Management ofIgA nephropathy: Evidence-based recommenglomerular diseases, whereas in Europe, it has been redations. The condition known as IgA nephropathy was first ported in 10 to 30% of glomerular disease series [8]. In identified when Berger observed mesangial staining for IgA in the United States, the overall prevalence is approxihealthy patients with isolated hematuria. These patients often mately 10 to 15% [9], although in specific groups such presented with recurrent synpharyngitic hematuria or less freas the American Indians in the Southwest, the rate is quently with asymptomatic microscopic hematuria and proteinuria. Although initially considered benign, we now recognize 35% [10]. IgAN is uncommon in blacks, whether they it as a common cause of end-stage renal failure. The overall live in the United States or in Africa [11, 12]. prognosis may be better than suggested in the literature, as Recurrence of IgAN after transplantation [13], evipatients with mild asymptomatic hematuria are often not biopdence showing that IgA glomerular deposits disappear in sied and, therefore, frequently are not included in published a kidney from an IgA donor [14], and IgA deposits obarticles. We reviewed prospective and retrospective adult studies published after 1976 and analyzed them to produce evidenceserved in other organs such as skin, lungs [15], or intesbased recommendations. Patients with proteinuria over 3 g/day,

A stent-graft was placed percutaneously in the right renal artery of a 50-year-old woman with hypertension and a fibromuscular dysplastic lesion consisting of severe stenoses and a 1.5-cm saccular aneurysm with a wide neck. At 1-year follow-up with arteriography, arterial luminal diameter was normal and no aneurysm was depicted. The patient's blood pressure was normal without blood pressure medication.

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