Objectives: Macrophages contribute to kidney injury by a variety of mechanisms. CD163, a M2-macrophage marker has been shown to be associated with glomerular inflammation and renal fibrosis. Microparticles (MPs) originate from cells on activation and injury. We performed this pilot study to evaluate M2 macrophage infiltration in renal biopsies of IgAN and correlate it with other parameters of monocyte activation including monocyte-derived MPs (MMPs) and urinary soluble CD163 (sCD163).   Methods: Ten patients of IgAN, diagnosed on histology and classified according to Oxford classification (MEST-C score) were included. Two age and sex-matched healthy controls and four Lupus Nephritis (LN) disease controls were also included. Plasma MMPs (AnnexinV+/CD14+) were quantified by flow cytometry and also estimated as a % of total MPs.  CD163 immunohistochemistry (clone-EP324) was performed on renal biopsies for quantification of macrophage infiltration in glomeruli and the tubulointerstitial compartments at 40x objective. Urinary sCD163 levels were estimated by ELISA.    Results: The mean age of patients of IgAN was 34.4±10 years, and seven were males. Mean level of circulating MPs in IgAN, healthy and LN were 3.1x105/µl, 6.7x103/µl and 2.4x105/µl, respectively. The MMPs in IgAN and healthy formed 63% and 40% of the total MPs. In renal biopsies of IgAN, CD163+ cells/glomeruli were 4.5±5.2 and correlated significantly with presence of endocapillary hypercellularity (E1) and crescents (C2). Mean levels of urinary sCD163 in IgAN, LN and healthy control group were 11.8ng/ml, 27ng/ml and 0.18ng/ml, respectively. sCD163 levels correlated significantly with the number of CD163+ cells in glomeruli. Conclusions: We found monocyte activation and M2 macrophage infiltration in renal biopsies of IgAN. The CD163+ M2 infiltration correlated with urinary sCD163 and with the severity of glomerular injury. Our findings suggest that in IgAN, urinary sCD163 may act as non-invasive biomarker in assessing the severity of glomerular injury.