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Objectives: (1) Evaluate mortality rate in patients with Shiga toxin-producing Escherichia coli hemolytic uremic syndrome, (2) determine the leading causes of death, and (3) identify predictors of mortality at hospital admission. Methods We conducted a multicentric, observational, retrospective, cross-sectional study. It included patients under 18 years old with Shiga toxin-producing Escherichia coli hemolytic uremic syndrome hospitalized between January 2005 and June 2016. Clinical and laboratory data were obtained from the Argentine National Epidemiological Surveillance System of Hemolytic Uremic Syndrome. Clinical and laboratory variables were compared between deceased and non-deceased patients. Univariate and multivariate analyses were performed. ROC curves and area under the curve were obtained. Results Seventeen (3.65%) out of the 466 patients died, being central nervous system involvement the main cause of death. Predictors of death were central nervous system involvement, the number of days since the beginning of diarrhea to hospitalization, hyponatremia, high hemoglobin, high leukocyte counts, and low bicarbonate concentration on admission. In the multivariate analysis, central nervous system involvement, sodium concentration, and hemoglobin were independent predictors. The best cut off for sodium was [less than or equal to] 128 meq/l and for hemoglobin [greater than or equal to] 10.8 g/dl. Conclusions 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., Author(s): Laura F. Alconcher [sup.1] , Paula A. Coccia [sup.2] , Angela del C. Suarez [sup.3] , Marta L. Monteverde [sup.4] , María Graciela Perez y Gutiérrez [sup.5] , Paula [...]

Background Angiotensin-converting enzyme inhibitors or angiotensin II type 1 receptor blockers decrease post-diarrheal hemolytic uremic syndrome (D + HUS) sequelar proteinuria. However, proteinuria may persist in some patients. In nephropathies other than D + HUS, an additive antiproteinuric effect with coadministration of both drugs has been observed. Methods To assess such an effect in D + HUS, 17 proteinuric children were retrospectively studied. After a median period of 1 year post-acute stage (range 0.5-1.9) patients received enalapril alone for a median of 2.6 years (range 0.33-12.0) at a median dose of 0.4 mg/kg/day (range 0.2-0.56). As proteinuria persisted, losartan was added at a median dose of1.0 mg/ kg/day (range 0.5-1.5) during 2.1 years (range 0.5-5.0). Results The decrease in proteinuria with enalapril was 58.0 %, which was further reduced to 83.8 % from the initial value after losartan introduction. The percentage of reduction was significantly greater with the association of both drugs (p-0.0006) compared with the effect of enalapril exclusively (p-0.023). Serum potassium, glomerular filtration rate, and blood pressure remained unchanged. Conclusions Our results suggest that adding losartan to persisting proteinuric D + HUS children already on enalapril is safe and reduces proteinuria more effectively. Whereas this effect is associated with long-term kidney protection, it should be determined by prospective controlled studies. Keywords Postdiarrheal hemolytic uremic syndrome * Proteinuria * Enalapril * Losartan * Combined therapy, Introduction Proteinuria is a major determinant of progression towards chronic kidney disease in children with renal damage secondary to postdiarrheal hemolytic uremic syndrome (D + HUS) [1, 2]. The renin-angiotensin [...]