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Benador et al investigated the occurrence of renal scars following presumed pyelonephritis in a population of hospitalized children aged 0-16 years. They divided the population into three age groups. These included 119 children less than 1 year old, 47 aged 1-5 years, and 35 older than 5 years. The diagnosis of urinary tract infection (UTI) was based on culture results of urine obtained by midstream collection, bagged specimens, or suprapubic aspiration. Parenchymal infection was based on clinical criteria. An attempt was made to identify first UTI based on history. Scarring was determined by abnormalities on cystourethrogram and repeat DMSA scintigraphy in those with initial lesions.
The results were surprising. The incidence of scar formation was 60% for the entire group, independent of whether it was the first or a recurrent UTI. Scarring was highest in the group aged 1-5 years (86%) while it was only 40% in those less than 1 year and a striking 64% in those older than 5 years, including 8-10 who allegedly had first UTIs. Reflux occurred in 29% of the entire group, but did not correlate well with the presence of a scar. That is, 24 had reflux and scarring, 14 had reflux without scarring, and 40 had scars but no reflux.
The authors conclude that renal parenchymal infection and subsequent scarring may occur in the absence of risk factors and is independent of age. Therefore, prevention of episodes of pyelonephritis should be the main objective in the management of UTIs in childhood.
Chronic pyelonephritis is responsible for 10% of end-stage renal disease (ESRD) in adults. Although it accounts for a significant number of people with ESRD, renal insufficiency is a distinctly uncommon sequela of UTI, a very common pediatric illness. For a long time we have believed that the risk of renal scarring, the precursor of renal insufficiency and/or hypertension, is greatest in the first 2-3 years of life.
Now along comes a study that seriously questions these commonly held beliefs. However, before we begin to change our approach to children with febrile UTIs and what we tell their families, there are several qualifications and limitations to the Benador study. First, the method of scar detection is DMSA scintigraphy, which is much more sensitive than ultrasonography or intravenous urography and may detect areas of mild scarring that are of no clinical, long-term significance. DMSA scanning is also very expensive and should not be used routinely, either to diagnose renal parenchymal infection or to replace serial ultrasonography to monitor renal growth and/or scar formation. Since the patients were followed for only two months, there are no data on impaired renal function, elevated blood pressure, or progressive scarring. Thus, there may be large discrepancy between DMSA-determined scarring and meaningful renal sequelae. Second, urine culture results were based on arguable clinical criteria, including bagged specimens, that may have led to over-diagnosis of UTIs in infants. Third, it is probably not accurate, and therefore not useful, to separate a group of patients with "documented first UTIs" when the cohort is determined by history alone. Another aspect of the study open to criticism is the large variability in the duration of treatment: 7-21 days. These concerns notwithstanding, the finding of frequent scarring after UTI, particularly in the age group over 5 years old, is impressive and worrisome and justifies the authors’ emphasis on doing everything we can to promptly diagnose and treat and preferably to prevent recurrent episodes of pyelonephritis.