Update on immunoglobulin A nephropathy, Part I: Pathophysiology

Figure 4 Pathways to glomerular damage and tubulointerstitial injury in Immunoglobulin A nephropathy. Deposition of IgA-ICs in the mesangium leads to activation of mesangial cells, triggering mesangial cell proliferation and release of proinflammatory and profibrotic mediators. Podocyte loss accentuates glomerular scarring and filtered mesangial cell-derived mediators and IgA-ICs stimulate PTEC to adopt a proinflammatory and profibrotic phenotype, which in turn drives tubulointerstitial scarring. IgA: Immunoglobulin A; PTEC: Proximal tubule epithelial cells.