Identification of Children and Adolescents at Risk for Renal Scarring After a First Urinary Tract Infection

Abstract

IMPORTANCE No studies have systematically examined the accuracy of clinical, laboratory, and imaging variables in detecting renal scarring in children and adolescents with a first urinary tract infection. OBJECTIVES To identify independent prognostic factors for the development of renal scarring and to combine these factors in prediction models that could be useful in clinical practice. DATA SOURCES MEDLINE and EMBASE. STUDY SELECTION We included patients aged 0 to 18 years with a first urinary tract infection who underwent follow-up renal scanning with technetium Tc 99m succimer at least 5 months later. DATA EXTRACTION AND SYNTHESIS We pooled individual patient data from 9 cohort studies. MAIN OUTCOMES AND MEASURES We examined the association between predictor variables assessed at the time of the first urinary tract infection and the development of renal scarring. Renal scarring was defined by the presence of photopenia on the renal scan. We assessed the following 3 models: clinical (demographic information, fever, and etiologic organism) and ultrasonographic findings (model 1); model 1 plus serum levels of inflammatory markers (model 2); and model 2 plus voiding cystourethrogram findings (model 3). RESULTS Of the 1280 included participants, 199 (15.5%) had renal scarring. A temperature of at least 39°C, an etiologic organism other than Escherichia coli, an abnormal ultrasonographic finding, polymorphonuclear cell count of greater than 60%, C-reactive protein level of greater than 40 mg/L, and presence of vesicoureteral reflux were all associated with the development of renal scars (P Յ .01 for all). Although the presence of grade IV or V vesicoureteral reflux was the strongest predictor of renal scarring, this degree of reflux was present in only 4.1% of patients. The overall predictive ability of model 1 with 3 variables (temperature, ultrasonographic findings, and etiologic organism) was only 3% to 5% less than the predictive ability of models requiring a blood draw and/or a voiding cystourethrogram. Patients with a model 1 score of 2 or more (21.7% of the sample) represent a particularly high-risk group in whom the risk for renal scarring was 30.7%. At this cutoff, model 1 identified 44.9% of patients with eventual renal scarring. CONCLUSIONS AND RELEVANCE Children and adolescents with an abnormal renal ultrasonographic finding or with a combination of high fever (Ն39°C) and an etiologic organism other than E coli are at high risk for the development of renal scarring.

Association Between Uropathogen and Pyuria

“…[8][9][10][11] This may partly explain why, in a recent meta-analysis, children with UTIs caused by non-E coli organisms were more likely to develop renal scarring. 12 Our results suggest that pyuria may not always be present in children with UTIs, especially those caused by Enterococcus species, Klebsiella species, or P aeruginosa. Accordingly, in acutely ill children suspected of having a UTI, empirical therapy while awaiting culture results may represent a reasonable approach if there are indications (see below) that organisms other than E coli may be involved.…”

Reaffirmation of AAP Clinical Practice Guideline: The Diagnosis and Management of the Initial Urinary Tract Infection in Febrile Infants and Young Children 2–24 Months of Age

“…NonEscherichia coli isolates are less frequently associated with pyuria than E coli, 5 but the significance of this association is not clear at present. Non-E coli uropathogens are of concern because they are more likely to result in scarring than E coli, 6 but animal studies demonstrate the host inflammatory response to be what causes scarring rather than the presence of organisms. 7 Moreover, the rate of asymptomatic bacteriuria is sufficient to account for the lack of association with pyuria.…”

Acute pyelonephritis in children

“…Escherichia coli (E. coli) is the most frequent bacteria, with a prevalence of about 80-90 % [6][7][8]. The primary reservoir of E. coli is the human gut, where this germ is a normal commensal.…”