Mortality was low in children with Shiga toxin-producing Escherichia coli hemolytic uremic syndrome, being central nervous system involvement the main cause of death. The best mortality predictors found were central nervous system involvement, hemoglobin, and sodium concentration. Hyponatremia may be a new Shiga toxin-producing Escherichia coli hemolytic uremic syndrome mortality predictor.

Hemolytic Uremic Syndrome (HUS) is the main cause of acute renal failure in children. The high percentage of patients who develop long-term sequelae constitutes an important medical concern. The identification of parameters that correlate with the degree of renal failure may be useful to plan the best treatment soon after hospitalization. Here, we investigated the functional state of neutrophils (PMN) from HUS patients on admission, before dialysis and/or transfusion, in relation to the severity of renal impairment reached during the acute period (AP). We found that all PMN activation parameters measured in severe cases of HUS (HUS AP3) were statistically lower comparing to children with mild cases of HUS (HUS AP1). As HUS PMN phenotype and dysfunction is compatible with that of cells undergoing cell death, we also studied spontaneous apoptosis. Not only were HUS PMN not apoptotic, but HUS AP3 PMN showed an increased survival. Almost all phenotypic and functional parameters measured on PMN correlated with severity. Our results revealed a marked deactivation of PMN in severe cases of HUS, and suggest that studying the functional state of PMN could be of prognostic value. (Pediatr Res 61: 123-128, 2007)

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The hemolytic uremic syndrome (HUS) is the most-common cause of acute renal failure in children. Several researchers have reported the presence of neutrophil (PMN) activating cytokines, such as interleukin-8 and tumor necrosis factor-alpha, in the sera of HUS patients. Moreover, PMN-derived products, such as elastase, were increased. These observations have lead to the hypothesis that activated PMN could act as mediators of endothelial damage. The objective of this investigation was to directly evaluate the activation status of peripheral PMN from children with HUS. For this purpose, 12 children with typical HUS were bled during the acute period, before dialysis and/or transfusion, and 8 of them were also bled after 1 month follow-up. Additionally, blood samples from healthy control children admitted for routine surgical procedures, chronic uremic children, and neutrophilic children with acute infections not related to HUS were collected and processed in an identical manner. The function and membrane activation markers of PMN from these groups were evaluated. We found that during the acute period of HUS, PMN had reduced expression of FcgammaRIII (CD16) and CD11b, were degranulated, and exhibited an impaired antibody-dependent cellular cytotoxicity. These parameters returned to normal after clinical recuperation. We conclude that PMN activation in HUS patients is a very early and transient event, and upon hospitalization before dialysis PMN show a phenotype and functional pattern of partial deactivation.

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