Current opinion in critical care
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Recent studies have provided a better understanding of the molecular mechanisms responsible for hemolytic uremic syndromes. In this review, we summarize biochemical and genetic data that may lead to new clinical approaches. ⋯ Shiga-like toxin-1 and Shiga-like toxin-2 regulate genes that encode for chemokines, cytokines, cell adhesion molecules, and transcription factors involved in immune response and apoptosis. Mutations in factor H, membrane cofactor protein and factor I have recently been identified. Reduced expression of compliment regulators might prevent restriction of complement deposition on glomerular endothelial cells, leading to microvascular cell damage and tissue injury. Shiga-like toxin hemolytic uremic syndrome in children has a favorable prognosis in 90% of cases; kidney transplantation shows a good graft survival rate (80%) in children who progress to end stage renal disease. As for non-Shiga-like toxin hemolytic uremic syndrome, treatment with plasma infusion or exchange has been used with controversial effects. Kidney transplantation is not recommended in those patients with mutations in factor H and factor I; however, a kidney transplant corrects membrane cofactor protein dysfunction. These findings vividly underscore the clinical heterogeneity of outcomes depending upon the nature of the underlying cause of the disease.
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Curr Opin Crit Care · Oct 2005
ReviewTransfusion practice and nosocomial infection: assessing the evidence.
To evaluate recent literature describing the potential relation between transfusion practice in the intensive care unit and the subsequent risk for nosocomial infection. ⋯ Packed red blood cell transfusion may substantially increase the risk for nosocomial infection. The likely link between transfusion practice and nosocomial infection should factor into the provider's decision when determining when to transfuse.