysis. These findings support uCD163 as a promising non-invasive candidate biomarker to complement conventional monitoring. Larger prospective and multi-centre studies are warranted to validate its clinical utility and establish evidence-based thresholds for routine use.
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Mosaad et al. (2026) studied this question.
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