Antibiotic prophylaxis in antenatal nonrefluxing hydronephrosis, megaureter and ureterocele

Observation is a conservative management option in infants with nonrefluxing hydronephrosis, primary nonrefluxing megaureter and ureterocele diagnosed postnatally following antenatal detection of hydronephrosis. Antibiotic prophylaxis might be a sensible regimen under these circumstances to prevent UTI in this population who are potentially at increased risk. However, studies examining the efficacy of prophylactic antibiotics are sparse in this setting. For each condition, prophylactic policies seem extremely variable, and UTI rates vary widely with comparable rates reported between patients followed on and off antibiotics. Overall, antibiotic prophylaxis seems unnecessary in patients with isolated low-grade hydronephrosis. Patients with high-grade nonrefluxing hydronephrosis seem at increased risk of UTI, with risk further increasing in patients with associated ureteral dilatation (hydroureteronephrosis) irrespective of the presence of a ureterocele. Obstruction might be an additional independent risk factor, but the diagnosis of obstruction is often possible only in retrospect. The data available suggest that infants are the most at risk of UTI during the first 6 months of life, particularly if they undergo catheterization during workup examinations. Thus, antibiotic prophylaxis might be prudent during the first 6-12 months of life in patients with high-grade hydronephrosis and hydroureteronephrosis with or without ureterocele, and particularly before completion of the diagnostic workup. Paediatric urologists are urged to embark on controlled trials to compare patients followed with and without antibiotic prophylaxis

Genetic susceptibility to polyI:C-induced IFNalpha/beta-dependent accelerated disease in lupus-prone mice

Systemic lupus erythematosus (SLE) is an autoimmune disease of unknown etiology. Associations between viral infections and the onset of SLE have been suggested, and recent studies have provided evidence that type I interferons (IFNalpha/beta) might play a role in the SLE disease process. Viruses and interferons have also been implicated in mouse models of SLE. We generated a model of accelerated proteinuria, in which lupus-prone mice were injected repeatedly with polyinosinic:polycytidylic acid (polyI:C), mimicking exposure to virus-derived double stranded RNA (dsRNA), leading to the production of IFNalpha/beta. PolyI:C-treated (B6.Nba2 x NZW)F1 and (B6 x NZW)F1 hybrid mice developed significantly increased levels of anti-dsDNA autoantibodies, characteristic of lupus. Most significantly, polyI:C-treated (B6.Nba2 x NZW)F1 mice, but not (B6 x NZW)F1 or parental strains, developed lupus-like nephritis in an accelerated fashion, which was dependent on IFNalpha/beta and associated with elevated deposition of total IgG, IgG2a and complement factor C3 in the glomerular capillary walls. These data suggest that reagents, which increase the levels of endogenous IFNalpha/beta (directly or indirectly), can accelerate the course of lupus-like nephritis, the development of which is dependent on the presence of both NZW- and Nba2-encoded genes