The mean annual incidence of hemolytic uremic syndrome in persons <15 years of age in Italy from 1988 to 2000 was 0.28 per 100,000 population. Laboratory investigations showed that Shiga toxin–producing Escherichia coli (STEC) infection occurred in 73.1% of patients. STEC O157 was the most common serotype, but a considerable number of cases were from infections by non-O157 STEC.
In a 3-year prospective study, 49 Italian children with the hemolytic-uremic syndrome (HUS) were examined for evidence of infection with Vero cytotoxin-producing Escherichia coli (VTEC). Diagnosis of infection was established in 37 patients (75.5%) by the combined use of stool examination for VTEC and for free fecal neutralizable Vero cytotoxin and serum analysis for antibodies to the Vero toxins and the lipopolysaccharides (LPS) of three major VTEC serogroups (O157, O26, O111). Anti-LPS antibodies were detected in sera from 30 patients: 25 had antibody to O157 LPS, 4 to O26, and 1 to O111. In as many as 27 patients (55.1%), diagnosis of infection relied only on serologic findings, and the presence of antibody to LPS was the sole evidence of VTEC infection in 20 patients (40.8%). The use of LPS from different E. coli serogroups provided evidence that in Italy O157 strains are the most prevalent VTEC involved in HUS.
Three patients are described who presented with a glomerulopathy suggestive of lupus nephritis in the absence of other clinical and biological evidence of systemic lupus erythematosus (SLE). Renal biopsies showed a "full-house" immunofluorescence pattern and two patients also had cytoplasmic tubuloreticular inclusions by electron microscopy. All these patients developed antinuclear and anti-double-stranded DNA antibodies 3, 5, and 10 years after their original presentation. Subsequently, 1 patient also developed clinical symptoms of lupus. Reviewing all renal biopsies performed in our department, we found 14 additional patients who presented with a "full-house" immunofluorescence glomerulonephritis in the absence of other features of SLE. After a mean follow-up of 5.8 years, these patients have not developed serological or clinical evidence of SLE. We conclude that a "full-house" glomerulopathy in children may be the first symptom of SLE, especially when cytoplasmic tubuloreticular inclusions are detected. The appearance of other clinical and biological symptoms may be delayed by several years.
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