You are here

Article Text

Article menu
Download PDFPDF
Electronic letters
Renoprotective efficacy of renin–angiotensin inhibitors in IgA nephropathy is influenced by ACE A2350G polymorphism
  1. I Narita,
  2. S Goto,
  3. N Saito,
  4. J Song,
  5. K Omori,
  6. D Kondo,
  7. M Sakatsume,
  8. F Gejyo
  1. Division of Clinical Nephrology and Rheumatology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
  1. Correspondence to:
 Dr I Narita
 Division of Clinical Nephrology and Rheumatology, Niigata University Graduate School of Medical and Dental Sciences, 757, Asahimachi-dori, Niigata, 951-8510, Japan; naritaimed.niigata-u.ac.jp

https://doi.org/10.1136/jmg.40.12.e130

Statistics from Altmetric.com

    Request Permissions

    If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

    Immunoglobulin A nephropathy (IgAN) is the most prevalent form of primary glomerulonephritis and one of the principal causes of end stage renal disease (ESRD) throughout the world.1,2 It is a complex disease, in which familial clustering suggests an inherited genetic predisposition. The disease has a variable clinical course, and one third of patients with IgAN progress to ESRD within 10–20 years of its onset.3,4 The mechanisms of interindividual differences in the rate of disease progression are unclear.5

    That increased production or activity of angiotensin II plays a detrimental role in the glomerular response to injury has been well documented. Recently, angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blocker (ARB) treatments have been shown to decrease proteinuria by improving glomerular permselectivity in IgAN,6,7 although the therapeutic effect was not recognised in about half of the patients.6

    An insertion/deletion (I/D) polymorphism of the angiotensin I converting enzyme gene has been shown to influence the concentration of ACE in the circulation and local tissues.8–10 Many studies have explored the association between the ACE I/D polymorphism and the development and progression of various cardiovascular diseases and renal diseases, including IgAN.11–13 Moreover, several studies have investigated associations between the ACE I/D polymorphism and the therapeutic efficacy of ACE inhibitors. The DD homozygote of the ACE I/D polymorphism has been reported as a risk factor for progression to ESRD in patients with IgAN, as well as a predictive marker for responsiveness to the antiproteinuric effects of ACE inhibitors.14 Other studies, however, reported that patients with the DD genotype were resistant to the renoprotective effects of ACE inhibitors, whether they had non-diabetic or diabetic nephropathy.15–17

    Recently, an informative set of 13 single nucleotide polymorphisms (SNPs) across the entire ACE gene has …

    View Full Text

    Footnotes

    • Declaration of interest: none declared.