Basic therapeutic requirements in the treatment of sepsis in acute renal failure

Acute renal failure (ARF) is a common manifestation of a septic condition which very often complicates surgical and traumatic events. The release of endotoxin, a lipopolysaccharide (LPS) from the cell wall of Gram-negative bacteria, and subsequently of numerous host mediators, is the initiating event of sepsis syndrome and eventually of septic shock. Particularly interesting is the observation that not only endotoxins but also Staphylococcus aureus which does not produce endotoxins induce the same cardiovascular changes of septic shock. The main aspect of septic shock is the inadequate oxygen supply to the body tissues. However, despite the documented myocardial depression in the course of septic shock, myocardial ischaemia is not to be considered a contributing factor, and the coronary blood flow is normal or even increased. Protein hypercatabolism can be at best only limited; in any case the optimal protein-sparing effect was observed with 1.5 g/kg proteins. Recently monoclonal antibodies to endotoxin core glycolipid have been developed; they are: (a) E5, a murine IgM anti-lipid A monoclonal antibody; (b) HA-1A, a human monoclonal antibody to endotoxin core glycolipid. In conclusion, hypercatabolic septic patients should be managed in an intensive care environment where a continuous monitoring of fluids, electrolytes, and acid-base disorders can be achieved. Surgical search of septic foci, and wide-spectrum antibiotic therapy are fundamental measures to combat cytokine and vasodilator production which impair tissue perfusion and create the premise of a shock status complicated by lactic acidosis. Dialysis treatment is a further complementary but fundamental approach that allows a large fluid and nutritional intake and a continuous correction of electrolyte and acid-base disorders.