Letter to the Editor
Lupus Nephritis Associated With Cytoplasmic Anti-neutrophil Cytoplasmic Antibodies
Nefritis lúpica asociada con c-ANCA
Marco Tobar-Marcilloa,b,
, Israel Destruge-Molinaa,b, Luis Torres-Orozcoc, Ricardo Santiago-Ramirezd
Corresponding author
a Universidad Nacional Autónoma de México, Mexico City, Mexico
b Departamento de Medicina interna, Hospital Regional Licenciado Adolfo López Mateos, Mexico City, Mexico
c Departamento de Nefrología, Hospital Regional Licenciado Adolfo López Mateos, Mexico City, Mexico
d Departamento de Reumatología, Hospital Regional Licenciado Adolfo López Mateos, Mexico City, Mexico
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A) Coloración de hematoxilina eosina 40×; se observa patrón membranoproliferativo con imagen de doble contorno (flecha roja), formación de semilunas (flechas negras). B) Coloración tricrómica de Masson 10×; se observa nefritis tubulointersticial con infiltrado mononuclear (flechas rojas), fibrosis intersticial (flecha negra). C) Coloración tricrómica de Masson 40×; con presencia de trombos y necrosis fibrinoide en asas capilares (flechas negras), fibrosis glomerular segmentaria (flecha roja). 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(A) Hematoxylin–eosin staining 40×; observe the membranoproliferative pattern with an image showing double contour (red arrow), formation of crescents (black arrows). (B) Masson trichrome staining 10×; observe tubulointerstitial nephritis with mononuclear infiltrate (red arrows) and interstitial fibrosis (black arrow). (C) Masson trichrome staining 40×; with presence of thrombi and fibrinoid necrosis in capillary loops (black arrows), segmental glomerular fibrosis (red arrow). (D) Immunofluorescence 40×; positive for immunoglobulin G with a focal granular pattern and only a few segments of capillary loops (red arrows).</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Systemic lupus erythematosus (SLE) and the vasculitides associated with antineutrophil cytoplasmic antibodies (ANCA) are well-differentiated diseases; although approximately a third of the patients with SLE are ANCA-positive,<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">1</span></a> this is rarely associated with vasculitis. The presence of ANCA in patients with SLE seems to predispose them to lupus nephritis (LN), low levels of complement C3 and a higher rate of complications.<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">We present the case of a 55-year-old man from Mexico City, who presented with a 5-month history of arthralgia in shoulders, wrists and ankles, that was bilateral and symmetrical; moreover, he had episodes of recurrent sinusitis, weight loss and edema arising from the lower limbs; there were no lesions affecting the skin. In the initial examination he underwent urinalysis which showed proteinuria of 200<span class="elsevierStyleHsp" style=""></span>mg/dL, innumerable erythrocytes, leukocytes 20 to 25 per field, red blood cell and leukocyte casts; creatinine: 1.66<span class="elsevierStyleHsp" style=""></span>mg/dL (reference range 0.6–1.3<span class="elsevierStyleHsp" style=""></span>mg/dL). Blood tests revealed hemoglobin concentration of 9.1<span class="elsevierStyleHsp" style=""></span>g/dL (reference range 13–17<span class="elsevierStyleHsp" style=""></span>g/dL), normocytic and normochromic; the remaining cell lines were normal; erythrocyte sedimentation rate (ESR): 55<span class="elsevierStyleHsp" style=""></span>mm/h (reference range 0–15<span class="elsevierStyleHsp" style=""></span>mm/h); C-reactive protein (CRP): 6.24<span class="elsevierStyleHsp" style=""></span>mg/dL (reference range 0–3<span class="elsevierStyleHsp" style=""></span>mg/dL). Immunological profile with a 1:160 titer of antinuclear antibodies (ANA), which had a homogeneous/fine speckled pattern by immunofluorescence and 78.0<span class="elsevierStyleHsp" style=""></span>IU/mL in enzyme-linked immunosorbent assay (ELISA) (reference range for high positive >60<span class="elsevierStyleHsp" style=""></span>IU/mL), anti-double stranded DNA (anti-ds DNA) by chemiluminescence: 1.4<span class="elsevierStyleHsp" style=""></span>IU/mL (reference range for negative <20<span class="elsevierStyleHsp" style=""></span>IU/mL), antiproteinase 3 (cytoplasmic [c-ANCA]) positive with titers reaching 1:320, granular pattern by immunofluorescence and higher than 100<span class="elsevierStyleHsp" style=""></span>IU/mL by ELISA (reference range 0–3.5<span class="elsevierStyleHsp" style=""></span>IU/mL), myeloperoxidase (perinuclear [p-ANCA]) were negative using the same technique, complement C3 was 71.7<span class="elsevierStyleHsp" style=""></span>mg/dL (reference range 90–180<span class="elsevierStyleHsp" style=""></span>mg/dL) and complement C4 was 17.6<span class="elsevierStyleHsp" style=""></span>mg/dL (reference range 10–40<span class="elsevierStyleHsp" style=""></span>mg/dL); human immunodeficiency virus (HIV) antibodies, cryoglobulins and hepatitis B and C negative; subsequently, 24<span class="elsevierStyleHsp" style=""></span>h urine was collected and revealed a proteinuria of 1.77<span class="elsevierStyleHsp" style=""></span>g.</p><p id="par0015" class="elsevierStylePara elsevierViewall">Given the presence of data compatible with nephritic syndrome, the patient underwent renal biopsy. The result was membranoproliferative and active diffuse extracapillary glomerulonephritis (crescents 80%) due to immune complexes, interstitial fibrosis, tubulointerstitial nephritis with mononuclear infiltrate, with no evidence of vasculitis; direct immunofluorescence with deposits of immunoglobulin G (IgG), immunoglobulin A (IgA), immunoglobulin M (IgM), complement C1q, complement C3 with a focal granular pattern (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>). With these data associated with the clinical presentation, the diagnosis was LN class IV-S (A), with an activity score of 18 and chronicity of 7.</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">Treatment was begun with 1<span class="elsevierStyleHsp" style=""></span>g intravenous cyclophosphamide every 30 days for a total of 6 doses, 1<span class="elsevierStyleHsp" style=""></span>g intravenous methylprednisolone every 24<span class="elsevierStyleHsp" style=""></span>h the first 3 days, followed by 60<span class="elsevierStyleHsp" style=""></span>mg of oral prednisone every 24<span class="elsevierStyleHsp" style=""></span>h for 4 weeks, 24-hour monitoring of proteinuria 1 month after treatment of 870<span class="elsevierStyleHsp" style=""></span>mg, creatinine of 1.54<span class="elsevierStyleHsp" style=""></span>mg/dL, at which time a trend toward a partial response was established.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">3</span></a> The patient continued with cyclophosphamide and steroids were tapered. During follow-up, there was an increase in proteinuria, persistence of dysmorphic erythrocytes at 0–5 per field, monitoring of positive c-ANCA at a titer of 1:160 in immunofluorescence, aside from a reduction in the glomerular filtration rate, with an increase >1<span class="elsevierStyleHsp" style=""></span>mg/dL in creatinine, leading to renal relapse.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">3</span></a><a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a> summarizes the 6-month follow-up. In line with the diagnosis of LN, given the symptoms of chronic sinusitis and positive c-ANCA, we studied a possible associated vasculitis. We performed computed tomography of the paranasal sinuses 20 days after the initiation of treatment (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>), which revealed swelling of the nasal mucosa, with slight bone erosion in left maxillary antral wall and turbinates justified by the chronic sinusitis process; chest radiograph was normal (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>C), and a biopsy of the nasal mucosa showed the absence of granulomas or other data suggesting a process of vasculitis.</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0025" class="elsevierStylePara elsevierViewall">This case corresponds to LN with failure of the first line of treatment, associated with high titers of positive c-ANCA, with no evidence of solid elements enabling the parallel diagnosis of vasculitis. A number of authors have observed that SLE patients can present these antibodies; that is the case of Galeazzi et al.,<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">4</span></a> who evaluated 566 patients with SLE in 11 European centers, presenting a prevalence of 16.4% (15.4% with p-ANCA and 1% with c-ANCA) in individuals in whom that relationship was detected; other reports demonstrate a highly variable relationship with prevalence of up to 37.3%,<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">5,6</span></a> predominantly with p-ANCA positivity.</p><p id="par0030" class="elsevierStylePara elsevierViewall">We recommend that all the patients with LN should undergo an intentional search for ANCA, because they have a higher positivity rate than SLE patients with no renal involvement; Pradhan et al.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">7</span></a> recorded a prevalence of 54.5%, and all of these individuals were positive for p-ANCA; subsequently, Pan et al.<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">2</span></a> evaluated 60 patients with a diagnosis of SLE, 28 of them with LN, observing a prevalence of ANCA of 53.6% and concluding that said association was related to higher activity and a poorer prognosis. Nasr et al.<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">8</span></a> reported 10 patients with LN associated with the presence of ANCA and described the histopathological features of the renal biopsy. It revealed a greater formation of crescents in our patient, involving 80% of the glomeruli, and areas of necrosis were also demonstrated by the histopathological study (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>). This suggests that their presence precipitated those findings, although the role they play in the pathophysiology of LN has not been made clear.</p><p id="par0035" class="elsevierStylePara elsevierViewall">With regard to treatment, the population with LN and ANCA-positivity should undergo follow-up studies of the scheme for the induction of conventional remission; given the failure of complete remission with first-line treatment in our patient, an alternative strategy should be proposed for initial treatment for patients of this type.</p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Tobar-Marcillo M, Destruge-Molina I, Torres-Orozco L, Santiago-Ramirez R. Nefritis lúpica asociada con c-ANCA. Reumatol Clin. 2018;14:246–248.</p>" ] ] "multimedia" => array:3 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1914 "Ancho" => 2500 "Tamanyo" => 695588 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Renal biopsy. (A) Hematoxylin–eosin staining 40×; observe the membranoproliferative pattern with an image showing double contour (red arrow), formation of crescents (black arrows). (B) Masson trichrome staining 10×; observe tubulointerstitial nephritis with mononuclear infiltrate (red arrows) and interstitial fibrosis (black arrow). (C) Masson trichrome staining 40×; with presence of thrombi and fibrinoid necrosis in capillary loops (black arrows), segmental glomerular fibrosis (red arrow). (D) Immunofluorescence 40×; positive for immunoglobulin G with a focal granular pattern and only a few segments of capillary loops (red arrows).</p>" ] ] 1 => array:7 [ "identificador" => "fig0010" "etiqueta" => "Fig. 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 836 "Ancho" => 2500 "Tamanyo" => 147368 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">(A and B) Computed tomography images of paranasal sinuses in simple phase: axial scan (A), coronal scan (B), swollen nasal mucosa, slight bone erosion involving left maxillary antral wall (red arrow) and inferior turbinates. (C) Normal posteroanterior chest radiograph; no lesions on lung parenchyma.</p>" ] ] 2 => array:8 [ "identificador" => "tbl0005" "etiqueta" => "Table 1" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at1" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:2 [ "leyenda" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">C-ANCA, cytoplasmic antineutrophil cytoplasmic antibodies.</p>" "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="table-head " align="" valign="top" scope="col" style="border-bottom: 2px solid black"> \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Diagnosis \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">First month \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Third month \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Sixth month \t\t\t\t\t\t\n \t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">24-Hour proteinuria (mg) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">1770 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">870 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">4055 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">2967 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Serum creatinine (mg/dL) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">1.66 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">1.54 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">2.57 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">2.48 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">C-ANCA by immunofluorescence \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">1:320 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="" valign="top"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">1:160 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="" valign="top"> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Complement C3 (90–180) (mg/dL) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">71.7 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">85.6 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">73.2 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">106.0 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Complement C4 (10–40) (mg/dL) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">17.6 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">26.8 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">18.4 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">28.2 \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab1823877.png" ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Changes in 24-hour Proteinuria, Serum Creatinine, Cytoplasmic Antineutrophil Cytoplasmic Antibodies and Complement Over a 6-month Follow-up Period.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:8 [ 0 => array:3 [ "identificador" => "bib0045" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Clinical implications of antineutrophil cytoplasmic antibody test in lupus nephritis" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "H. 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