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A Clinicopathologic Study of Thrombotic Microangiopathy in IgA Nephropathy

2011; American Society of Nephrology; Volume: 23; Issue: 1 Linguagem: Inglês

10.1681/asn.2010111130

1533-3450

Khalil El Karoui, Gary S. Hill, Alexandre Karras, C. Jacquot, L Moulonguet, O Kourilsky, Véronique Frémeaux‐Bacchi, Michel Delahousse, Jean–Paul Duong Van Huyen, Alexandre Loupy, Patrick Bruneval, Dominique Nochy,

Vasculitis and related conditions

Thrombotic microangiopathy (TMA) occurs in IgA nephropathy, but its clinical significance is not well described. We retrospectively examined a series of 128 patients diagnosed with IgA nephropathy between 2002 and 2008 who had a mean follow-up of 44±27 months. In our series, 53% presented with lesions of TMA, acute or organized, in arteries and/or arterioles. Among patients with TMA, 4% were normotensive, 25% had controlled hypertension, and 71% had uncontrolled hypertension. Of those with uncontrolled hypertension, 26% had malignant hypertension. Histologically, the group with TMA had a significantly greater percentage of sclerotic glomeruli and worse tubulointerstitial fibrosis than those of the group without TMA. However, a significant minority of patients had near-normal histology, with minimal tubular atrophy (20%) and/or <20% interstitial fibrosis (24%). TMA rarely occurred in the absence of significant proteinuria. During follow-up, a doubling of serum creatinine or ESRD occurred in all patients with laboratory evidence of TMA, in 42% of those with morphologic evidence but no laboratory evidence of TMA, and in 11% of those without TMA. In summary, lesions of TMA are frequent in IgA nephropathy and may occur in normotensive patients with near-normal renal histology. Although the pathophysiologic mechanisms involved remain undetermined, the current study rules out severe hypertension or advanced renal disease as sole causes.