We determined the prevalence, anatomical variants and coexisting complications of duplex collecting systems in children with a history of UTI. Additionally, we compared the prevalence and severity of the coexisting anomalies with those found in single systems. We reviewed the records of children younger than 6 years who were evaluated following a first UTI during a 9-year period to identify those with duplex systems. Children without duplication anomalies comprised the control group. Of 774 evaluated children 63 (8%), more commonly females than males, had duplex systems. CDS were as common as IDS. VUR was the most commonly associated anomaly, with a higher prevalence in CDS (66%) and IDS (47%) compared to single systems (26%, p <0.0001 and p = 0.007, respectively). Ectopic ureterocele, which was the second most common associated anomaly, was found in 20% of the CDS but in none of the IDS or single systems. The occurrence of renal scarring was similar among CDS, IDS (13%) and single systems (10%). Poorly functioning pole moieties occurred more often in CDS (40%) compared to IDS (4%, p = 0.003), and were observed in none of the single systems. The resolution rate of reflux tended to be higher in IDS compared to CDS. CDS were a common finding among children with UTI who had duplication anomalies. Although CDS and IDS were accompanied by VUR more often than were single systems, CDS were associated more often with severe VUR, other serious complications and poor renal function.

OBJECTIVE: To evaluate prospectively whether normal scintigraphic results during urinary tract infections (UTIs) in neonates were predictive of the absence of dilating vesicoureteral reflux (VUR) (grade ≥III) and permanent renal damage (PRD).

Traditionally a disease of adults, type 2 diabetes (T2D) has been increasingly diagnosed in youth, particularly among adolescents and young adults of minority ethnic groups. Especially, during the recent COVID-19 pandemic, obesity and prediabetes have surged not only in minority ethnic groups but also in the general population, further raising T2D risk. Regarding its pathogenesis, a gradually increasing insulin resistance due to central adiposity combined with a progressively defective β-cell function are the main culprits. Especially in youth-onset T2D, a rapid β-cell activity decline has been observed, leading to higher treatment failure rates, and early complications. In addition, it is well established that both the quantity and quality of food ingested by individuals play a key role in T2D pathogenesis. A chronic imbalance between caloric intake and expenditure together with impaired micronutrient intake can lead to obesity and insulin resistance on one hand, and β-cell failure and defective insulin production on the other. This review summarizes our evolving understanding of the pathophysiological mechanisms involved in defective insulin secretion by the pancreatic islets in youth- and adult-onset T2D and, further, of the role various micronutrients play in these pathomechanisms. This knowledge is essential if we are to curtail the serious long-term complications of T2D both in pediatric and adult populations.