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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?
Age-related decline in the capacity of the kidney to repair itself is a significant contributor to mortality associated with acute renal failure. In this well-balanced overview of renal and bone-marrow stem cells, Lloyd Cantley summarizes current knowledge and speculates on mechanisms of regeneration that have therapeutic potential.
Thiazolidinediones are synthetic agonists of peroxisome proliferator-activated receptors that have shown promise inin vitroand animal models of nephropathy. Encouraging early-stage data have also been generated in patients with diabetic nephropathy. Carol Pollock and colleagues outline what we know and what we need to find out before thiazolidinediones such as pioglitazone and rosiglitazone can fulfill their clinical potential.
Despite the implications of the term 'focal segmental glomerulosclerosis', subtypes of this form of idiopathic nephrotic syndrome are not always focal, segmental or sclerotic. Here, Alain Meyrier presents a comprehensive update of our understanding of the processes that underlie the development of variants of this condition, with emphasis on the unifying role of the podocyte.
