Figure 621

The pathogenesis of falciparum malarial renal complications. Note the infection triggers two initially independent pathways: red cell parasitization and monocyte activation. These subsequently interact, as the infected red cells express abnormal proteins that induce an immune reaction by their own right, in addition to providing sticky points (knobs) for clumping and adherence to platelets and capillary endothelium. TNF-a released from the activated monocytes shares in the endothelial activation. As both pathways proceed and interact, a variety of renal complications develop, including acute tubular necrosis, acute interstitial nephritis and acute glomerulonephritis. B—B-lymphocyte; CD8—cytotoxic T cell; CIC—circulating immune complexes; TH—T-helper cells (1 and 2); TNF-a—tumor necrosis factor-a.

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