In autopsy studies or 0-hour renal allograft biopsies, IgA nephropathy (IgAN) can be found in up to 1.5% of the normal population.1 Thus, the vast majority of patients seem not to need us and do well without a nephrologist. Patients who are in need of renal care and therapy are those with a proteinuria level of >0.5 to 1.0 g/d and/or a decline in GFR. A favorable outcome was noted in observational studies when proteinuria was reduced to <1 g/d in such patients.2 Similarly, loss of GFR can be retarded, albeit not absolutely prevented, with angiotensin-converting enzyme inhibitor (ACEI) therapy,3 corticosteroid therapy,4 or combined corticosteroid and ACEI therapy.5,6 There is uncertainty, however, whether an even more intense therapy might result in even better outcomes. In this issue of JASN , Pozzi et al. 7 describe the outcome of a long-awaited Italian and Swiss multicenter, randomized, controlled trial (RCT)8 in which they tested the hypothesis that adding a 6-month course of azathioprine to a 6-month corticosteroid regimen would further reduce the loss of GFR in high-risk, adult patients with IgAN. At inclusion, all patients exhibited a GFR of >50 ml/min per d and a proteinuria level of 1.5 to 3.5 g/d. Most also had advanced inflammatory and/or sclerosing histologic lesions in their baseline …
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Floege et al. (2010) studied this question.
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