There are two main reasons for trying to actively prevent UTIs:
a. To prevent morbidity/ mortality associated with acute cystitis & pyelonephritis.
Young children are especially at risk of severe infections, with 6% of UTIs in the first year of life associated with bacteraemia, 2% requiring fluid resuscitation at diagnosis, and 1% requiring ventilatory support (Craig et al., 1998). The incidence of death from urinary sepsis was as high as 11% during the 1960s, but is now rare. Because UTIs often recur -12% to 30% of children with their first UTI have another infection during the ensuing 12 months (Winberg et al., 1974) - these occasional severe outcomes may justify offering preventive interventions to young children with UTI.
b. To prevent long-term sequelae of hypertension and end-stage renal disease.
The combination of vesicoureteric reflux (VUR) and renal damage from recurrent UTIs has traditionally been thought to lead to end-stage renal disease (ESRD) (Bailey, 2000). In recent years, however, evidence has emerged that hypertension (HT), renal impairment, and ESRD may not be causally linked with VUR and recurrent UTIs (Figure 20.1) (Wennerstrom et al., 2000b; Yeung et al., 1997; Pope et al., 1999; Marr et al., 2004). Long-term sequelae of HT and renal dysfunction were addressed in a Swedish cohort of children who were examined 16-26 years after their first symptomatic UTI (Wennerstrom et al., 2000a). Sixty-eight participants with renal parenchymal defects on dimerccaptosuccinic acid (DMSA) scan at the time of childhood UTI diagnosis were matched for age and gender with 51 controls (who had UTI with normal DMSA scans). Hypertension was found in 9% of the group with defects and 6% of the group without defects (difference not statistically significant). Glomerular filtration rate (GFR) was well preserved in both study groups, and neither had substantial rates of proteinuria (Wennerstrom et al., 2000a). Although the sample size was small, these data suggest that childhood UTI is not associated with high rates of renal impairment or HT, even if an abnormal DMSA scan is present initially.
These results stand in contrast to previous case-series, in which 18-25% of patients with evidence of renal "scarring" developed hypertension on follow-up 15-30 years after their first UTI (Goonasekera et al., 1996; Smellie et al., 1998). However, those studies selected patients with severe renal parenchymal defects and used conventional and not ambulatory BP measurements, which may account for the discrepancy in results. Jacobson et al. found three of 30 patients followed up 27 years after the detection of non-obstructive pyelonephritic renal scarring had ESRD, and the remainder had significantly lower GFR than matched controls (Jacobson et al., 1989). Martinell et al. followed 54 female patients with renal scarring continuously for 15 years (Martinell et al., 1996). GFR was reduced compared to controls only in those with severe scarring. In summary, there is no clear evidence that renal scarring is a risk factor for the future development of HT, but severe renal scarring may be a risk factor for future reduction in GFR.
VUR -► UTI -► Renal scars -► Renal damage-► ESRD
Renal dysplasia / hypoplasia ESRD
Genetic and/or _ . . . Environmental -► Embryo[ogical
factors dysfunction ^
VUR, vesico-ureteric reflux; UTI, urinary tract infection; ESRD, end-stage renal disease
The natural history of renal parenchymal defects as detected by DMSA scans is resolution over time. Forty percent of DMSA scans performed at the time of acute UTI will demonstrate defects. This reduces to 5% three years later (Stokeland et al., 1998). Many of the defects found at the time of a UTI may have been present prior to the infection, possibly due to congenital renal dysplasia (Figure 20.1) (Polito et al., 2000; Wennerstrom et al., 2000b). This may be diagnosed antenatally and may be progressive despite medical and surgical intervention.
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