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He was well until his skin eruptions have erosen one month ago&#46; Hydroxychloroquine and topical corticosteroid were prescribed to him for cutaneous lupus erythematosus diagnosed by skin biopsy&#46; His blood pressure was 120&#47;80<span class="elsevierStyleHsp" style=""></span>mmHg&#46; Trace pretibial edema and hypopigmented lesions on forearms were detected&#46; Biochemically&#44; his serum creatinine &#40;Cr&#41; level was 1&#46;28<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; estimated glomerular filtration rate &#40;eGFR&#41; Chronic Kidney Disease Epidemiology Collaboration equation &#40;CKD&#8211;EPI-cre based&#41;&#58; 66<span class="elsevierStyleHsp" style=""></span>mL&#47;min&#47;1&#46;73<span class="elsevierStyleHsp" style=""></span>m<span class="elsevierStyleSup">2</span>&#44; serum albumin level was 3&#46;6<span class="elsevierStyleHsp" style=""></span>g&#47;dL&#44; proteinuria was 660<span class="elsevierStyleHsp" style=""></span>mg&#47;day&#44; his urine sediment was inactive at admission&#46; 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by IFA&#44; presence of perinuclear &#40;myeloperoxidase&#41; anti-neutrophil cytoplasmic antibodies &#40;ANCA&#41; was observed by IFA with a serum titration between 1&#47;32 and 1&#47;100 together with positive anti-SS-A&#44; anti-Smith &#40;anti-Sm&#41;&#44; anti-histone&#44; and anti-nucleosome antibodies tested by immunoblot analysis&#46;</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 &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; Six of the 17 glomeruli were globally sclerotic&#46; No cellular&#47;fibrous crescent and necrosis was noticed&#46; Direct immunofluorescence microscopy displayed granular full-house staining with predominant intense C3 staining &#40;severity degree of &#43;3&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#41;&#44; followed by C1q &#40;mild staining&#41;&#44; and IgG &#40;mild staining&#41;&#44; in addition to lambda &#40;moderate staining&#41;&#44; kappa &#40;mild staining&#41; and fibrin &#40;severe staining&#41;&#46; C4d staining showed presence of C4d deposition&#46; Autoantibody test results and findings of skin biopsy made us thought lupus nephritis at first&#46; However kidney biopsy revealed findings associated with both lupus nephritis class IV-G &#40;A&#47;C&#41; and C3 dominant glomerulopathy&#46; The dominant C3 deposition made it necessary to research molecular genetic complement disorders&#46;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">3&#44;4</span></a> In our patient&#44; further examinations in order to enlighten C3 glomerulopathy&#44; yielded homozygous p&#46;His402Tyr mutation due to c&#46;1204C&#62;T change in the complement factor H &#40;CFH&#41; gene and homozygous p&#46;Val306fs mutation due to c&#46;914&#95;915insA insertion in the complement 3 &#40;C3&#41; gene and heterozygous p&#46;Lys565Glu mutation due to c&#46;1693A<span class="elsevierStyleHsp" style=""></span>g&#47;day&#46; Methylprednisolone and mycophenolate mofetil were given to the patient because he developed hypersensitivity to cyclophosphamide&#46; Proteinuria level decreased to 2&#46;56<span class="elsevierStyleHsp" style=""></span>g&#47;day&#44; serum creatinine level decreased to 1<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; and serum albumin level increased to 3&#46;9<span class="elsevierStyleHsp" style=""></span>g&#47;dL after 1 year of follow-up&#46;</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 &#40;ACR&#41; criteria and by the 2012 Systemic Lupus International Collaborating Clinics &#40;SLICC&#41; criteria&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">5</span></a> The signature of lupus nephritis in renal pathology is polyclonal staining of IgG&#44; IgA&#44; IgM&#44; C3 and C1q with dominant or codominant IgG&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> There was no dominant IgG deposits&#44; even no uniform involvement of IgG and C3 deposits in our case&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">6</span></a> Instead&#44; C3 dominance fulfilled the criterion necessary to diagnose C3 glomerulopathy defined by consensus report of International Society of Nephrology&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> Dysregulation of complement system due to mutations or antibodies lead to C3 glomerulopathy&#46; Only &#8773;25&#37; of cases diagnosed as C3 glomerulopathy were reported to have genetic mutations in genes of C3 &#40;encoding complement factor 3&#41;&#44; CFB &#40;encoding complement factor B&#41;&#44; CFH &#40;encoding complement factor H&#44; the regulatory protein of compleman activation&#41;&#44; CFI &#40;encoding complement factor I&#44; inactivator of C3b&#41;&#44; and CFHR5 &#40;encoding complement factor H-related protein 5&#44; enhancer of complement activation&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> The c&#46;1204c&#62;T&#59; p&#46;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&#46;<a class="elsevierStyleCrossRefs" href="#bib0090"><span class="elsevierStyleSup">8&#44;9</span></a> This variant of CFH put our patient at an increased risk for liability to complement-mediated diseases which emerge in adulthood&#46; The second variant in genetic sequence of complement factor B gene was probably pathogenic for complement mediated disorders like thrombotic microangiopathy as reported previously&#46;<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&#46; 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&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">In conclusion&#44; as far as we know this is the first case showing the togetherness of C3 glomerulopathy and lupus nephritis&#46; After one year of treatment with methylprednisolone and mycophenolate mofetil&#44; renal improvement was achieved&#46; Further studies will enlighten the best therapeutic approach for this new entity in the future&#46;</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>&#58; Kubra Kaynar&#46; <span class="elsevierStyleItalic">Design</span>&#58; Kubra Kaynar&#44; Beyhan G&#252;vercin&#46; <span class="elsevierStyleItalic">Control</span>&#58; Kubra Kaynar&#44; Beyhan G&#252;vercin&#44; Sahile Safarl&#305;&#44; Sevdeg&#252;l Mungan&#44; Mustafa &#350;ahin&#46; <span class="elsevierStyleItalic">Data Collection</span>&#58; Sahile Safarl&#305;&#44; Sevdeg&#252;l Mungan&#44; Mustafa &#350;ahin&#46; <span class="elsevierStyleItalic">Literature review</span>&#58; Kubra Kaynar&#46; <span class="elsevierStyleItalic">Writing the manuscript</span>&#58; Kubra Kaynar&#46;</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&#46; Informed consent was obtained from patient&#46;</p></span></span>"
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Letter to the Editor
C3 glomerulonephritis accompanied with lupus nephritis
Lomerulonefritis C3 acompañada de nefritis lúpica
Kubra Kaynara,
Corresponding author
kkaynar@yahoo.com

Corresponding author.
, Beyhan Güvercina, Sahile Safarlıb, Sevdegül Munganc, Mustafa Şahinb
a Department of Nephrology, School of Medicine, Karadeniz Technical University, Trabzon, Turkey
b Department of Internal MedicineSchool of Medicine, Karadeniz Technical University, Trabzon, Turkey
c Department of Pathology, School of Medicine, Karadeniz Technical University, Trabzon, Turkey
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Complement 3 &#40;C3&#41; glomerulopathy is diagnosed when C3 dominant glomerulonephritis is seen in kidney biopsy with C3 only deposition without immunoglobulin &#40;Ig&#41;&#44; or dominant C3 with up to 1<span class="elsevierStyleHsp" style=""></span>&#43;<span class="elsevierStyleHsp" style=""></span>IgM&#44; or dominant C3 of &#43;2 orders of magnitude of intensity by immunoflourescent &#40;IF&#41; greater than any other immune reactant &#40;using a scale of 0 to 3&#44; including 0&#44; trace&#44; 1&#43;&#44; 2&#43;&#44; 3&#43;&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> Systemic lupus erythematosus &#40;SLE&#41; lead to renal damage through immune deposition such as IgG&#44; IgA&#44; IgM&#44; C3&#44; and C1q&#44; with IgG dominance or codominance in a specific pattern known as full-house&#46;<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&#46; He was well until his skin eruptions have erosen one month ago&#46; Hydroxychloroquine and topical corticosteroid were prescribed to him for cutaneous lupus erythematosus diagnosed by skin biopsy&#46; His blood pressure was 120&#47;80<span class="elsevierStyleHsp" style=""></span>mmHg&#46; Trace pretibial edema and hypopigmented lesions on forearms were detected&#46; Biochemically&#44; his serum creatinine &#40;Cr&#41; level was 1&#46;28<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; estimated glomerular filtration rate &#40;eGFR&#41; Chronic Kidney Disease Epidemiology Collaboration equation &#40;CKD&#8211;EPI-cre based&#41;&#58; 66<span class="elsevierStyleHsp" style=""></span>mL&#47;min&#47;1&#46;73<span class="elsevierStyleHsp" style=""></span>m<span class="elsevierStyleSup">2</span>&#44; serum albumin level was 3&#46;6<span class="elsevierStyleHsp" style=""></span>g&#47;dL&#44; proteinuria was 660<span class="elsevierStyleHsp" style=""></span>mg&#47;day&#44; his urine sediment was inactive at admission&#46; Kidneys were ultrasonographically normal in size and echogenicity&#46; Double-checked result of proteinuria level was 1&#46;87<span class="elsevierStyleHsp" style=""></span>g&#47;day&#44; complement 3 &#40;C3&#41; and complement 4 &#40;C4&#41; levels were normal &#40;104<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; normal range<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>90&#8211;180&#59; and 16<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; normal range<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>10&#8211;40 respectively&#41;&#44; antinuclear antibody &#40;ANA&#41; was detected positive at 1&#47;1000&#8211;1&#47;3200 titration by IFA &#40;immunofluorescence assay&#41;&#44; anti-double-stranded deoxyribonucleic acid &#40;anti-dsDNA&#41; antibody level was found as 176&#46;2<span class="elsevierStyleHsp" style=""></span>IU&#47;mL &#40;negative titration<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>&#60;100<span class="elsevierStyleHsp" style=""></span>IU&#47;mL&#41; by IFA&#44; presence of perinuclear &#40;myeloperoxidase&#41; anti-neutrophil cytoplasmic antibodies &#40;ANCA&#41; was observed by IFA with a serum titration between 1&#47;32 and 1&#47;100 together with positive anti-SS-A&#44; anti-Smith &#40;anti-Sm&#41;&#44; anti-histone&#44; and anti-nucleosome antibodies tested by immunoblot analysis&#46;</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 &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; Six of the 17 glomeruli were globally sclerotic&#46; No cellular&#47;fibrous crescent and necrosis was noticed&#46; Direct immunofluorescence microscopy displayed granular full-house staining with predominant intense C3 staining &#40;severity degree of &#43;3&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#41;&#44; followed by C1q &#40;mild staining&#41;&#44; and IgG &#40;mild staining&#41;&#44; in addition to lambda &#40;moderate staining&#41;&#44; kappa &#40;mild staining&#41; and fibrin &#40;severe staining&#41;&#46; C4d staining showed presence of C4d deposition&#46; Autoantibody test results and findings of skin biopsy made us thought lupus nephritis at first&#46; However kidney biopsy revealed findings associated with both lupus nephritis class IV-G &#40;A&#47;C&#41; and C3 dominant glomerulopathy&#46; The dominant C3 deposition made it necessary to research molecular genetic complement disorders&#46;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">3&#44;4</span></a> In our patient&#44; further examinations in order to enlighten C3 glomerulopathy&#44; yielded homozygous p&#46;His402Tyr mutation due to c&#46;1204C&#62;T change in the complement factor H &#40;CFH&#41; gene and homozygous p&#46;Val306fs mutation due to c&#46;914&#95;915insA insertion in the complement 3 &#40;C3&#41; gene and heterozygous p&#46;Lys565Glu mutation due to c&#46;1693A<span class="elsevierStyleHsp" style=""></span>g&#47;day&#46; Methylprednisolone and mycophenolate mofetil were given to the patient because he developed hypersensitivity to cyclophosphamide&#46; Proteinuria level decreased to 2&#46;56<span class="elsevierStyleHsp" style=""></span>g&#47;day&#44; serum creatinine level decreased to 1<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; and serum albumin level increased to 3&#46;9<span class="elsevierStyleHsp" style=""></span>g&#47;dL after 1 year of follow-up&#46;</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 &#40;ACR&#41; criteria and by the 2012 Systemic Lupus International Collaborating Clinics &#40;SLICC&#41; criteria&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">5</span></a> The signature of lupus nephritis in renal pathology is polyclonal staining of IgG&#44; IgA&#44; IgM&#44; C3 and C1q with dominant or codominant IgG&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> There was no dominant IgG deposits&#44; even no uniform involvement of IgG and C3 deposits in our case&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">6</span></a> Instead&#44; C3 dominance fulfilled the criterion necessary to diagnose C3 glomerulopathy defined by consensus report of International Society of Nephrology&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> Dysregulation of complement system due to mutations or antibodies lead to C3 glomerulopathy&#46; Only &#8773;25&#37; of cases diagnosed as C3 glomerulopathy were reported to have genetic mutations in genes of C3 &#40;encoding complement factor 3&#41;&#44; CFB &#40;encoding complement factor B&#41;&#44; CFH &#40;encoding complement factor H&#44; the regulatory protein of compleman activation&#41;&#44; CFI &#40;encoding complement factor I&#44; inactivator of C3b&#41;&#44; and CFHR5 &#40;encoding complement factor H-related protein 5&#44; enhancer of complement activation&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> The c&#46;1204c&#62;T&#59; p&#46;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&#46;<a class="elsevierStyleCrossRefs" href="#bib0090"><span class="elsevierStyleSup">8&#44;9</span></a> This variant of CFH put our patient at an increased risk for liability to complement-mediated diseases which emerge in adulthood&#46; The second variant in genetic sequence of complement factor B gene was probably pathogenic for complement mediated disorders like thrombotic microangiopathy as reported previously&#46;<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&#46; 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&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">In conclusion&#44; as far as we know this is the first case showing the togetherness of C3 glomerulopathy and lupus nephritis&#46; After one year of treatment with methylprednisolone and mycophenolate mofetil&#44; renal improvement was achieved&#46; Further studies will enlighten the best therapeutic approach for this new entity in the future&#46;</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>&#58; Kubra Kaynar&#46; <span class="elsevierStyleItalic">Design</span>&#58; Kubra Kaynar&#44; Beyhan G&#252;vercin&#46; <span class="elsevierStyleItalic">Control</span>&#58; Kubra Kaynar&#44; Beyhan G&#252;vercin&#44; Sahile Safarl&#305;&#44; Sevdeg&#252;l Mungan&#44; Mustafa &#350;ahin&#46; <span class="elsevierStyleItalic">Data Collection</span>&#58; Sahile Safarl&#305;&#44; Sevdeg&#252;l Mungan&#44; Mustafa &#350;ahin&#46; <span class="elsevierStyleItalic">Literature review</span>&#58; Kubra Kaynar&#46; <span class="elsevierStyleItalic">Writing the manuscript</span>&#58; Kubra Kaynar&#46;</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&#46; Informed consent was obtained from patient&#46;</p></span></span>"
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ISSN: 20132514
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