The Clinical Significance of Uric Acid and Complement Activation in the Progression of IgA Nephropathy
Abstract Background/Aims: The aim of this study is to investigate the utility of clinical [age, gender, mean arterial pressure (MAP)] and laboratory parameters [eGFR, hemoglobin (Hgb), serum levels of creatinine, uric acid, albumin, proteinuria, hematuria] and also histopathological lesions (Oxford...
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| Veröffentlicht in: | Kidney & blood pressure research 2016-03, Vol.41 (2), p.148-157 |
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| creator | Caliskan, Yasar Ozluk, Yasemin Celik, Dilara Oztop, Nida Aksoy, Aysun Ucar, Ayse Serra Yazici, Halil Kilicaslan, Isin Sever, Mehmet Sukru |
| description | Abstract
Background/Aims: The aim of this study is to investigate the utility of clinical [age, gender, mean arterial pressure (MAP)] and laboratory parameters [eGFR, hemoglobin (Hgb), serum levels of creatinine, uric acid, albumin, proteinuria, hematuria] and also histopathological lesions (Oxford classification parameters, crescents, intensity and pattern of staining for C3, C1Q, IgA, IgG, IgM) as progression markers in patients with IgA Nephropathy (IgAN). Methods: A total of 111 IgAN patients with a follow-up period >1 year or who reached kidney failure [GFR category G5 chronic kidney disease (CKD)] 30 ml/min/m2. Conclusions: Hyperuricemia and the deposition of C3 are independent risk factors for IgAN progression. |
| doi_str_mv | 10.1159/000443415 |
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Background/Aims: The aim of this study is to investigate the utility of clinical [age, gender, mean arterial pressure (MAP)] and laboratory parameters [eGFR, hemoglobin (Hgb), serum levels of creatinine, uric acid, albumin, proteinuria, hematuria] and also histopathological lesions (Oxford classification parameters, crescents, intensity and pattern of staining for C3, C1Q, IgA, IgG, IgM) as progression markers in patients with IgA Nephropathy (IgAN). Methods: A total of 111 IgAN patients with a follow-up period >1 year or who reached kidney failure [GFR category G5 chronic kidney disease (CKD)] <1 year were investigated. Primary endpoint was the development of kidney failure or eGFR decline ≥50% from the baseline. Kaplan-Meier and Cox proportional hazards analyses were performed. Results: Mean follow-up period was 33±29 months. Thirty-seven (33.3%) patients progressed to kidney failure and 4 (3.6%) patients developed eGFR decline ≥50% from the baseline after a median of 23 and 65 months, respectively. In multivariate Cox regression analysis, baseline levels of Hgb (HR:0.782, 95% CI 0.559-0.973, p=0.037), serum uric acid (HR:1.293, 95% CI 1.023-1.621, p=0.046), eGFR (HR:0.966, 95% CI 0.947-0.984, p=0.004) and intensity of C3 staining (HR:1.550, 95% CI 1.198-1.976, p=0.049) predicted primary endpoint. Serum uric acid level was associated independently with T score (β=0.303, p=0.005) in patients with eGFR>30 ml/min/m2. Conclusions: Hyperuricemia and the deposition of C3 are independent risk factors for IgAN progression.</description><identifier>ISSN: 1420-4096</identifier><identifier>EISSN: 1423-0143</identifier><identifier>DOI: 10.1159/000443415</identifier><identifier>PMID: 26914454</identifier><identifier>CODEN: RPBIEL</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Adolescent ; Adult ; Age ; Aged ; Albumin ; Atrophy ; Biological markers ; Biomarkers ; Biomarkers - blood ; Biopsy ; Blood pressure ; Body mass index ; Care and treatment ; Chronic kidney failure ; Classification ; Clinical medicine ; Complement ; Complement (Immunology) ; Complement activation ; Complement Activation - physiology ; Complement C3 ; Creatinine ; Development and progression ; Disease Progression ; End stage renal disease ; Epidermal growth factor receptors ; Failure ; Female ; Females ; Genetic aspects ; Glomerulonephritis, IGA - blood ; Glomerulonephritis, IGA - diagnosis ; Health aspects ; Hematuria ; Hemoglobin ; HIV ; Human immunodeficiency virus ; Humans ; Hypertension ; Hyperuricemia ; Hyperuricemia - blood ; Hyperuricemia - diagnosis ; Identification and classification ; IgA glomerulonephritis ; IgA Nephropathy ; Immunoglobulin A ; Immunoglobulin G ; Immunoglobulin M ; Kidney diseases ; Kidneys ; Laboratories ; Male ; Males ; Medical prognosis ; Middle Aged ; Original Paper ; Parameters ; Patients ; Proteinuria ; Regression analysis ; Renal failure ; Retrospective Studies ; Risk factors ; Serum levels ; Staining ; Uric acid ; Uric Acid - blood ; Young Adult</subject><ispartof>Kidney & blood pressure research, 2016-03, Vol.41 (2), p.148-157</ispartof><rights>2016 The Author(s) Published by S. Karger AG, Basel</rights><rights>2016 The Author(s) Published by S. Karger AG, Basel.</rights><rights>COPYRIGHT 2016 S. Karger AG</rights><rights>2016 The Author(s) Published by S. Karger AG, Basel. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the associated terms available at: https://uk.sagepub.com/en-gb/eur/reusing-open-access-and-sage-choice-content</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c625t-a2e76da76dcdeb34d7cff38602bd27c55ed02d3339de22e203018834292784783</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,864,2102,27635,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26914454$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Caliskan, Yasar</creatorcontrib><creatorcontrib>Ozluk, Yasemin</creatorcontrib><creatorcontrib>Celik, Dilara</creatorcontrib><creatorcontrib>Oztop, Nida</creatorcontrib><creatorcontrib>Aksoy, Aysun</creatorcontrib><creatorcontrib>Ucar, Ayse Serra</creatorcontrib><creatorcontrib>Yazici, Halil</creatorcontrib><creatorcontrib>Kilicaslan, Isin</creatorcontrib><creatorcontrib>Sever, Mehmet Sukru</creatorcontrib><title>The Clinical Significance of Uric Acid and Complement Activation in the Progression of IgA Nephropathy</title><title>Kidney & blood pressure research</title><addtitle>Kidney Blood Press Res</addtitle><description>Abstract
Background/Aims: The aim of this study is to investigate the utility of clinical [age, gender, mean arterial pressure (MAP)] and laboratory parameters [eGFR, hemoglobin (Hgb), serum levels of creatinine, uric acid, albumin, proteinuria, hematuria] and also histopathological lesions (Oxford classification parameters, crescents, intensity and pattern of staining for C3, C1Q, IgA, IgG, IgM) as progression markers in patients with IgA Nephropathy (IgAN). Methods: A total of 111 IgAN patients with a follow-up period >1 year or who reached kidney failure [GFR category G5 chronic kidney disease (CKD)] <1 year were investigated. Primary endpoint was the development of kidney failure or eGFR decline ≥50% from the baseline. Kaplan-Meier and Cox proportional hazards analyses were performed. Results: Mean follow-up period was 33±29 months. Thirty-seven (33.3%) patients progressed to kidney failure and 4 (3.6%) patients developed eGFR decline ≥50% from the baseline after a median of 23 and 65 months, respectively. In multivariate Cox regression analysis, baseline levels of Hgb (HR:0.782, 95% CI 0.559-0.973, p=0.037), serum uric acid (HR:1.293, 95% CI 1.023-1.621, p=0.046), eGFR (HR:0.966, 95% CI 0.947-0.984, p=0.004) and intensity of C3 staining (HR:1.550, 95% CI 1.198-1.976, p=0.049) predicted primary endpoint. Serum uric acid level was associated independently with T score (β=0.303, p=0.005) in patients with eGFR>30 ml/min/m2. Conclusions: Hyperuricemia and the deposition of C3 are independent risk factors for IgAN progression.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Age</subject><subject>Aged</subject><subject>Albumin</subject><subject>Atrophy</subject><subject>Biological markers</subject><subject>Biomarkers</subject><subject>Biomarkers - blood</subject><subject>Biopsy</subject><subject>Blood pressure</subject><subject>Body mass index</subject><subject>Care and treatment</subject><subject>Chronic kidney failure</subject><subject>Classification</subject><subject>Clinical medicine</subject><subject>Complement</subject><subject>Complement (Immunology)</subject><subject>Complement activation</subject><subject>Complement Activation - physiology</subject><subject>Complement C3</subject><subject>Creatinine</subject><subject>Development and progression</subject><subject>Disease Progression</subject><subject>End stage renal disease</subject><subject>Epidermal growth factor receptors</subject><subject>Failure</subject><subject>Female</subject><subject>Females</subject><subject>Genetic aspects</subject><subject>Glomerulonephritis, IGA - blood</subject><subject>Glomerulonephritis, IGA - diagnosis</subject><subject>Health aspects</subject><subject>Hematuria</subject><subject>Hemoglobin</subject><subject>HIV</subject><subject>Human immunodeficiency virus</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Hyperuricemia</subject><subject>Hyperuricemia - blood</subject><subject>Hyperuricemia - diagnosis</subject><subject>Identification and classification</subject><subject>IgA glomerulonephritis</subject><subject>IgA Nephropathy</subject><subject>Immunoglobulin A</subject><subject>Immunoglobulin G</subject><subject>Immunoglobulin M</subject><subject>Kidney diseases</subject><subject>Kidneys</subject><subject>Laboratories</subject><subject>Male</subject><subject>Males</subject><subject>Medical prognosis</subject><subject>Middle Aged</subject><subject>Original Paper</subject><subject>Parameters</subject><subject>Patients</subject><subject>Proteinuria</subject><subject>Regression analysis</subject><subject>Renal failure</subject><subject>Retrospective Studies</subject><subject>Risk factors</subject><subject>Serum levels</subject><subject>Staining</subject><subject>Uric acid</subject><subject>Uric Acid - blood</subject><subject>Young Adult</subject><issn>1420-4096</issn><issn>1423-0143</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DOA</sourceid><recordid>eNqNksuLFDEQxhtR3IcevIs0eFkPs-bZ6RzHwcfgoqK755BOKj0Zu5PedI-w_72Z7XEEEZEQUnz86ktVUUXxDKNLjLl8jRBijDLMHxSnmBG6QJjRh_cxWjAkq5PibBy3GeMIkcfFCakkZoyz08Jdb6BcdT54o7vym2-DdzkMBsroypvkTbk03pY62HIV-6GDHsKUtcn_0JOPofShnLLHlxTbBOO4l3Lmul2Wn2DYpDjoaXP3pHjkdDfC08N7Xty8e3u9-rC4-vx-vVpeLUxF-LTQBERldb7GQkOZFcY5WleINJYIwzlYRCylVFogBAiiCNc1ZUQSUTNR0_NiPfvaqLdqSL7X6U5F7dW9EFOrdJq86UBVmmNba42cs4w3TAqOrG6aSpqaMEmy18XsNaR4u4NxUr0fDXSdDhB3o8JCCFkTKVFGX_6BbuMuhdyponnoFDFK-b8oXGNCRIUoztTlTLU6V-mDi1PSJh8LvTcxgPNZX4paSEHybP43oaKCCCar_ZBezQkmxXFM4I6DwkjtF0odFyqzLw4175oe7JH8tUG_m_quUwvpCHx883W2UIN1mXr-V-rwy08cXtXt</recordid><startdate>20160301</startdate><enddate>20160301</enddate><creator>Caliskan, Yasar</creator><creator>Ozluk, Yasemin</creator><creator>Celik, Dilara</creator><creator>Oztop, Nida</creator><creator>Aksoy, Aysun</creator><creator>Ucar, Ayse Serra</creator><creator>Yazici, Halil</creator><creator>Kilicaslan, Isin</creator><creator>Sever, Mehmet Sukru</creator><general>S. Karger AG</general><general>Karger Publishers</general><scope>M--</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IAO</scope><scope>3V.</scope><scope>7QL</scope><scope>7T7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>S0X</scope><scope>7X8</scope><scope>DOA</scope></search><sort><creationdate>20160301</creationdate><title>The Clinical Significance of Uric Acid and Complement Activation in the Progression of IgA Nephropathy</title><author>Caliskan, Yasar ; Ozluk, Yasemin ; Celik, Dilara ; Oztop, Nida ; Aksoy, Aysun ; Ucar, Ayse Serra ; Yazici, Halil ; Kilicaslan, Isin ; Sever, Mehmet Sukru</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c625t-a2e76da76dcdeb34d7cff38602bd27c55ed02d3339de22e203018834292784783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Age</topic><topic>Aged</topic><topic>Albumin</topic><topic>Atrophy</topic><topic>Biological markers</topic><topic>Biomarkers</topic><topic>Biomarkers - blood</topic><topic>Biopsy</topic><topic>Blood pressure</topic><topic>Body mass index</topic><topic>Care and treatment</topic><topic>Chronic kidney failure</topic><topic>Classification</topic><topic>Clinical medicine</topic><topic>Complement</topic><topic>Complement (Immunology)</topic><topic>Complement activation</topic><topic>Complement Activation - physiology</topic><topic>Complement C3</topic><topic>Creatinine</topic><topic>Development and progression</topic><topic>Disease Progression</topic><topic>End stage renal disease</topic><topic>Epidermal growth factor receptors</topic><topic>Failure</topic><topic>Female</topic><topic>Females</topic><topic>Genetic aspects</topic><topic>Glomerulonephritis, IGA - blood</topic><topic>Glomerulonephritis, IGA - diagnosis</topic><topic>Health aspects</topic><topic>Hematuria</topic><topic>Hemoglobin</topic><topic>HIV</topic><topic>Human immunodeficiency virus</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Hyperuricemia</topic><topic>Hyperuricemia - blood</topic><topic>Hyperuricemia - diagnosis</topic><topic>Identification and classification</topic><topic>IgA glomerulonephritis</topic><topic>IgA Nephropathy</topic><topic>Immunoglobulin A</topic><topic>Immunoglobulin G</topic><topic>Immunoglobulin M</topic><topic>Kidney diseases</topic><topic>Kidneys</topic><topic>Laboratories</topic><topic>Male</topic><topic>Males</topic><topic>Medical prognosis</topic><topic>Middle Aged</topic><topic>Original Paper</topic><topic>Parameters</topic><topic>Patients</topic><topic>Proteinuria</topic><topic>Regression analysis</topic><topic>Renal failure</topic><topic>Retrospective Studies</topic><topic>Risk factors</topic><topic>Serum levels</topic><topic>Staining</topic><topic>Uric acid</topic><topic>Uric Acid - blood</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Caliskan, Yasar</creatorcontrib><creatorcontrib>Ozluk, Yasemin</creatorcontrib><creatorcontrib>Celik, Dilara</creatorcontrib><creatorcontrib>Oztop, Nida</creatorcontrib><creatorcontrib>Aksoy, Aysun</creatorcontrib><creatorcontrib>Ucar, Ayse Serra</creatorcontrib><creatorcontrib>Yazici, Halil</creatorcontrib><creatorcontrib>Kilicaslan, Isin</creatorcontrib><creatorcontrib>Sever, Mehmet Sukru</creatorcontrib><collection>Karger Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale Academic OneFile</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Kidney & blood pressure research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Caliskan, Yasar</au><au>Ozluk, Yasemin</au><au>Celik, Dilara</au><au>Oztop, Nida</au><au>Aksoy, Aysun</au><au>Ucar, Ayse Serra</au><au>Yazici, Halil</au><au>Kilicaslan, Isin</au><au>Sever, Mehmet Sukru</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Clinical Significance of Uric Acid and Complement Activation in the Progression of IgA Nephropathy</atitle><jtitle>Kidney & blood pressure research</jtitle><addtitle>Kidney Blood Press Res</addtitle><date>2016-03-01</date><risdate>2016</risdate><volume>41</volume><issue>2</issue><spage>148</spage><epage>157</epage><pages>148-157</pages><issn>1420-4096</issn><eissn>1423-0143</eissn><coden>RPBIEL</coden><abstract>Abstract
Background/Aims: The aim of this study is to investigate the utility of clinical [age, gender, mean arterial pressure (MAP)] and laboratory parameters [eGFR, hemoglobin (Hgb), serum levels of creatinine, uric acid, albumin, proteinuria, hematuria] and also histopathological lesions (Oxford classification parameters, crescents, intensity and pattern of staining for C3, C1Q, IgA, IgG, IgM) as progression markers in patients with IgA Nephropathy (IgAN). Methods: A total of 111 IgAN patients with a follow-up period >1 year or who reached kidney failure [GFR category G5 chronic kidney disease (CKD)] <1 year were investigated. Primary endpoint was the development of kidney failure or eGFR decline ≥50% from the baseline. Kaplan-Meier and Cox proportional hazards analyses were performed. Results: Mean follow-up period was 33±29 months. Thirty-seven (33.3%) patients progressed to kidney failure and 4 (3.6%) patients developed eGFR decline ≥50% from the baseline after a median of 23 and 65 months, respectively. In multivariate Cox regression analysis, baseline levels of Hgb (HR:0.782, 95% CI 0.559-0.973, p=0.037), serum uric acid (HR:1.293, 95% CI 1.023-1.621, p=0.046), eGFR (HR:0.966, 95% CI 0.947-0.984, p=0.004) and intensity of C3 staining (HR:1.550, 95% CI 1.198-1.976, p=0.049) predicted primary endpoint. Serum uric acid level was associated independently with T score (β=0.303, p=0.005) in patients with eGFR>30 ml/min/m2. Conclusions: Hyperuricemia and the deposition of C3 are independent risk factors for IgAN progression.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>26914454</pmid><doi>10.1159/000443415</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adolescent Adult Age Aged Albumin Atrophy Biological markers Biomarkers Biomarkers - blood Biopsy Blood pressure Body mass index Care and treatment Chronic kidney failure Classification Clinical medicine Complement Complement (Immunology) Complement activation Complement Activation - physiology Complement C3 Creatinine Development and progression Disease Progression End stage renal disease Epidermal growth factor receptors Failure Female Females Genetic aspects Glomerulonephritis, IGA - blood Glomerulonephritis, IGA - diagnosis Health aspects Hematuria Hemoglobin HIV Human immunodeficiency virus Humans Hypertension Hyperuricemia Hyperuricemia - blood Hyperuricemia - diagnosis Identification and classification IgA glomerulonephritis IgA Nephropathy Immunoglobulin A Immunoglobulin G Immunoglobulin M Kidney diseases Kidneys Laboratories Male Males Medical prognosis Middle Aged Original Paper Parameters Patients Proteinuria Regression analysis Renal failure Retrospective Studies Risk factors Serum levels Staining Uric acid Uric Acid - blood Young Adult |
| title | The Clinical Significance of Uric Acid and Complement Activation in the Progression of IgA Nephropathy |
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