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cartas al director Tabla 1. Intervalos de confianza del 95 % en el gráfico de Bland-Altman Proteinuria 24 h (mg) Todos < 300 300-3499 > 3500 n 159 60 77 22 Diferencia media 252,7 -10,9 -85,8 2156 Desviación estándar (DE) 1508 117 808 3208 Intervalo de confianza 95 % (-2763, 3269) (-245, 223) (-1702, 1530) (-4260, 8572) (diferencia media ± 2 DE) 1. Sexton D. Correlation versus agreement; protein/creatinine ratio in spot urine and 24-hour urine protein. Nefrologia 2013;33(1):134. 2. Müller R, Büttner P. A critical discussion of intraclass correlation coefficients. Stat Med 1994;13:2465-76. 3. Shrout PE, Fleiss JL. Intraclass correlations: uses in assessing rater reliability. Psychol Bull 1979;86(2):420-8. Nuria Montero 1 , Sergio Mojal 2 , Julio Pascual 1 , María José Soler 1 1 Servicio de Nefrología. Hospital del Mar. Barcelona. 2 Institut del Mar d’Insvestigacions Mèdiques. Barcelona. Correspondencia: María José Soler Servicio de Nefrología. Hospital del Mar. Passeig Marítim, 25-29. 08003 Barcelona. Msoler@parcdesalutmar.cat Msoler1@imim.es Comment on “Membranous glomerulonephritis associated with mieloperoxidase antineutrophil cytoplasmic antibodyassociated glomerulonephritis” Nefrologia 2013;33(1):135-6 doi:10.3265/Nefrologia.pre2012.Sep.11692 Nefrologia 2013;33(1):134-54 Dear Editor, We read with interest the report of Dr. Guang-Yu Zhou, about a case of Membranous Glomerulonephritis with crescentic transformation. 1 Acute crescentic transformation is a rare but well described event in patients with membranous glomerulonephritis. 2 The concomitant occurrence of a vasculitic glomerulonephritis and membranous nephropathy in the same patient is unusual. 3 We report herein our similar experience. A caucasic 66-year-old man presented for rapid declining of renal function. For nearly 10 years he was suffering from hypertension and for 4 years he is having paresthesias, muscle aches in the legs and significant reduction in muscle strength with an ataxic walking. This condition was interpreted as a mixed sensori-motor polyneuropathy. He performed therapy with prednisone and azatioprine, suspended for 1 year; six months before, laboratory tests showed a serum creatinine concentration 220µmol/L and a 24-h protein excretion 0,75g/d. On admission, the physical examination showed edema and severe hypertension; we detected a 24-h protein excretion 1.1g/d, Hb: 9.1g/dl, serum creatinine concentration 550.8µmol/L, the urinalysis 2 + urine protein and 1 + urine blood. ANCA determined in serum screening test by indirect immunofluorescence and other immunological tests, including anti-nuclear antibodies (ANAs), anti-Sm antibody, anti-dsDNA antibody, anti-cyclic citrullinated peptide (CCP) antibody, and anti-glomerular basement membrane (GBM) antibody were negative; serum complement and immunoglobulin levels were normal. Liver function tests and other routine parameters were within the normal range. There was no evidence of systemic lupus erythematosus (SLE), infection, malignancy. For the clinical suspicion of a vasculitis leading to renal and neurological involvement, we performed a kidney biopsy. In the light microscopic visualization of renal tissue, 11 out of 17 glomeruli were globally sclerotic; the remaining glomeruli showed: diffuse, global and marked thickening of capillary wall (Figure 1), focal and diffuse sub-epithelial vacuolation; global and segmental sub epithelial deposits with sub-epithelial spikes, formation of 11 crescents (n° 3 cellular crescents, n° 1 fibrocellular crescent and n° 7 fibrotic crescents (Figure 2). Immunofluorescence examination displayed granular deposition of IgG, kappa and lambda light chains and a strong, diffuse and global granular staining along the glomerular capillary (subepithelial) walls. Therefore renal histology and laboratory examinations supported diagnosis of membranous GN with crescentic overlap. We diagnosed a vasculitis ANCA-negative and the patient was treated initially with methylprednisolone pulse 125mg/d for 3 days followed by prednisone 50mg/d, and i.v. cyclophosphamide 0.25g once every 21 days. Because of no sign of improvement shown 2 months later, we stopped the cyclophosphamide therapy and the patient started chronic haemodialysis treatment. Several authors have reported acute crescentic transformation in patients with pri- Figure 1. PAS stain shows global and prominent thickening of the glomerular basement membranes, in the absence of evidence of cellular proliferation (PAS, x 400). 135
cartas al director Figure 2. PAS stain shows a fibrocellular crescent in the urinary space that compresses the residual glomerulus and its tuft (PAS, x 400). Dear Editor, We were very interested by the comment submitted by Dr. Gioacchino Li Cavoli and his collaborators, regarding their similar experience of a membranous glomerulonephritis with crescentic overmary membranous glomerulonephritis. Vasculitic or crescentic glomerulonephritis is rarely seen in membranous nephropathy, except in those cases associated with systemic lupus. The immunopathogenesis of this unusual transformation is unclear. It is well recognized that patients with a crescentic glomerulonephritis have severe and often rapidly deteriorating failure. Unlike membranous nephropathy, which often has an insidious course progressing to renal failure over a period of years, patients with superimposed crescentic glomerulonephritis appear to have a more aggressive clinical course. The importance of recognizing this group of patients with membranous nephropathy and crescentic glomerulonephritis is that immunosuppressive therapy may ameliorate the progression of renal damage and in some cases early treatment was associated with useful recovery of renal function. 4 In our case, the discontinuation of prednisone and azathioprine therapy may have facilitated the rapid progression of kidney disease. Conflict of interest The authors declare that there is no conflict of interest associated with this manuscript. 1. Zhou GY. Membranous glomerulonephritis associated with myeloperoxidase antineutrophil cytoplasmic antibody-associated glomerulonephritis. Nefrologia 2012;32(4):548-51. 2. Kwan JT, Moore RH, Dodd SM, Cunningham J. Crescentic transformation in primary membranous glomerulonephritis. Postgrad Med J 1991;67:574-6. 3. Tse WY, Howie AJ, Adu D, Savage CO, Richards NT, Wheeler DC, et al. Association of vasculitic glomerulonephritis with membranous nephropathy: a report of 10 cases. Nephrol Dial Transplant 1997;12:1017-27. 4. Nasr SH, Said SM, Valeri AM, Stokes MB, Masani NN, D'Agati VD, et al. Membranous glomerulonephritis with ANCA-associated necrotizing and crescentic glomerulonephritis. Clin J Am Soc Nephrol 2009;4:299-308. Gioacchino Li Cavoli 1 , Angelo Ferrantelli 1 , Luisa Bono 1 , Calogera Tortorici 1 , Carlo Giammarresi 1 , Rita Passantino 2 , Ugo Rotolo 1 1 Division of Nephrology. Civic and Di Cristina Hospital. Palermo (Italy) 2 Anatomical Pathology Department. Civic and Di Cristina Hospital. Palermo (Italy) Correspondence: Gioacchino Li Cavoli Division of Nephrology. Civic and Di Cristina Hospital. Via Francesco Cilea 43. 90144 Palermo, Italy. gioacchinolicavoli@libero.it Respuesta Response to “Comment on 'Membranous glomerulonephritis associated with mieloperoxidase antineutrophil cytoplasmic antibody associated glomerulonephritis'” Nefrologia 2013;33(1):136-7 doi:10.3265/Nefrologia.pre2012.Oct.11763 lap. First of all, we would like to thank them for their input. They reported a case of membranous glomerulonephritis (MGN) with crescentic transformation in a ANCA-negative vasculitis which revealed no evidence of systemic lupus erythematosus (SLE), anti-glomerular basement membrane (GBM) glomerulonephritis, infection, malignancy and showed no improvement after immunosuppressive treatments. The case they presented was similar to the patient that Kwan JT et al. described previously. 1 Although several authors have demonstrated the concomitance of MGN and ANCA-associated glomerulonephritis, 2-6 MGN accompanied by ANCAnegative crescentic glomerulonephritis has been rarely encountered. The light microscopic visualization of renal tissue in their case showed the formation of 11 crescents (3 cellular crescents, 1 fibrocellular crescent and 7 fibrotic crescents) and 11 out of 17 glomeruli were globally sclerotic. These histopathological changes indicate the patient has reached to an advanced stage of crescentic glomerulonephritis and the renal disease has progressed to the sclerotic phase at the time of renal biopsy. Nasr SH et al. reported that the percentage of globally sclerotic glomeruli correlated with nonresponse to immunosuppressive agents. 5 This is why the patient showed no improvement after treated with steroid plus cyclophosphamide and started chronic haemodialysis treatment eventually. By contrast, our case showed 2 sclerosed glomeruli out of 19 glomeruli, the formation of 9 crescents including 4 cellular crescents and 5 fibrocellular crescents, as well as the fibrinoid necrosis lesions upon light microscopy. This indicates our patient might be at the relatively early stage of crescentic glomerulonephritis and the renal biopsy findings may interpret the better response to immunosuppressive treatments in our case. Concerning the prognosis of this group of patients, Nasr SH et al. reported that 50% of patients had reached endpoints of end-stage renal stage (ESRD) or 136 Nefrologia 2013;33(1):134-54
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