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Does erythropoietin have the potential to ameliorate renal injury in humans? This article addresses this question in the context of our current understanding of the pathophysiology of acute renal failure. Recent findings from experimental models are presented, and their relevance to mechanisms of acute renal failure—including endothelial and tubular cell injury, and inflammation—are discussed.
In 1955, the Swiss hematologist Conrad von Gasser coined the term ‘hemolytic uremic syndrome’ to describe the combined symptoms of diarrhea, hemolytic anemia, thrombocytopenia and acute renal failure, which he had observed in five children. Since then, investigators have realized that some forms of hemolytic uremic syndrome can be attributed to genetic abnormalities in circulating and membrane-bound proteins that regulate the complement system. How do these abnormalities influence the course and outcome of the disease, and how should they affect its treatment?
