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M. Praga, MD, Servicio Nefrología, Hospital l° Octubre, Carretera Andalucia km 5.400, E-28041 Madrid (Spain) Dear Sir, Boyce and Holdsworth [1] reported a case of fatal pulmonary haemorrhage associated with crescentic glomerulonephritis (GN) in the absence of immunereac-tant deposition (idiopathic Goodpasture’s syndrome). We read this report with great interest because recently we have reviewed our experience with diffuse pulmonary haemorrhage (DPH) associated with crescentic GN. In 54 cases of crescentic GN, 12 (22.2%) showed DPH: 3 cases had a systemic vasculitis, 5 showed circulating antiglomerular basement membrane antibody (anti-GBM Ab) with linear deposits of IgG on glomerular capillary walls (anti-GBM Ab mediated Goodpasture’s syndrome) and the other 4 patients had a crescentic GN with negative immunofluorescence (IF) and without clinical or histological data of vasculitis. The latter 4 cases are, then, similar to that reported by Boyce and Holdsworth [1] (idiopathic Goodpasture’s syndrome). When comparing patients with anti-GBM Ab Goodpasture’s syndrome (group I) and those with idiopathic Goodpasture’s syndrome (group II), several interesting findings arose: the bouts of DPH were accompanied by important decreases of haematocrit and p02 in every case, without differences between the two groups. The percent of glom-eruli with crescents and the degree of renal failure were similar in both groups (table I), and no differences were observed in the radiological picture. Some patients showed localized lung consolidations like the case of Boyce and Holdsworth [1], although diffuse pulmonary infiltrates were more frequently seen. Every patient was treated with intravenous prednisolone pulses and cyclo-phosphamide, in addition with plasmapheresis in 4 patients of group I. Prednisolone pulses had a clear beneficial effect on DPH, although 1 patient from each group died as a consequence of massive DPH. Table I.