Angiotensin-converting enzyme gene polymorphism in children with idiopathic nephrotic syndrome.
OBJECTIVE
To investigate the genetic polymorphism of angiotensin-converting enzyme (ACE) insertion/deletion (I/D) in children with idiopathic nephrotic syndrome (INS), as well as its relationship with patient's clinical response to steroid therapy.


METHODS
Fifty-nine patients with INS were recruited and divided into 2 groups according to their clinical response to steroids: steroid-sensitive (SS) with 19 patients and non-SS with 40 patients, which was further divided into steroid-dependent (SD) and steroid-resistant (SR) groups with 35 and 5 patients, respectively. Seventy-nine children without previous renal diseases and negative proteinuria were enrolled as a control group. The genotypes for ACE I/D polymorphism, including DD, ID, and II, were analyzed.


RESULTS
The distribution of ACE DD, ID, and II genotypes in INS patients were 52.5, 10.2 and 37.3%, respectively; the corresponding numbers for the control group were 2.5, 25.3 and 72.2%, respectively. Patients with INS had a significantly higher percentage of DD genotype (p <0.001) than the control group. This higher incidence of the DD genotype was observed in both the SS and non-SS groups. A higher percentage of the DD genotype in the non-SS group and in the SD group as compared to the SS group (both p < 0.05) was also noted.


CONCLUSIONS
Our data shows that INS is associated with a higher incidence of the DD genotype, especially in non-SS patients. This finding suggests that the DD genotype may be a risk factor for INS and play a role in the clinical response to steroids.
Tsai
I-Jung
IJ
Department of Pediatrics, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan.
Yang
Yao-Hsu
YH
Lin
Yen-Hung
YH
Wu
Vin-Cent
VC
Tsau
Yong-Kwei
YK
Hsieh
Fon-Jou
FJ
D000483:Alleles; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D005260:Female; D005838:Genotype; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D015994:Incidence; D007223:Infant; D008297:Male; D009404:Nephrotic Syndrome / Q000188:drug therapy / Q000201:enzymology / Q000453:epidemiology / Q000235:genetics* / Q000473:pathology; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D011239:Prednisolone / Q000627:therapeutic use; D011507:Proteinuria / Q000188:drug therapy; D013624:Taiwan / Q000453:epidemiology
D005938:Glucocorticoids; D011239:Prednisolone; D007703:Peptidyl-Dipeptidase A