A. Amoroso et al., Polymorphisms in angiotensin-converting enzyme gene and severity of renal disease in Henoch-Schoenlein patients, NEPH DIAL T, 13(12), 1998, pp. 3184-3188
Background. The influence of angiotensin converting enzyme (ACE) gene polym
orphism on the progression of primary IgA nephropathy (pIgAN) is still deba
ted. Even though the allele frequency was reported to be similar to control
s, in some studies D/D patients had a faster decline of renal function and
need of dialysis. Since Henoch-Schoenlein purpura (HSP) nephritis is consid
ered a systemic vasculitis with renal lesions indistinguishable from pIgAN,
we investigated the effect of the ACE polymorphism on presentation and pro
gression of HSP IgAN.
Methods. We examined the insertion (I) and deletion (D) polymorphism in int
ron 16 of ACE gene by PCR amplification of genomic DNA of 82 patients (37 c
hildren), with biopsy-proven IgAN associated with HSP enrolled in a collabo
rative study.
Results. No significant association with clinical presentation at onset or
with final outcome was found (functional impairment at outcome in 31.8% D/D
, 27.4% I/D and 44% I/I, heavy proteinuria in 36.3% D/D, 21.6% I/D, and 11.
1% I/I). Patients homozygous for the D allele had a greater number of extra
renal relapses (P = 0.0028). No association was found between the ACE genot
ype and the presence of hypertension at onset and at the end of the follow-
up. No difference was found between adults and children.
Conclusions. In this cohort of HSP IgAN, no ACE I/D polymorphisms were foun
d to be associated with progressive deterioration of renal function. Differ
ent genes possibly involved in vasculitis might more strictly modulate expr
ession and evolution of HSP IgAN.