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  • Title: Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers for IgA nephropathy.
    Author: Dillon JJ.
    Journal: Semin Nephrol; 2004 May; 24(3):218-24. PubMed ID: 15156527.
    Abstract:
    The lengthy course of IgA nephropathy and the possibility of good outcomes without therapy suggest nontoxic therapies such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs.) Among patients with IgA nephropathy, both ACE inhibitors and ARBs reduce the transglomerular passage of large, but not small, molecules, reducing proteinuria. The antiproteinuric effects of ACE inhibitors and ARBs are probably equivalent. Dual ACE inhibitor-ARB therapy reduces proteinuria by 54% to 73% and is more effective than either agent alone. To determine whether ACE inhibitors or ARBs preserve renal function long-term, one must rely on trials studying nondiabetic, proteinuric renal diseases rather than on trials specific to IgA nephropathy. Among this group of patients, several randomized, controlled trials, including the AIPRI trial, the REIN trial, and a metaanalysis of 11 randomized, controlled trials, have established clearly that the ACE inhibitors preserve renal function. There is no reason to believe that this information is not applicable to IgA nephropathy. The COOPERATE trial, in which 50% of the subjects had IgA nephropathy, established that ACE inhibitors and ARBs preserve renal function equally, and that dual ACE inhibitor-ARB therapy preserves renal function more effectively than either therapy alone. These data suggest that most individuals with proteinuric renal diseases, including IgA nephropathy, should be treated with ACE inhibitors and ARBs, ideally in combination. Polymorphisms of the angiotensinogen gene, the ACE gene, and the angiotensin II type I receptor gene have, so far, failed to predict either susceptibility to or progression of IgA nephropathy. However, the D allele of the ID polymorphism, particularly the DD genotype, could predict a favorable response to renin-angiotensin blockade.
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