Silicosis Associated with Crescentic IgA Mesangial Nephropathy

A. Bonnin, Department of Nephrology and Reanimation, Hôpital du Bocage, 2 boulevard de-Lattre-de-Tassigny, F-21034 Dijon Cédex (France) Dear Sir, IgA mesangial nephropathy can be observed in association with diseases involving IgA-secreting epithelia, including the lungs [1]. On the other hand, exposure to silica can result in renal function abnormalities, so called ‘silicon nephropathy’ [2]. But as far as we know, an association silicosis-IgA mesangial nephropathy has not yet been described. Three men, (50,67 and 69 years old) have had a history of pulmonary silicosis diagnosed 10,20 and 23 years ago. They were seen because of a recent discovery of a glomer-ular type proteinuria ranging from 1.1 to 3 g/24 h, with microscopic hematuria, mild renal failure in 2 cases (serum creatinine levels: 165 and 210 μmol/l) and high blood pressure (2 cases). Light microscopic examination of a kidney biopsy specimen showed in the 3 cases an increase in mesangial matrix associated in 1 case with focal and segmental proliferation of mesangial cells and extracap-illary proliferation in 20% (2 cases) and 50% (1 case) of the glomeruli. Immunofluorescence studies revealed diffuse IgA and C3 mesangial deposits compatible with IgA mesangial nephropathy. Serum IgA levels were 1.3, 6.3 and 6.7 g/l (normal range: 0.9–4.5 g/l). One patient died from respiratory failure 11 months later. One patient with 20%o crescents still has a normal renal function and a stable proteinuria after 16 months. The other one experienced a cutaneous vasculitis with arteriolar IgA deposits and decline of renal function (50% fresh crescents) 1 year after the diagnosis. After plasma exchange and corti-costeroid treatment, renal function improved, then gradually decreased and has been stable for 17 months (serum creatinine level: 510 μmol/l). The antigens of the major histocompatibility complex were A30, Ax, B13, B35, DR5, DR7 in case 1 and A2, A9, B5, Bl2, DR3⁄8, DR10 in case 2 (table I, ∏). Such histological findings, including crescents, have already been described as silicon nephropathy, but without diffuse IgA mesangial deposits [2]. So, we could postulate that these patients have simultaneously silicon nephropathy and Berger’s disease. Alternatively ‘primitive’ IgA nephropathy can also result in such histological features. However, two kinds of arguments could support the hypothesis of a causal relationship between silicosis and IgA nephropathy. At