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"https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2013251421001097?idApp=UINPBA000064" "url" => "/20132514/0000004100000005/v1_202112230647/S2013251421001097/v1_202112230647/en/main.assets" ] "en" => array:15 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Letter to the Editor</span>" "titulo" => "C3 glomerulonephritis accompanied with lupus nephritis" "tieneTextoCompleto" => true "saludo" => "Dear Editor:" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "595" "paginaFinal" => "597" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "Kubra Kaynar, Beyhan Güvercin, Sahile Safarlı, Sevdegül Mungan, Mustafa Şahin" "autores" => array:5 [ 0 => 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" ] ] ] 1 => array:3 [ "nombre" => "Beyhan" "apellidos" => "Güvercin" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 2 => array:3 [ "nombre" => "Sahile" "apellidos" => "Safarlı" "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" => "Mustafa" "apellidos" => "Şahin" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] ] "afiliaciones" => array:3 [ 0 => array:3 [ "entidad" => "Department of Nephrology, School of Medicine, Karadeniz Technical University, Trabzon, Turkey" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Department of Internal MedicineSchool of Medicine, Karadeniz Technical University, Trabzon, Turkey" "etiqueta" => "b" "identificador" => "aff0010" ] 2 => array:3 [ "entidad" => "Department of Pathology, School of Medicine, Karadeniz Technical University, Trabzon, Turkey" "etiqueta" => "c" "identificador" => "aff0015" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Lomerulonefritis C3 acompañada de nefritis lúpica" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 678 "Ancho" => 900 "Tamanyo" => 139066 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Renal biopsy which shows diffuse global basal membrane thickening, lymphocyte dominant tubulointerstitial inflammation, increased fibrosis, and tubular atrophy by light microscopy, H.E. 400×.</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Complement 3 (C3) glomerulopathy is diagnosed when C3 dominant glomerulonephritis is seen in kidney biopsy with C3 only deposition without immunoglobulin (Ig), or dominant C3 with up to 1<span class="elsevierStyleHsp" style=""></span>+<span class="elsevierStyleHsp" style=""></span>IgM, or dominant C3 of +2 orders of magnitude of intensity by immunoflourescent (IF) greater than any other immune reactant (using a scale of 0 to 3, including 0, trace, 1+, 2+, 3+).<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> Systemic lupus erythematosus (SLE) lead to renal damage through immune deposition such as IgG, IgA, IgM, C3, and C1q, with IgG dominance or codominance in a specific pattern known as full-house.<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">A 49 year old male patient applied to our clinic due to high serum creatinine levels noticed at dermatology department during examination for discoid rash. He was well until his skin eruptions have erosen one month ago. Hydroxychloroquine and topical corticosteroid were prescribed to him for cutaneous lupus erythematosus diagnosed by skin biopsy. His blood pressure was 120/80<span class="elsevierStyleHsp" style=""></span>mmHg. Trace pretibial edema and hypopigmented lesions on forearms were detected. Biochemically, his serum creatinine (Cr) level was 1.28<span class="elsevierStyleHsp" style=""></span>mg/dL, estimated glomerular filtration rate (eGFR) Chronic Kidney Disease Epidemiology Collaboration equation (CKD–EPI-cre based): 66<span class="elsevierStyleHsp" style=""></span>mL/min/1.73<span class="elsevierStyleHsp" style=""></span>m<span class="elsevierStyleSup">2</span>, serum albumin level was 3.6<span class="elsevierStyleHsp" style=""></span>g/dL, proteinuria was 660<span class="elsevierStyleHsp" style=""></span>mg/day, his urine sediment was inactive at admission. Kidneys were ultrasonographically normal in size and echogenicity. Double-checked result of proteinuria level was 1.87<span class="elsevierStyleHsp" style=""></span>g/day, complement 3 (C3) and complement 4 (C4) levels were normal (104<span class="elsevierStyleHsp" style=""></span>mg/dL, normal range<span class="elsevierStyleHsp" style=""></span>=<span class="elsevierStyleHsp" style=""></span>90–180; and 16<span class="elsevierStyleHsp" style=""></span>mg/dL, normal range<span class="elsevierStyleHsp" style=""></span>=<span class="elsevierStyleHsp" style=""></span>10–40 respectively), antinuclear antibody (ANA) was detected positive at 1/1000–1/3200 titration by IFA (immunofluorescence assay), anti-double-stranded deoxyribonucleic acid (anti-dsDNA) antibody level was found as 176.2<span class="elsevierStyleHsp" style=""></span>IU/mL (negative titration<span class="elsevierStyleHsp" style=""></span>=<span class="elsevierStyleHsp" style=""></span><100<span class="elsevierStyleHsp" style=""></span>IU/mL) by IFA, presence of perinuclear (myeloperoxidase) anti-neutrophil cytoplasmic antibodies (ANCA) was observed by IFA with a serum titration between 1/32 and 1/100 together with positive anti-SS-A, anti-Smith (anti-Sm), anti-histone, and anti-nucleosome antibodies tested by immunoblot analysis.</p><p id="par0015" class="elsevierStylePara elsevierViewall">Renal biopsy revealed membranoproliferative glomerulonephritis with diffuse glomerular basal membrane thickening and global mesangial matrix expansion by light microscopy (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>). Six of the 17 glomeruli were globally sclerotic. No cellular/fibrous crescent and necrosis was noticed. Direct immunofluorescence microscopy displayed granular full-house staining with predominant intense C3 staining (severity degree of +3) (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>), followed by C1q (mild staining), and IgG (mild staining), in addition to lambda (moderate staining), kappa (mild staining) and fibrin (severe staining). C4d staining showed presence of C4d deposition. Autoantibody test results and findings of skin biopsy made us thought lupus nephritis at first. However kidney biopsy revealed findings associated with both lupus nephritis class IV-G (A/C) and C3 dominant glomerulopathy. The dominant C3 deposition made it necessary to research molecular genetic complement disorders.<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">3,4</span></a> In our patient, further examinations in order to enlighten C3 glomerulopathy, yielded homozygous p.His402Tyr mutation due to c.1204C>T change in the complement factor H (CFH) gene and homozygous p.Val306fs mutation due to c.914_915insA insertion in the complement 3 (C3) gene and heterozygous p.Lys565Glu mutation due to c.1693A<span class="elsevierStyleHsp" style=""></span>g/day. Methylprednisolone and mycophenolate mofetil were given to the patient because he developed hypersensitivity to cyclophosphamide. Proteinuria level decreased to 2.56<span class="elsevierStyleHsp" style=""></span>g/day, serum creatinine level decreased to 1<span class="elsevierStyleHsp" style=""></span>mg/dL, and serum albumin level increased to 3.9<span class="elsevierStyleHsp" style=""></span>g/dL after 1 year of follow-up.</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">Our patient was diagnosed as SLE by fulfillment of either the 1997 American Collage of Rheumatology (ACR) criteria and by the 2012 Systemic Lupus International Collaborating Clinics (SLICC) criteria.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">5</span></a> The signature of lupus nephritis in renal pathology is polyclonal staining of IgG, IgA, IgM, C3 and C1q with dominant or codominant IgG.<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> There was no dominant IgG deposits, even no uniform involvement of IgG and C3 deposits in our case.<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">6</span></a> Instead, C3 dominance fulfilled the criterion necessary to diagnose C3 glomerulopathy defined by consensus report of International Society of Nephrology.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> Dysregulation of complement system due to mutations or antibodies lead to C3 glomerulopathy. Only ≅25% of cases diagnosed as C3 glomerulopathy were reported to have genetic mutations in genes of C3 (encoding complement factor 3), CFB (encoding complement factor B), CFH (encoding complement factor H, the regulatory protein of compleman activation), CFI (encoding complement factor I, inactivator of C3b), and CFHR5 (encoding complement factor H-related protein 5, enhancer of complement activation).<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> The c.1204c>T; p.His402Tyr variant in the CFH gene has been reported to be highly associated with dense deposit disease and favorable outcomes in age-related macular degeneration.<a class="elsevierStyleCrossRefs" href="#bib0090"><span class="elsevierStyleSup">8,9</span></a> This variant of CFH put our patient at an increased risk for liability to complement-mediated diseases which emerge in adulthood. The second variant in genetic sequence of complement factor B gene was probably pathogenic for complement mediated disorders like thrombotic microangiopathy as reported previously.<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a> It remains to be determined whether the third genetical variant in complement 3 gene is capable of causing complement mediated disease. The data about mutation in the complement factor B gene of our patient and its clinical importance for enhanced formation and delay in inactivation of C3bBb convertase needs to be searched.</p><p id="par0025" class="elsevierStylePara elsevierViewall">In conclusion, as far as we know this is the first case showing the togetherness of C3 glomerulopathy and lupus nephritis. After one year of treatment with methylprednisolone and mycophenolate mofetil, renal improvement was achieved. Further studies will enlighten the best therapeutic approach for this new entity in the future.</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Authorship contributions</span><p id="par0030" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Concept</span>: Kubra Kaynar. <span class="elsevierStyleItalic">Design</span>: Kubra Kaynar, Beyhan Güvercin. <span class="elsevierStyleItalic">Control</span>: Kubra Kaynar, Beyhan Güvercin, Sahile Safarlı, Sevdegül Mungan, Mustafa Şahin. <span class="elsevierStyleItalic">Data Collection</span>: Sahile Safarlı, Sevdegül Mungan, Mustafa Şahin. <span class="elsevierStyleItalic">Literature review</span>: Kubra Kaynar. <span class="elsevierStyleItalic">Writing the manuscript</span>: Kubra Kaynar.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Compliance with ethical standards</span><p id="par0035" class="elsevierStylePara elsevierViewall">All authors declare that there are no conflicts of interests related to the study and no fund was taken. Informed consent was obtained from patient.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:3 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Authorship contributions" ] 1 => array:2 [ "identificador" => "sec0010" "titulo" => "Compliance with ethical standards" ] 2 => 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" => 678 "Ancho" => 900 "Tamanyo" => 139066 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Renal biopsy which shows diffuse global basal membrane thickening, lymphocyte dominant tubulointerstitial inflammation, increased fibrosis, and tubular atrophy by light microscopy, H.E. 400×.</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" => 678 "Ancho" => 900 "Tamanyo" => 45193 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Renal biopsy which shows peripheral and mesangial granular pattern severe (+3) C3 deposition in glomerulus by immunoflourescence microscopy, 400×.</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" => "C3 glomerulopathy: consensus report" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "M.C. 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Year/Month | Html | Total | |
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2024 November | 12 | 10 | 22 |
2024 October | 98 | 64 | 162 |
2024 September | 107 | 44 | 151 |
2024 August | 97 | 67 | 164 |
2024 July | 105 | 50 | 155 |
2024 June | 95 | 55 | 150 |
2024 May | 107 | 66 | 173 |
2024 April | 84 | 56 | 140 |
2024 March | 91 | 33 | 124 |
2024 February | 75 | 35 | 110 |
2024 January | 60 | 28 | 88 |
2023 December | 65 | 33 | 98 |
2023 November | 75 | 45 | 120 |
2023 October | 145 | 32 | 177 |
2023 September | 322 | 48 | 370 |
2023 August | 413 | 27 | 440 |
2023 July | 430 | 36 | 466 |
2023 June | 192 | 32 | 224 |
2023 May | 114 | 38 | 152 |
2023 April | 83 | 21 | 104 |
2023 March | 67 | 33 | 100 |
2023 February | 63 | 33 | 96 |
2023 January | 66 | 53 | 119 |
2022 December | 86 | 35 | 121 |
2022 November | 83 | 45 | 128 |
2022 October | 115 | 57 | 172 |
2022 September | 97 | 48 | 145 |
2022 August | 106 | 42 | 148 |
2022 July | 98 | 51 | 149 |
2022 June | 61 | 47 | 108 |
2022 May | 93 | 38 | 131 |
2022 April | 65 | 46 | 111 |
2022 March | 62 | 51 | 113 |
2022 February | 34 | 45 | 79 |
2022 January | 55 | 57 | 112 |
2021 December | 26 | 21 | 47 |