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.

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.