POLYMORPHISM IN IGA NEPHROPATHY

Authors
Citation
Zh. Liu et Ls. Li, POLYMORPHISM IN IGA NEPHROPATHY, Nephrology, 3(1), 1997, pp. 63-66
Citations number
32
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
13205358
Volume
3
Issue
1
Year of publication
1997
Pages
63 - 66
Database
ISI
SICI code
1320-5358(1997)3:1<63:PIIN>2.0.ZU;2-A
Abstract
IgA nephropathy (IgAN) is polyphormic in its clinical manifestation, c ourse and prognosis. Patients with isolated IgA deposit in glomeruli t end to have a high incidence of macroscopic haematuria and carry a bet ter prognosis. In contrast, patients with deposits of IgA and IgG and IgM have a higher incidence of nephrotic syndrome and hypertension. In parallel, patients with IgA and IgG and IgM tend to have more glomeru losclerosis and tubulointestitial lesions. Recently, the angiotensin c onverting enzyme (ACE) gene polymorphism and its association in diseas e risk provided interesting exploration leading us to speculate about a possible mechanism to explain the variation in the rate of progressi on of IgAN; although, the results are still controversial. The variabi lity of plasma ACE concentration has been shown to be associated with an insertion/deletion polymorphism. The frequencies of ACE genotype in 177 Chinese patients with IgAN has been observed. We found that patie nts with IgAN showed a higher frequency of DD genotype than normal pop ulation. In contrast to the previous reports, we did not find any asso ciation between ACE genotype and the rate of progression of IgAN. As d ifferent genotypes of IL-1 receptor antagonist (IL-1ra) are also respo nsible for the circulating levels of IL-1ra, the polymorphism of IL-1r a gene has been analyzed in 100 IgAN patients. There was no significan t difference in the frequency of IL1RN2 allele between normal subject s and IgAN. However, patients with recurrent macroscopic haematuria sh owed a higher carriage rate of IL1RN2. Hereditable factors, in combin ation with a number of recognized environmental risk factors, are impo rtant determinants of the pathogenesis and natural history of IgAN. Th e notion that the gene polymorphism might be responsible for the clini cal features and progression of IgAN is both intriguing and provocativ e. The lessons from previous multiple small size studies have produced conflicting results illustrating the need for observation of large nu mbers of cases in further studies to verify these observed association s.