Microsoft Word - NEF335BF

نویسندگان

  • C. D. Diaz Gallo
  • J. M. Mauri
  • R. Poveda
  • A. M. Castelao
  • M. T. Gonzalez
  • M. Carreras
  • J. Alsina
چکیده

C. Diaz Gallo, Servei de Nefrologia, Hospital de Bellvitge, Feixa Llarga s/n, L’Hospitalet de Llebregat, E-08907 Barcelona (Spain) Dear Sir, Amyloidosis is a systemic disease characterized by the presence of extracellular deposits of insoluble fibrillar proteins. There are several varieties of amyloid, identified by the nature of the proteins involved; among them, we found the secondary amyloidosis, associated with chronic diseases. The involvement of several organs depends on the type of amyloidosis. Renal involvement occurs in a 75–100% in secondary amyloidosis. Renal amyloidosis is diagnosed observing amyloid deposits especially in glomerular mesangium, although they can also be found in capillaries, vessels and interstitium. These deposits are characterized by their Congo red and/or thioflavine T stain positiveness [1]. Rapidly progressive glomerulonephritis (RPGN) is characterized by a rapid deterioration of renal function and cellular proliferation of the parietal epithelium of Bowman capsule. Without treatment, 80–90% of the patients develop terminal renal failure in less than 6 months. Immunofluorescence allows to differentiate this disease in three types: type I with linear deposits of immunoglobulins (Ig) IgG often accompanied by C3 deposition, type II with granular deposits of Ig, and type III with no deposits. RPGN can be divided into primary or secondary. Secondary RPGN may be associated with other glomerulopathies, infections or systemic diseases [2]; however, association of RPGN and renal amyloidosis is rare. We report the case of a 71-year-old woman with chronic rheumatoid arthritis (RA) and rapidly progressive renal failure. Renal biopsy showed amyloid deposition and RPGN, with the particularity of the presence of antiglomerular basement membrane (anti-GBM) antibodies (lineal IgG) that, as far as we know, has not been reported previously. A 71-year-old female was admitted to our department because of oligoanuria and acute renal failure. She had been suffering from RA since she was 15. She had been treated with several nonsteroid antiinflammatory drugs (NSAID). No antecedents such as hypertension, diabetes mellitus, hematuria or hemoptysis were referred to. Four months prior to hospitalization pretibial edema and mild proteinuria were noted, with normal renal function. Three months before

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تاریخ انتشار 2008