Figure 610

Common pathogenetic mechanisms of renal injury in tropical bacterial infections. Depending on the bacterial species and strain, as well as on the host's resistance and genetic background, bacteria may directly invade the renal parenchyma, induce an immune reaction, injure the capillary endothelium or provoke a nonspecific humoral or hematologic response. The subsequent evolution of these pathways may lead to different forms of renal injury. The asterisk indicates that the role of hemolysis is augmented in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency. ATN—acute tubular necrosis; DIC—disseminated intravascular coagulation; IL—interleukin; NO—nitric oxide; ROM—reactive oxygen molecules; TNF-a—tumor necrosis factor-a.

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