Incomplete hemolytic-uremic syndrome in Argentinean children with bloody diarrhea

López, Eduardo; Contrini, María Marta; Devoto, Susana; Rosa, María Fabiana De; Graña, Marı́a; Aversa, Luis; Gomez, Henry F.; Genero, Mario H.; Cleary, Thomas G.

doi:10.1016/s0022-3476(95)70064-1

Cited by 46 publications

(30 citation statements)

References 20 publications

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“…We showed that Stx2 is more toxic to human glomerular cells than to tubular cells. This supports studies that have failed to find cases of renal disease in the absence of microvascular and hemolytic symptoms following bloody diarrhea caused by STEC (37,52). In contrast to the polyuria and dilute urine of the mice challenged with Stx2 plus LPS, most HUS patients are oligoanuric (66).…”

Section: Vol 77 2009supporting

confidence: 79%

Shiga Toxin 2 Targets the Murine Renal Collecting Duct Epithelium

et al. 2009

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Hemolytic-uremic syndrome (HUS) caused by Shiga toxin-producingEscherichia coli infection is a leading cause of pediatric acute renal failure. Bacterial toxins produced in the gut enter the circulation and cause a systemic toxemia and targeted cell damage. It had been previously shown that injection of Shiga toxin 2 (Stx2) and lipopolysaccharide (LPS) caused signs and symptoms of HUS in mice, but the mechanism leading to renal failure remained uncharacterized. The current study elucidated that murine cells of the glomerular filtration barrier were unresponsive to Stx2 because they lacked the receptor glycosphingolipid globotriaosylceramide (Gb 3 ) in vitro and in vivo. In contrast to the analogous human cells, Stx2 did not alter inflammatory kinase activity, cytokine release, or cell viability of the murine glomerular cells. However, murine renal cortical and medullary tubular cells expressed Gb 3 and responded to Stx2 by undergoing apoptosis. Stx2-induced loss of functioning collecting ducts in vivo caused production of increased dilute urine, resulted in dehydration, and contributed to renal failure. Stx2-mediated renal dysfunction was ameliorated by administration of the nonselective caspase inhibitor Q-VD-OPH in vivo. Stx2 therefore targets the murine collecting duct, and this Stx2-induced injury can be blocked by inhibitors of apoptosis in vivo.

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Section: Vol 77 2009supporting

confidence: 79%

Shiga Toxin 2 Targets the Murine Renal Collecting Duct Epithelium

et al. 2009

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“…This is of particular importance because long-term follow-up examinations will be missed in unrecognized cases. There are only few reports describing the various features of iHUS, even in large surveys of cHUS; additionally the case definitions were not universally the same [22,23,33]. In rare cases, HUS can originate from UTI [16,29]; in three patients of this series, iHUS was consequence of a STEC-associated UTI.…”

Section: Discussionmentioning

confidence: 88%

“…The observed proportion of iHUS is likely to represent an underestimate since many such patients, especially in case of even milder forms are unlikely to reach the hospital, or even to be diagnosed. Of note, in a prospective study in Argentina the incidence of iHUS complicating bloody diarrhea was twice that of cHUS [22]. This is of particular importance because long-term follow-up examinations will be missed in unrecognized cases.…”

Section: Discussionmentioning

confidence: 98%

Hemolytic-uremic syndrome in Switzerland: a nationwide surveillance 1997–2003

et al. 2009

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Hemolytic-uremic syndrome (HUS) is a leading cause of acute renal failure in childhood. In its typical presentation, it is preceded by an episode of diarrhea mostly due to Shiga-toxin-producing Escherichia coli. There is important geographical variation of many aspects of this syndrome. Nationwide data on childhood HUS in Switzerland have not been available so far. In a prospective national study through the Swiss Pediatric Surveillance Unit 114 cases (median age 21 months, 50% boys) were reported between April 1997 and March 2003 by 38 pediatric units (annual incidence 1.42 per 10(5) children < or =16 years). Shiga-toxin-producing E. coli were isolated in 32 (60%) of tested stool samples, serotype O157:H7 in eight. Sixteen children presented with only minimal renal involvement, including three with underlying urinary tract infection. Six patients presented with atypical hemolytic-uremic syndrome, and six with HUS due to invasive Streptococcus pneumoniae infection. Mortality was 5.3%, including two out of six children with S. pneumoniae infection. The severity of thrombocytopenia and the presence of central nervous system involvement significantly correlated with mortality. In conclusion, childhood HUS is not rare in Switzerland. Contrasting other countries, E. coli O157:H7 play only a minor role in the etiology. Incomplete manifestation is not uncommon.

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“…It appears unlikely that family physicians in Canada may have treated children or adolescents with D+ HUS without any involvement from paediatricians. However, we cannot exclude that incomplete forms of D+ HUS [11,18] may have been under-recognised, since physicians do not systematically perform screening blood tests when children with STEC enteritis seek consultation. The provinces of Ontario, Quebec, and Alberta accounted for 89% of cases in Canada, reflecting in part, the relative size of their populations compared to other provinces and territories.…”

Section: Discussionmentioning

confidence: 99%

Prospective surveillance of Canadian children with the haemolytic uraemic syndrome

Proulx

Sockett

2005

Pediatr Nephrol

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We determined prospectively the incidence of childhood diarrhoea associated haemolytic uraemic syndrome (D+ HUS) or HUS due to Streptococcus pneumoniae (SP+ HUS) in Canada through the Canadian Paediatric Surveillance Program (CPSP) network. From April 2000, to March 2002, 82% (1,886/2,300) of all Canadian paediatricians reported possible new cases of D+ HUS or SP+ HUS. Diagnosis was validated with a second questionnaire. There were a total of 136 children with D+ HUS (epidemic, n =15; endemic, n =121), corresponding to an annual incidence rate of 1.11 cases per 100,000 children under 16 years of age. Excluding incomplete forms, the annual incidence rate among endemic cases was 0.74 cases per 100,000. The provinces of Ontario (40%), Quebec (31%), and Alberta (18%) accounted for 89% of cases. Evidence of E. coli O157 or O157:H7 were found in 94% (79/84) of children who had positive stool cultures. The mortality rate was 4% (n =5) and 34% (n =41) of children underwent dialysis for a median of 12 days (2-60 days). SP-HUS was diagnosed in four children with pneumonia and pleural effusion (n =2) or meningitis (n =2) who survived. One child with positive direct Coombs testing had definitive evidence of SP+ HUS. The remaining three were considered possible cases. We conclude that SP+ HUS is rare in Canada. Over the last 15 years, the incidence of childhood D+ HUS in Canadian children may have decreased.

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Incomplete hemolytic-uremic syndrome in Argentinean children with bloody diarrhea

Cited by 46 publications

References 20 publications

Shiga Toxin 2 Targets the Murine Renal Collecting Duct Epithelium

Shiga Toxin 2 Targets the Murine Renal Collecting Duct Epithelium

Hemolytic-uremic syndrome in Switzerland: a nationwide surveillance 1997–2003

Prospective surveillance of Canadian children with the haemolytic uraemic syndrome

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