Table 1.

Pathophysiology in urosepsis. Inflammatory mediators and their reactions.

Innate immunity	activation of macrophages, monocytes, neutrophils and NK T cells when binding with PAMPs	secretion of proinflammatory cytokines	leukocyte activation and proliferation, complement activation, overexpression of endothelial adhesion molecules, tissue factor production
		inflammasomes determine cytokines and caspase production	apoptosis
Coagulation disorders	destroyed endothelial cells, monocytes and polymorphonuclear cells release the tissue factor	thrombin production, platelet activation and platelet-fibrin clot formation	microthrombi cause local hypoperfusion that leads to tissue hypoxia and organ dysfunction
	increase levels of TNFα and IL-1β determine plasminogen tissue activators to be secreted in the endothelium	microthrombosis
	low levels of plasma C protein, S protein and thrombomodulin	Activation of the coagulation cascade
Immunosuppression	Apoptosis and decrease of inflammatory cytokines IL-6 and TNF	low number of helper and natural killer T cells	the immune system is not able to organize an effective response to secondary infection
	neutrophils express fewer chemokine receptors	decreased chemotaxis