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Pauci-immune necrotizing glomerulonephritis in a patient with ankylosing spondylitis
Glomerulonefritis necrotizante pauciinmune en un paciente con espondilitis anquilosante
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AMR: antibody mediated rejection; CAMR: chronic active antibody mediated rejection; Cya: ciclosporin; MFM: mycophenolate mofetil; Cg: transplant glomerulopathy; Ci: interstitial fibrosis; Ct; tubular atrophy; iIFTA: inflammation in areas of interstitial fibrosis/tubular atrophy.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Lina M. León Machado, María O. Lopéz Oliva, Yanieli H. Hernandez Perdomo, Tamara Peréz, Elena González Garcia, Rafael Selgas Gutierrez, Carlos Jiménez Martín" "autores" => array:7 [ 0 => array:2 [ "nombre" => "Lina M." "apellidos" => "León Machado" ] 1 => array:2 [ "nombre" => "María O." "apellidos" => "Lopéz Oliva" ] 2 => array:2 [ "nombre" => "Yanieli H." 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patient with ankylosing spondylitis" "tieneTextoCompleto" => true "saludo" => "Dear Editor:" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "496" "paginaFinal" => "498" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "Beyhan Güvercin, Kubra Kaynar, Hasibe Bilge Gür, Sevdegül Mungan, Emre Selim, Muammer Cansız, Şükrü Ulusoy" "autores" => array:7 [ 0 => array:3 [ "nombre" => "Beyhan" "apellidos" => "Güvercin" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 1 => array:4 [ "nombre" => "Kubra" "apellidos" => "Kaynar" "email" => array:1 [ 0 => "kkaynar@yahoo.com" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "cor0005" ] ] ] 2 => array:3 [ "nombre" => "Hasibe Bilge" "apellidos" => "Gür" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] 3 => array:3 [ "nombre" => "Sevdegül" "apellidos" => "Mungan" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">c</span>" "identificador" => "aff0015" ] ] ] 4 => array:3 [ "nombre" => "Emre" "apellidos" => "Selim" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] 5 => array:3 [ "nombre" => "Muammer" "apellidos" => "Cansız" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 6 => array:3 [ "nombre" => "Şükrü" "apellidos" => "Ulusoy" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] ] "afiliaciones" => array:3 [ 0 => array:3 [ "entidad" => "Faculty of Medicine, Department of Nephrology, Trabzon 61080, Turkey" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Faculty of Medicine, Department of Internal Medicine, Trabzon 61080, Turkey" "etiqueta" => "b" "identificador" => "aff0010" ] 2 => array:3 [ "entidad" => "Faculty of Medicine, Department of Pathology, Trabzon 61080, Turkey" "etiqueta" => "c" "identificador" => "aff0015" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "<span class="elsevierStyleItalic">Corresponding author</span>." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Glomerulonefritis necrotizante pauciinmune en un paciente con espondilitis anquilosante" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0010" "etiqueta" => "Fig. 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 683 "Ancho" => 905 "Tamanyo" => 180386 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Renal biopsy showing diffuse tubulointerstitial inflammation and extensive necrosis destructing the normal structure of the tubuli and glomeruli on light microscopy (hematoxylin–eosin staining, original magnification 200×).</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Ankylosing spondylitis (AS) is an autoimmune disease that emerged from the interaction of genetic tendency and environmental risk factors.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> Patients with AS are mostly diagnosed at the end of their third decade of life after approximately 10 years of insidious course.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> Membranous glomerulopathy secondary to etanercept therapy, immunoglobulin A (Ig A) nephropathy, and renal amyloidosis were reported as kidney diseases associated with AS.<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2–4</span></a> Anti-neutrophil cytoplasmic antibody (ANCA)-negative pauci-immune necrotizing glomerulonephritis (PING) is also one of the auto-immune diseases.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">5</span></a> The association of PING with AS has not been reported. Herein, we report for the first time the development of ANCA-negative PING accompanied by pulmonary hemorrhage in a patient with AS.</p><p id="par0010" class="elsevierStylePara elsevierViewall">A 39-year-old male patient was diagnosed as having AS on the basis of bilateral grade 2 sacroileitis (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>) and inflammatory low back pain that had woken him up at nights for 1 year.<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">6</span></a> He had been treated with sulfasalazine 1<span class="elsevierStyleHsp" style=""></span>g twice daily and acemetacin 120<span class="elsevierStyleHsp" style=""></span>mg/d for 1 year, and methotrexate 15<span class="elsevierStyleHsp" style=""></span>mg once weekly, methylprednisolone 32<span class="elsevierStyleHsp" style=""></span>mg/d and colchicine 0.5<span class="elsevierStyleHsp" style=""></span>mg/d for 2 months in another hospital. Some of the patient's symptoms including swelling and pain of the fingers (dactylitis), and buttocks pain, did not resolve with this management. After the first year of follow-up, a skin lesion biopsy was performed for the leukocytoclastic vasculitis that appeared on his left lower leg. By that time his serum creatinine levels had increased to 4.0<span class="elsevierStyleHsp" style=""></span>mg/dL from the basal levels of 0.77<span class="elsevierStyleHsp" style=""></span>mg/dL in a period of 1 month. He was hospitalized at our department because of the rapid increase in his serum creatinine level and nephrotic range proteinuria (3.9<span class="elsevierStyleHsp" style=""></span>g/d) with urinary dysmorphic erythrocytes. His serum complement 3 (C3) and 4 (C4) levels were normal (0.94<span class="elsevierStyleHsp" style=""></span>g/L; normal range, 0.9–1.8; and 0.2<span class="elsevierStyleHsp" style=""></span>g/L; normal range, 0.1–0.4, respectively), and no antinuclear antibody, anti-double-stranded deoxyribonucleic acid antibody, ANCA, anti-SS-A, anti-Smith (anti-Sm), anti-histone, and anti-nucleosome antibodies were found. Renal biopsy revealed PING, as evidenced by 8% of glomeruli having cellular crescents without immune deposition, 26% of glomeruli having fibrinoid necrosis, fibrosis, and edema in 80% of the interstitium, and subintimal fibrosis in middle-sized vessels (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>). As soon as the renal biopsy results were released, the patient received pulse (high-dose intravenous [i.v.]) methylprednisone 12.5<span class="elsevierStyleHsp" style=""></span>mg/kg/d for 3 days.<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> The rest of the previous medications were stopped. Meanwhile, oliguria, uremic symptoms with hypervolemia, and hemoptysis due to pulmonary hemorrhage developed, and hemodialysis and plasma exchange with albumin replacement were initiated via temporary jugular venous catheter. Subsequently, daily oral methylprednisone 1<span class="elsevierStyleHsp" style=""></span>mg/kg/d with three doses of i.v. cyclophosphamide 0.5<span class="elsevierStyleHsp" style=""></span>g/m<span class="elsevierStyleSup">2</span> every 2 weeks were administered to the patient. However, pulmonary hemorrhage relapsed 4 weeks after initiation of the treatment, so rituximab (i.v. 375<span class="elsevierStyleHsp" style=""></span>mg/m<span class="elsevierStyleSup">2</span>) four times weekly were prescribed to the patient. Renal recovery without the need for hemodialysis was observed nearly 2 months after the start of cyclophosphamide treatment and on the third week of rituximab therapy. Azathioprine, methylprednisolone, spironolactone, nifedipine, nebivolol, furosemide, pantoprazole, and calcitriol with calcium carbonate were prescribed. The patient is currently followed up in the nephrology outpatient clinic (without dialysis and pulmonary hemorrhage), with a serum creatinine level of 1.7<span class="elsevierStyleHsp" style=""></span>mg/dL, serum albumin level of 3.6<span class="elsevierStyleHsp" style=""></span>g/dL, and proteinuria of 1<span class="elsevierStyleHsp" style=""></span>g/d.</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0015" class="elsevierStylePara elsevierViewall">One of the well-known etiologies of rapidly progressive glomerulonephritis is PING. ANCA plays a major role in the pathogenesis of PING. However, 10% of PING cases have been reported to occur without ANCA, similar to our case.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">8</span></a> The activation mechanism of the neutrophils that are the primary responsible immune cells in the development of ANCA-negative PING has not been clarified yet.<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a> More severe complement and neutrophil activation and thus greater renal damage were found in ANCA-negative PING cases than in ANCA-positive ones.<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a> The main pathogenetic mechanism of AS is impaired regulation of interleukin-17 production and genetic mutations involving antigen presentation.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> As knowledge is lacking about the common pathogenic mechanism that leads to both PING and AS, this coexistence may be coincidental. In spite of the worse renal prognosis of patients with ANCA-negative PING, our patient recovered after 2 months of dialysis-dependent renal failure. Renal involvement was reported to be found in 21.7% of cases with AS.<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a> The renal pathologies (tubulointerstitial nephritis, IgA nephropathy, nonsteroidal anti-inflammatory drug-induced nephropathy, and amyloidosis) associated with AS were not found in our case. The renal pathology of the present case was PING. This case is important because of the rarity of cases with PING without ANCA, and the present case is the first to show the association of PING with AS.</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Funding</span><p id="par0020" class="elsevierStylePara elsevierViewall">No funding was obtained for this article</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Inform consent</span><p id="par0030" class="elsevierStylePara elsevierViewall">Written informed consent for publication of this case report was obtained from the patient</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">Conflict of interest</span><p id="par0040" class="elsevierStylePara elsevierViewall">The authors declare no conflict of interest regarding the publication of this article.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:4 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Funding" ] 1 => array:2 [ "identificador" => "sec0010" "titulo" => "Inform consent" ] 2 => array:2 [ "identificador" => "sec0015" "titulo" => "Conflict of interest" ] 3 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "multimedia" => array:2 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1020 "Ancho" => 905 "Tamanyo" => 107557 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Plain (anteroposterior oblique) radiograph of the sacroiliac joint, showing ankylosis, pseudo-widening, and subchondral sclerosis in the right sacroiliac joint (grade 3 sacroiliitis) and subchondral sclerosis pseudo-widening in the left sacroiliac joint (grade 2 sacroiliitis).</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" => 683 "Ancho" => 905 "Tamanyo" => 180386 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Renal biopsy showing diffuse tubulointerstitial inflammation and extensive necrosis destructing the normal structure of the tubuli and glomeruli on light microscopy (hematoxylin–eosin staining, original magnification 200×).</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:10 [ 0 => array:3 [ "identificador" => "bib0055" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Pathogenesis of ankylosing spondylitis – recent advances and future directions" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:5 [ 0 => "V. 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| año/Mes | Html | Total | |
|---|---|---|---|
| 2024 Noviembre | 4 | 8 | 12 |
| 2024 Octubre | 44 | 42 | 86 |
| 2024 Septiembre | 60 | 46 | 106 |
| 2024 Agosto | 65 | 58 | 123 |
| 2024 Julio | 50 | 38 | 88 |
| 2024 Junio | 61 | 50 | 111 |
| 2024 Mayo | 65 | 43 | 108 |
| 2024 Abril | 57 | 43 | 100 |
| 2024 Marzo | 53 | 45 | 98 |
| 2024 Febrero | 52 | 44 | 96 |
| 2024 Enero | 57 | 32 | 89 |
| 2023 Diciembre | 51 | 45 | 96 |
| 2023 Noviembre | 84 | 47 | 131 |
| 2023 Octubre | 173 | 34 | 207 |
| 2023 Septiembre | 309 | 33 | 342 |
| 2023 Agosto | 221 | 28 | 249 |
| 2023 Julio | 86 | 32 | 118 |
| 2023 Junio | 135 | 41 | 176 |
| 2023 Mayo | 124 | 53 | 177 |
| 2023 Abril | 90 | 24 | 114 |
| 2023 Marzo | 81 | 33 | 114 |
| 2023 Febrero | 50 | 28 | 78 |
| 2023 Enero | 62 | 40 | 102 |
| 2022 Diciembre | 66 | 36 | 102 |
| 2022 Noviembre | 69 | 44 | 113 |
| 2022 Octubre | 86 | 58 | 144 |
| 2022 Septiembre | 56 | 51 | 107 |
| 2022 Agosto | 68 | 50 | 118 |
| 2022 Julio | 82 | 74 | 156 |
| 2022 Junio | 64 | 36 | 100 |
| 2022 Mayo | 64 | 24 | 88 |
| 2022 Abril | 87 | 47 | 134 |
| 2022 Marzo | 85 | 33 | 118 |
| 2022 Febrero | 87 | 62 | 149 |
| 2022 Enero | 132 | 32 | 164 |
| 2021 Diciembre | 68 | 34 | 102 |
| 2021 Noviembre | 50 | 29 | 79 |
| 2021 Octubre | 68 | 53 | 121 |
| 2021 Septiembre | 54 | 33 | 87 |
| 2021 Agosto | 51 | 46 | 97 |
| 2021 Julio | 46 | 67 | 113 |
| 2021 Junio | 35 | 30 | 65 |
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