Evidence of infection with organisms producing Shiga-like toxins in household contacts of children with the hemolytic uremic syndrome.

We conducted a prospective study in 87 household contacts of 51 children with hemolytic uremic syndrome to determine the frequency of infection with Shiga-like toxin-producing bacteria. Gastrointestinal tract symptoms occurred in only 1 of 87 contacts. Free fecal toxin was detected in 25 of 64 (39%) of the household members. Neutralization with specific antisera to Shiga-like toxins I and II (SLT-I, SLT-II) revealed that in 6 of these household contacts only SLT-I was present in stool, in 10 only SLT-II was present and in 9 both toxins were found. Thirty-three percent of the hemolytic uremic syndrome families in which 2 or more members were studied had more than 1 household member with free fecal toxin in stool. None of the household contacts was found to have E. coli O157:H7 in feces. Serum samples were available in 77 household contacts; 75% (58 of 77) had serum neutralizing titers of greater than or equal to 1:4 to 1 or both toxins. In those contacts for whom paired sera were available, seroconversion was found in 10 of 24 (42%). These data show that household contacts of children with hemolytic uremic syndrome are commonly colonized with Shiga-like toxin-producing E. coli and seroconversion to Shiga-like toxins occurs frequently in family members of children with hemolytic uremic syndrome.

Hemolytic uremic syndrome and diarrhea in Argentine children: the role of Shiga-like toxins.

Shiga-like toxin-producing Escherichia coli have been associated with hemorrhagic colitis and the hemolytic uremic syndrome (HUS). Because Argentina has the highest reported frequency of HUS in the world, Argentine children were prospectively studied during the HUS seasons for evidence of Shiga-like toxin-related diseases. On the basis of serology, fecal cytotoxin neutralization, stool cultures, and DNA hybridization of colony lysates, most children with HUS had evidence of infection with Shiga-like toxin-producing organisms. Children with spring-summer diarrhea also commonly (32%, confidence interval 18%-46%) had clear-cut evidence of such infection. No controls (children without gastrointestinal, renal, or hemolytic disease) had free fecal cytotoxin, positive cultures for E. coli O157:H7, or DNA probe-positive organisms; 20% of them had low serum titers of antibodies to Shiga-like toxins. E. coli O157:H7 was not common in either HUS or diarrhea patients. The high frequency of Shiga-like toxin-induced diarrhea in young children in Argentina probably explains the high incidence of HUS in this country and suggests that HUS is a relatively uncommon complication of Shiga-like toxin-related disease.

Diagnóstico y seguimiento de 42 casos pediátricos de glomerulonefritis membranoproliferativa / Diagnosis and follow-up of 42 pediatric cases of membranoproliferative glomerulonephritis

Se analizaron 42 historias clínicas de niños con glomerulonefritis membranoproliferativa (GNMP) diagnosticadas a través de la biopsia renal. Los pacientes se controlaron en la Unidad de Nefrología del Hospital de Niños. La media de tiempo de seguimiento fue de 5,16 años. Se excluyeron los pacientes que presentaban GNMP secundarias, y se clasificaron en GNMP tipo I (27 pacientes) y tipo II (15 pacientes). En el comienzo de la enfermedad todos los niños presentaron hematuria, la mitad hipertensión arterial, un tercio de los niños anemia (3 de tipo hemolítico) no relaccionada con la caída del filtrado glomerular, y el 70% de los mismos C3 disminuido. En un paciente se detectó deficiencia familiar de C3. Ninguno de estos hallazgos clínicos o de laboratorio estuvo relacionado con la evalución posterior. La presencia de insuficiencia renal aguda persistente al comienzo de la enfermedad o de síndrome nefrótico (clínico o de laboratorio) fueron indicadores de mal pronóstico. La curva de sobrevida actuarial de los 42 pacientes fue de 65% a los 5 años y de 30% a los 10 años. Se remarca la posibilidad de remisión espontánea y/o de detención de la enfermedad independiente de la terapéutica utilizada (AU)

Diagnóstico y seguimiento de 42 casos pediátricos de glomerulonefritis membranoproliferativa / Diagnosis and follow-up of 42 pediatric cases of membranoproliferative glomerulonephritis

Se analizaron 42 historias clínicas de niños con glomerulonefritis membranoproliferativa (GNMP) diagnosticadas a través de la biopsia renal. Los pacientes se controlaron en la Unidad de Nefrología del Hospital de Niños. La media de tiempo de seguimiento fue de 5,16 años. Se excluyeron los pacientes que presentaban GNMP secundarias, y se clasificaron en GNMP tipo I (27 pacientes) y tipo II (15 pacientes). En el comienzo de la enfermedad todos los niños presentaron hematuria, la mitad hipertensión arterial, un tercio de los niños anemia (3 de tipo hemolítico) no relaccionada con la caída del filtrado glomerular, y el 70% de los mismos C3 disminuido. En un paciente se detectó deficiencia familiar de C3. Ninguno de estos hallazgos clínicos o de laboratorio estuvo relacionado con la evalución posterior. La presencia de insuficiencia renal aguda persistente al comienzo de la enfermedad o de síndrome nefrótico (clínico o de laboratorio) fueron indicadores de mal pronóstico. La curva de sobrevida actuarial de los 42 pacientes fue de 65% a los 5 años y de 30% a los 10 años. Se remarca la posibilidad de remisión espontánea y/o de detención de la enfermedad independiente de la terapéutica utilizada

Urinary kallikrein in hypertension secondary to hemolytic uremic syndrome: response to diuretic stimulus.

Urinary kallikrein excretion was measured in 43 children, mean age 8 years, who had the hemolytic uremic syndrome (HUS) during the first year of life. Twenty eight were normotensive and fifteen hypertensive. We found no difference in urinary kallikrein excretion between the normotensive and hypertensive groups. Twenty three of these children received a combination of 1 mg/kg/day of hydrochlorothiazide plus amiloride for ten days. 14 of these patients were normotensive and 9 hypertensive. The rate of kallikrein excretion did not change in the hypertensive children whereas normotensive children had a three fold increase following administration of the diuretic. The different behaviour of kallikrein excretion in both groups may reflect a change in the reactive capabilities of the vasodilator system in this form of hypertension.