ACE gene polymorphism and renal scar in children with acute pyelonephritis

Abstract.

The pathogenesis of renal scarring after acute pyelonephritis (APN) in children is multifactorial. In addition to well-known risk factors (young age, high grade of vesicoureteral reflux, P-fimbriated Escherichia coli, and treatment delay), a role for genetic predisposition has been suggested. Since the ACE gene deletion polymorphism is a known risk factor for progressive glomerulosclerosis in chronic renal diseases, we have investigated the relationship between the ACE genotypes and the development of renal scarring after APN. Fifty-nine children (43 males and 16 females) with APN diagnosed by urine culture and technetium-99m-dimercaptosuccinic acid (⁹⁹Tc-DMSA) renal scan were studied. ACE genotypes were determined as II, ID, and DD using the polymerase chain reaction technique. A follow-up ⁹⁹Tc-DMSA renal scan was performed to evaluate the development of renal scars 3–6 months after treatment. The distribution of ACE genotypes and the allele frequencies were compared in the renal scar-positive (n=39) and -negative group (n=20). ACE genotype frequency after stratification by risk factors was also evaluated. The distribution of ACE genotypes did not differ between the renal scar-positive (II 25.9%, ID 35.9%, DD 28.2%) and -negative group (II 35.0%, ID 45.0%, DD 20.0%), before and after stratification by each risk factor. ACE gene deletion polymorphism did not affect the development of renal scar as an independent variable in children with APN.