Background: The pathogenesis of renal scarring (RS) after first febrile urinary tract infection (UTI) in children is multifactorial. In addition to well-known risk factors, a role for genetic predisposition has been suggested. Aims: To determine whether deoxyribonucleic acid (DNA) polymorphisms at the plasminogen activator inhibitor -1 (PAI-1) gene were associated with evolution to RS following a febrile UTI in infants. Materials and Methods: Our research included 100 infants, 84 girls and 16 boys, ages up to 1 year with a first febrile UTI, increased inflammatory parameters and positive urine culture treated at the Pediatric Clinic II of the University Clinical Center Sarajevo (UCCS). The diagnostic was based on the imaging studies: ultrasonography, voiding cystourethrography (VCUG) and initial and control static renal scintigraphy (DMSA renal scan), to assess the renal parenchymal damage (RPD). The polymorphisms of the PAI-1 were determined based on polymerase chain reaction technique. The distribution of PAI-1 genotypes and the allele frequencies were compared between different groups of patients with febrile UTI. Results: Results presented that 66 infants had acute pyelonephritis (APN) and 22 had vesicoureteral reflux (VUR). On initial DMSA renal scan examination, we detected no RPD in any patient. After 6 months, the repeat DMSA renal scan revealed the presence of RPD in 18 (27%) out of 66 infants with APN. Distribution of PAI-1 genotypes was not different between various groups of patients with febrile UTI. Conclusions: The results of our study have not shown that individual genetic variation in PAI-1 is an independent variable that predispose same of children for RS after first febrile UTI. Maybe that yet unknown gene polymorphisms together with geographical and /or socio-economic differences can influence on the development of RS.
Key words: urinary tract infection, plasminogen activator inhibitor -1, renal scarring.
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