Over the last 10 years the syndrome of severe acute renal failure has
progressively changed in its epidemiology. It is now most frequently
seen in critically ill patients, typically in the context of sepsis and
multiorgan failure. This epidemiologic change has meant that intensive
care physicians and nephrologists must now work in close cooperation at
all times and must take many com- plex issues of prevention,
pathogenesis, and management into account that they did not previously
have to tackle. Simultaneously, the last 10 years have seen the
development of major technical and conceptual changes in the field of
renal replacement therapy. There are now previously unavailable
therapeutic options that provide physicians with a flexible and rapidly
evolving armamentarium. The nutrition of these patients, previously
limited by the par- tial efficacy of renal replacement therapies, has
also become more aggressive and more in tune with the needs of
critically ill patients. Increased understanding of the pathogenesis of
the multi- organ failure syndrome has focused on the role of many
soluble "mediators of injury" (cytokines, leukotrienes, prostanoids
etc.). These molecules are likely to participate in the pathogenesis of
acute renal failure. Their generation and disposal is also affected by
different techniques of artificial renal support.