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On examination&#44; blood pressure 170&#47;100&#8239;mmHg&#44; sinus rhythm&#44; crackles in both lung bases and edema&#46; Hemogram and blood chemistry&#58; normocytic normochromic anemia&#44; without microangiopathic hemolytic anemia &#40;MHA&#41;&#44; creatinine 6&#8239;mg&#47;dl&#44; nephrotic proteinuria with normal serum albumin and microhematuria&#46; Chest X-ray&#58; bilateral interstitial infiltrate&#44; with diagnosis of pulmonary hemorrhage with immunological study with ANCAp positive 1&#47;320&#44; rest normal&#47;negative&#44; including anti-glomerular basement membrane antibodies&#46; Plasmapheresis&#44; corticosteroids and intravenous cyclophosphamide were started&#46; One week after admission&#44; MHA with smear showing schistocytes and undetectable haptoglobin&#44; with negative stool culture&#44; normal ADAMTS13&#44; we decided to start eculizumab treatment&#44; with normal genetic follow-up Renal biopsy&#58; 49 glomeruli&#44; 10 sclerosed&#44; 29 with epithelial crescents&#44; some with segmental necrosis&#44; PAS and Jones silver positive&#46; No signs of TMA&#46; Direct immunofluorescence was strongly positive for IgG with linear pattern&#44; kappa and lambda positive&#44; weak C3 with parietal and mesangial granular pattern&#44; IgG4 positive &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0015" class="elsevierStylePara elsevierViewall">At hospital discharge&#44; the patient presented remission of pulmonary hemorrhage and resolution of MHA&#44; creatinine of 3&#46;8&#8239;mg&#47;dl&#44; proteinuria and microhematuria&#44; and continued treatment with cyclophosphamide&#44; corticosteroids and eculizumab up to 2 months after resolution of MHA&#46; Thirty days after discontinuation of eculizumab&#44; she presented a new episode of probable TMA and the ME result was received&#58; dense deposits&#44; in glomerular basement membrane &#40;GBM&#41; and mesangium&#44; consisting of random fibrils&#44; with an average thickness of 18&#46;41&#8239;nm&#44; compatible with fibrillary glomerulopathy&#44; with linear IgG deposits &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; DNAJB9 testing by immunohistochemistry was positive&#44; and we restarted eculizumab&#44; with suspicion of secondary TMA&#46; After 6 months of cyclophosphamide&#44; we maintained treatment with azathioprine&#46; For 2&#46;5 months&#44; she presented clinical and renal function stability&#44; with no MHA data&#59; treatment with eculizumab was maintained for 3 months and subsequently renal function improved with no MHA data&#46; Three months after discontinuation&#44; the patient presented deterioration of renal function&#44; and eculizumab was reinitiated until her inclusion in chronic treatment with peritoneal dialysis&#44; 9 months later &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#41;&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">Fibrillary glomerulonephritis rarely presents as it did in this case&#44; with acute renal failure and pulmonary hemorrhage&#46; Different authors suggest the possibility of a circulating factor in GF&#44; which may be responsible for the existence of fibrillar material at pulmonary level&#44; triggering pulmonary hemorrhage&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> For the diagnosis of FGN&#44; EM is necessary&#44; or DNAJB9 by immunohistochemistry if EM is not available&#46; In our case&#44; despite diagnosis made by EM&#44; we tested for DNAJB9 with a positive result&#46;<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">7&#8211;9</span></a> The linear&#47;pseudolinear IgG deposits described in FGN and in our patient resembles a GBM antibody disease&#44; which makes us rule out FGN when present or suggest coexistence&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;2</span></a> The presence of RPG and TMA is rare&#44; but may occur in FGN&#44; 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Letter to the Editor
Fibrillary glomerulonephritis simulating glomerular basal antimembrane antibody disease with associated thrombotic microangiopathy and ANCAp
Glomerulonefritis con depósitos fibrilares simulando enfermedad por anticuerpos antimembrana basal glomerular con microangiopatía trombótica asociada y ANCAp
M. Dolores Sánchez de la Nieta Garcíaa,
Corresponding author
sanchezdelanieta@senefro.org

Corresponding author.
, Lucía González Lópezb, Paz Castro Fernándezc, Minerva Arambarri Seguraa, Alberto Martínez-Caleroa, Marina Alonso Riañod, Ana Sánchez-Fructuosoa
a Servicio de Nefrología, Hospital Universitario Clínico San Carlos, Madrid, Spain
b Servicio de Anatomía Patológica, Hospital General Universitario de Ciudad Real, Ciudad Real, Spain
c Servicio de Nefrología, Hospital General Universitario de Ciudad Real, Ciudad Real, Spain
d Servicio de Anatomía Patológica, Hospital Universitario 12 de Octubre, Madrid, Spain
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On examination&#44; blood pressure 170&#47;100&#8239;mmHg&#44; sinus rhythm&#44; crackles in both lung bases and edema&#46; Hemogram and blood chemistry&#58; normocytic normochromic anemia&#44; without microangiopathic hemolytic anemia &#40;MHA&#41;&#44; creatinine 6&#8239;mg&#47;dl&#44; nephrotic proteinuria with normal serum albumin and microhematuria&#46; Chest X-ray&#58; bilateral interstitial infiltrate&#44; with diagnosis of pulmonary hemorrhage with immunological study with ANCAp positive 1&#47;320&#44; rest normal&#47;negative&#44; including anti-glomerular basement membrane antibodies&#46; Plasmapheresis&#44; corticosteroids and intravenous cyclophosphamide were started&#46; One week after admission&#44; MHA with smear showing schistocytes and undetectable haptoglobin&#44; with negative stool culture&#44; normal ADAMTS13&#44; we decided to start eculizumab treatment&#44; with normal genetic follow-up Renal biopsy&#58; 49 glomeruli&#44; 10 sclerosed&#44; 29 with epithelial crescents&#44; some with segmental necrosis&#44; PAS and Jones silver positive&#46; No signs of TMA&#46; Direct immunofluorescence was strongly positive for IgG with linear pattern&#44; kappa and lambda positive&#44; weak C3 with parietal and mesangial granular pattern&#44; IgG4 positive &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0015" class="elsevierStylePara elsevierViewall">At hospital discharge&#44; the patient presented remission of pulmonary hemorrhage and resolution of MHA&#44; creatinine of 3&#46;8&#8239;mg&#47;dl&#44; proteinuria and microhematuria&#44; and continued treatment with cyclophosphamide&#44; corticosteroids and eculizumab up to 2 months after resolution of MHA&#46; Thirty days after discontinuation of eculizumab&#44; she presented a new episode of probable TMA and the ME result was received&#58; dense deposits&#44; in glomerular basement membrane &#40;GBM&#41; and mesangium&#44; consisting of random fibrils&#44; with an average thickness of 18&#46;41&#8239;nm&#44; compatible with fibrillary glomerulopathy&#44; with linear IgG deposits &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; DNAJB9 testing by immunohistochemistry was positive&#44; and we restarted eculizumab&#44; with suspicion of secondary TMA&#46; After 6 months of cyclophosphamide&#44; we maintained treatment with azathioprine&#46; For 2&#46;5 months&#44; she presented clinical and renal function stability&#44; with no MHA data&#59; treatment with eculizumab was maintained for 3 months and subsequently renal function improved with no MHA data&#46; Three months after discontinuation&#44; the patient presented deterioration of renal function&#44; and eculizumab was reinitiated until her inclusion in chronic treatment with peritoneal dialysis&#44; 9 months later &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#41;&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">Fibrillary glomerulonephritis rarely presents as it did in this case&#44; with acute renal failure and pulmonary hemorrhage&#46; Different authors suggest the possibility of a circulating factor in GF&#44; which may be responsible for the existence of fibrillar material at pulmonary level&#44; triggering pulmonary hemorrhage&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> For the diagnosis of FGN&#44; EM is necessary&#44; or DNAJB9 by immunohistochemistry if EM is not available&#46; In our case&#44; despite diagnosis made by EM&#44; we tested for DNAJB9 with a positive result&#46;<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">7&#8211;9</span></a> The linear&#47;pseudolinear IgG deposits described in FGN and in our patient resembles a GBM antibody disease&#44; which makes us rule out FGN when present or suggest coexistence&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;2</span></a> The presence of RPG and TMA is rare&#44; but may occur in FGN&#44; 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ISSN: 20132514
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