Fig. 6

Putative etiology of the pathological condition of this patient summarizing 2 toxic agents of Streptococcal pyogenes locally induce inflammation in the glomeruli and tubulointerstitium in different ways. Infection with Streptococcal pyogenes, which produces the nephritis-associated plasmin receptor (NAPlr) and neuraminidase, induces the release of NAPlr and neuraminidase into the circulation. On one hand, circulating NAPlr accumulates on the inner side of the glomerular tufts, and then traps and maintains the activity of plasmin, which induces plasmin-associated glomerular damage leading to the development of endocapillary proliferative glomerulonephritis with massive infiltration of neutrophils (Ref. 12). On the other hand, the circulating neuraminidase (Ref. 18) affects renal tubular epithelial cells, vascular endothelial cells, and red blood cells, leading to the exposure of the T-antigen on these cells, resulting in the development of tubulointerstitial nephritis with T-cells and macrophage (MФ) infiltration, capillaritis, and thrombotic microangiopathy (TMA). Thus, the 2 toxic agents of Streptococcal pyogenes locally induce inflammation in the glomeruli and tubulointerstitium in different ways, resulting in the accumulation of different cell populations in the two regions