Renal CD163+ and CD68+ Macrophage Infiltration and Urinary sCD163 Levels in IgA Nephropathy

Background IgA Nephropathy (IgAN) often affects young adults and leads to significant renal failure in many patients in India. Macrophages are linked to renal inflammation and fibrosis. We examined CD68+ and CD163+ macrophage infiltration in renal biopsies and measured urinary and serum soluble CD163 (sCD163) levels. Materials and Methods The study included 70 patients with IgAN, 20 with lupus nephritis (LN), and healthy controls (n = 20). Tissue macrophage infiltration was assessed by immunohistochemistry using a pan-macrophage marker, CD68, and an M2 macrophage marker, CD163. The soluble CD163 (sCD163) levels were measured in urine and serum by ELISA, and correlated with biochemical parameters and histological MEST-C scores. Results Glomerular CD68+ cells significantly correlated with the presence of endocapillary hypercellularity (E1) ( p <0.001). A cutoff of ≥4 CD68+ cells in any glomerulus predicted E1 with 88.9% sensitivity and 100% specificity. The tubulointerstitial CD163+ cells correlated with tubular atrophy ( p = 0.01). Urinary sCD163 levels were significantly higher in patients with IgAN and LN than in controls. The levels correlated with serum creatinine (r = 0.303, p = 0.01), tubulointerstitial CD163+ cells, and glomerular CD68+ cells. Follow-up urinary sCD163 levels decreased significantly ( p = 0.001),. At a median follow-up of 12 months, E1 on renal histology was associated with a 5-fold higher risk of progression (95% CI, 1.46-17.46). Conclusion Tissue macrophage infiltration is associated with disease activity and fibrosis in IgAN. Urinary sCD163 levels decline with treatment response, although follow-up was available only for a small subset. Larger studies are needed to evaluate its potential as a non-invasive biomarker for monitoring disease activity.