Bacterial infections promote important alterations in immune, hemodynamic, and metabolic function which can result in irreversible shock. These changes are mediated by host-secreted cytokines rather than by direct action of the endotoxin lipopolysaccharide (LPS) derived from the cell wall of bacteria. One cytokine that has been extensively studied for its role in infection is macrophage-derived tumor necrosis factor alpha (TNFα) [1]. Three observations suggest that TNFα has a central involvement in endotoxic shock: (i) High levels of TNFα can be found in blood of animals and humans with endotoxic shock; (ii) When injected to animals, TNFα causes a syndrome similar to endotoxic shock, with hypotension, decreased tissue perfusion, organ failure, and lactic acidosis; (iii) The effects of LPS can be prevented by prior passive immunization of animals with polyclonal or monoclonal antibody directed against TNFα.During severe bacterial infections, acute renal insufficiency occurs frequently and contributes significantly to the morbidity and mortality of the shock. In vivo studies indicate that LPS induces an increase in renal vascular resistance and a decrease in glomerular filtration rate [2]. A variety of mediators could contribute to these hemodynamic changes. They include: arachidonic acid metabolites (thromboxane A2, TXA2; leukotrienes, LT), platelet activating factor (PAF), adenosine, catecholamines, angiotensin II and cytokines. Their synthesis is probably initiated by the release of TNFα [3]. The present paper discusses the cellular origin of TNFα within the kidney, and reviews the mechanisms whereby factors released in response to TNFα participate in controlling the secretion of this cytokine.