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).
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.
Absolute Event Rate: 0% vs 0%
Abstract 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.
Bazzi et al. (Fri,) reported a other. 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).