Key result
ACEi use is linked to ~68% less progression in IgA nephropathy with high urinary IgG.
Why the study?
Factors affecting responsiveness to ACE inhibitors, the role of proteinuria components and histological lesions, and criteria to identify patients who benefit in IgA nephropathy were poorly defined.
Do ACE inhibitors reduce end-stage renal disease and doubling of serum creatinine in patients with IgA nephropathy?
Do ACE inhibitors reduce end-stage renal disease and doubling of serum creatinine in patients with IgA nephropathy?
Fractional urinary excretion of IgG is a strong predictor of which patients with IgA nephropathy will derive renoprotective benefits from ACE inhibitor therapy.
May guide ACE inhibitor selection by FEIgG in IgA nephropathy; supports consensus but leaves open need for randomized confirmation.
Background: Several aspects of renoprotection by angiotensin-converting enzyme inhibitors (ACEi) in IgA nephropathy (IgAN) are poorly defined: fac tors affecting responsiveness, role of proteinuria components and histological lesions, and crite ria to identify patients who may benefit from ACEi. Methods: In an observational study of 140 IgAN patients (follow up 62 ± 36 months), 73 untreated and 67 ACEi treated for 53 ± 28 months, 9 baseline risk factors (RFs) (blood pressure, serum creatinine, proteinuria/day, frac tional excretion of IgG [FEIgG] and α1-microglobulin, global and segmental [SS] glomerular sclerosis, tu bulointerstitial damage and arteriolar hyalinosis [AH] score), each divided into 2 subgroups according to a cutoff with the highest sensitivity and specificity for progression, were evaluated for ability to predict reno protection. Primary end point: end-stage renal dis ease (ESRD) and doubling of serum creatinine (sCr); secondary end point: increase ≥25% of sCr with last sCr ≥1.58 mg/dL; total progression: sum of end points. Results: Patients with RFs below cutoffs did not ben efit from ACEi. All clinical and proteinuric and 2 histo logical RFs (SS, AH score) with values above cutoffs showed significant reduction of progression in ACEi treated vs. untreated patients; FEIgG showed the high est prediction of renoprotection: ESRD/sCr×2: 20% vs. 62% (p=0.0004); total progression: 40% vs. 85% (p=0.0003). By multivariate analysis, independent pre dictors of progression were FEIgG, sCr and no ACEi treatment. Proteinuria reduction from -100% to -30%, spontaneous or after ACEi treatment, did not affect progression in treated vs. untreated patients (19% vs.13%, p=0.85). Patients with proteinuria increased or re duced <30% showed a reduction of total progression if ACEi-treated (15% vs. 77%, p=0.0002). Presence of 1 clinical or proteinuric RF above the cutoff may be a cri terion to identify patients who may benefit from ACEi. Conclusions:Renoprotection by ACEi is a multifacto rial phenomenon: the best predictor of renoprotection is FEIgG, a marker of disruption of glomerular barrier to proteins; renoprotection depends not only on ability to reduce proteinuria, but probably also on antiinflam matory and antifibrotic activity.
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Bazzi et al. (2009) studied this question. In IgA nephropathy, ACE inhibitors reduce progression significantly in patients with high fractional urinary excretion of IgG: 20% vs. 62% ESRD/sCr×2 (p=0.0004).
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