The purpose of this retrospective cohort study was to report the clinical course of children with primary vesicoureteral reflux (VUR). Between 1970 and 2004, 735 patients were diagnosed with VUR and were systematically followed in a single tertiary renal unit. Patients were followed up for a mean time of 76 months (6 months to 411 months). The events of interest were reflux resolution, renal damage, urinary tract infection (UTI), chronic kidney disease (CKD), and hypertension. Survival analysis was performed in order to evaluate reflux resolution and CKD. Renal damage was detected at admission in 319 patients (43.4%). Continuous low-dose antibiotic prophylaxis was administered to 624 patients (91.2%); 499 (73%) patients subsequently had no UTI or fewer than three episodes. The median time of persistence of reflux according to Kaplan-Meier analysis was 38 months for grade I/II [95% confidence interval (95% CI), 33-43], 98 months for grade III (95% CI, 78.5-105), and 156 months for grade IV/V (95% CI, 122-189). Twenty patients (3%) developed hypertension. It was estimated that the probability of CKD was 5% at 10 years after diagnosis of VUR; for children diagnosed after 1990 the probability of CKD was only 2%. Renal function impairment occurred in patients with severe bilateral reflux or in patients with contralateral renal hypoplasia. There has been an improvement of prognosis for patients diagnosed in the past 15 years.

Our findings suggest that the combination of fetal and postnatal renal pelvic dilatation is able to increase the diagnostic accuracy for detecting infants who need a more comprehensive postnatal investigation for upper urinary tract obstruction.

We report a case of acute myocardial infarction in a nephrotic child. A 7-year-old boy with a 4-year history of steroid-unresponsive nephrotic syndrome due to mesangial proliferation disease presented with acute vomiting and chest pain. An electrocardiogram showed ST elevation and pathological Q waves in leads consistent with anterior and septal myocardial infarction. Subsequent cardiac catheterization showed no evidence of atherosclerotic coronary artery disease, and thrombotic occlusion of the anterior descending coronary artery was the likely cause of the event. Myocardial scintigraphy showed extensive myocardial damage. The child had no long history of extreme hypercholesterolemia or hypertriglyceridemia. The case suggests that children with long-lasting nephrotic syndrome may be at increased risk for ischemic cardiovascular events, due to hyperlipidemia as well as a hypercoagulability state. The literature is reviewed regarding the relationship between nephrotic syndrome and the incidence of ischemic heart disease.

The association between Helicobacter pylori infection and gastric motility abnormalities is still controversial, partly because of the lack of an appropriate animal model. H. heilmannii type 1 (Hh1), a spiral bacterium that infects the stomach of both man and pigs, easily colonises and induces an in¯ammatory response in the gastric mucosa of rodents. For these reasons, the present study investigated the relationship between gastric motility in rats experimentally infected with Hh1 and correlated the results with serum gastrin and gastric somatostatin concentrations, as these hormones seem to be involved in gastric motility. Ten rats were inoculated with gastric mucus from an Hh1-positive pig and 10 animals with gastric mucus from an Hh1-negative pig (control group). After 56 days, gastric emptying was studied in vivo by scintigraphy. The animals were then killed, blood samples were collected for serum gastrin measurement, strips of the gastric wall were obtained for an in-vitro motor study and fragments of the gastric antrum were obtained for somatostatin content evaluation, Hh1 diagnosis and histological study. There was a signi®cant increase in gastric emptying in the test group compared with the controls as demonstrated by the in-vivo and in-vitro studies. Serum gastrin levels were signi®cantly higher and somatostatin levels were lower in the test group than in the controls. In addition, infected animals showed evidence of gastritis on histological examination. Gastric motility is altered in rats infected with Hh1, a fact possibly related to concurrent abnormalities of gastrin and somatostatin secretion.