In IgA Nephropathy, Glomerulosclerosis Is Associated with Increased Urinary CD80 Excretion and Urokinase-Type Plasminogen Activator Receptor-Positive Podocyturia

Background: Podocyturia may determine the evolution to podocytopenia, glomerulosclerosis, and renal failure. According to the Oxford classification of IgA nephropathy (IgAN), the S1 lesion describes glomerulosclerosis. Urokinase-type plasminogen activator receptor (uPAR) participates in podocyte att...

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Veröffentlicht in:Nephron extra 2017-05, Vol.7 (2), p.52-61
Hauptverfasser: Trimarchi, Hernán, Canzonieri, Romina, Schiel, Amalia, Costales-Collaguazo, Cristian, Stern, Aníbal, Paulero, Matías, Rengel, Tatiana, Andrews, José, Iotti, Alejandro, Forrester, Mariano, Lombi, Fernando, Pomeranz, Vanesa, Iriarte, Romina, Muryan, Alexis, Zotta, Elsa
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container_issue 2
container_start_page 52
container_title Nephron extra
container_volume 7
creator Trimarchi, Hernán
Canzonieri, Romina
Schiel, Amalia
Costales-Collaguazo, Cristian
Stern, Aníbal
Paulero, Matías
Rengel, Tatiana
Andrews, José
Iotti, Alejandro
Forrester, Mariano
Lombi, Fernando
Pomeranz, Vanesa
Iriarte, Romina
Muryan, Alexis
Zotta, Elsa
description Background: Podocyturia may determine the evolution to podocytopenia, glomerulosclerosis, and renal failure. According to the Oxford classification of IgA nephropathy (IgAN), the S1 lesion describes glomerulosclerosis. Urokinase-type plasminogen activator receptor (uPAR) participates in podocyte attachment, while CD80 increases in glomerulosclerosis. We measured uPAR-positive urinary podocytes and urinary CD80 (uCD80) in controls and in IgAN subjects with M1E0S0T0 and M1E0S1T0 Oxford scores to assess a potential association between podocyturia, inflammation, and glomerulosclerosis. Methods: The groups were as follows: controls (G1), n = 20 and IgAN group (G2), n = 39, subdivided into M1E0S0T0 (G2A), n = 21 and M1E0S1T0 (G2B), n = 18. Among the included variables, we determined uPAR-positive podocytes/gram of urinary creatinine (gUrCr) and uCD80 ng/gUrCr. Biopsies with interstitial fibrosis and tubular atrophy
doi_str_mv 10.1159/000473888
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According to the Oxford classification of IgA nephropathy (IgAN), the S1 lesion describes glomerulosclerosis. Urokinase-type plasminogen activator receptor (uPAR) participates in podocyte attachment, while CD80 increases in glomerulosclerosis. We measured uPAR-positive urinary podocytes and urinary CD80 (uCD80) in controls and in IgAN subjects with M1E0S0T0 and M1E0S1T0 Oxford scores to assess a potential association between podocyturia, inflammation, and glomerulosclerosis. Methods: The groups were as follows: controls (G1), n = 20 and IgAN group (G2), n = 39, subdivided into M1E0S0T0 (G2A), n = 21 and M1E0S1T0 (G2B), n = 18. Among the included variables, we determined uPAR-positive podocytes/gram of urinary creatinine (gUrCr) and uCD80 ng/gUrCr. Biopsies with interstitial fibrosis and tubular atrophy &lt;10% were included. Results: Groups were not different in age and gender; urinary protein-creatinine (uP/C) ratio, Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) equation, uPAR-positive podocytes/gUrCr, and uCD80 were significantly increased in G2 versus G1. G2A and G2B were not different in age, gender, hypertension, and follow-up. G2B displayed significantly higher uP/C, uPAR-positive podocytes, uCD80, and lower CKD-EPI versus G2A. Strong significant correlations were encountered between uCD80 and podocyturia in G2A and G2B. However, when G1 was compared to G2A and G2B separately, the differences with respect to uP/C, uPAR-positive podocytes, and podocyturia were significantly stronger versus G2B than versus G2A. Conclusions: IgAN presents elevated uCD80 excretion and uPAR-positive podocyturia, while CD80 correlates with podocyturia. Glomerulosclerosis (S1) at the time of biopsy is associated with higher uP/C, lower renal function, increased uPAR-positive podocyturia, and CD80 excretion, and is independent of M1. In IgAN, uPAR may participate in podocyte detachment.</description><identifier>ISSN: 1664-5529</identifier><identifier>EISSN: 1664-5529</identifier><identifier>DOI: 10.1159/000473888</identifier><identifier>PMID: 28626472</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Original Paper</subject><ispartof>Nephron extra, 2017-05, Vol.7 (2), p.52-61</ispartof><rights>2017 The Author(s). Published by S. Karger AG, Basel</rights><rights>Copyright © 2017 by S. Karger AG, Basel 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c424t-673d1484989f7a2f53e9e8acd02a7dc2bd1b0011788176eb8390b6b37cd2f49c3</citedby><cites>FETCH-LOGICAL-c424t-673d1484989f7a2f53e9e8acd02a7dc2bd1b0011788176eb8390b6b37cd2f49c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5473063/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5473063/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27626,27915,27916,53782,53784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28626472$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Trimarchi, Hernán</creatorcontrib><creatorcontrib>Canzonieri, Romina</creatorcontrib><creatorcontrib>Schiel, Amalia</creatorcontrib><creatorcontrib>Costales-Collaguazo, Cristian</creatorcontrib><creatorcontrib>Stern, Aníbal</creatorcontrib><creatorcontrib>Paulero, Matías</creatorcontrib><creatorcontrib>Rengel, Tatiana</creatorcontrib><creatorcontrib>Andrews, José</creatorcontrib><creatorcontrib>Iotti, Alejandro</creatorcontrib><creatorcontrib>Forrester, Mariano</creatorcontrib><creatorcontrib>Lombi, Fernando</creatorcontrib><creatorcontrib>Pomeranz, Vanesa</creatorcontrib><creatorcontrib>Iriarte, Romina</creatorcontrib><creatorcontrib>Muryan, Alexis</creatorcontrib><creatorcontrib>Zotta, Elsa</creatorcontrib><title>In IgA Nephropathy, Glomerulosclerosis Is Associated with Increased Urinary CD80 Excretion and Urokinase-Type Plasminogen Activator Receptor-Positive Podocyturia</title><title>Nephron extra</title><addtitle>Nephron Extra</addtitle><description>Background: Podocyturia may determine the evolution to podocytopenia, glomerulosclerosis, and renal failure. According to the Oxford classification of IgA nephropathy (IgAN), the S1 lesion describes glomerulosclerosis. Urokinase-type plasminogen activator receptor (uPAR) participates in podocyte attachment, while CD80 increases in glomerulosclerosis. We measured uPAR-positive urinary podocytes and urinary CD80 (uCD80) in controls and in IgAN subjects with M1E0S0T0 and M1E0S1T0 Oxford scores to assess a potential association between podocyturia, inflammation, and glomerulosclerosis. Methods: The groups were as follows: controls (G1), n = 20 and IgAN group (G2), n = 39, subdivided into M1E0S0T0 (G2A), n = 21 and M1E0S1T0 (G2B), n = 18. Among the included variables, we determined uPAR-positive podocytes/gram of urinary creatinine (gUrCr) and uCD80 ng/gUrCr. Biopsies with interstitial fibrosis and tubular atrophy &lt;10% were included. Results: Groups were not different in age and gender; urinary protein-creatinine (uP/C) ratio, Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) equation, uPAR-positive podocytes/gUrCr, and uCD80 were significantly increased in G2 versus G1. G2A and G2B were not different in age, gender, hypertension, and follow-up. G2B displayed significantly higher uP/C, uPAR-positive podocytes, uCD80, and lower CKD-EPI versus G2A. Strong significant correlations were encountered between uCD80 and podocyturia in G2A and G2B. However, when G1 was compared to G2A and G2B separately, the differences with respect to uP/C, uPAR-positive podocytes, and podocyturia were significantly stronger versus G2B than versus G2A. Conclusions: IgAN presents elevated uCD80 excretion and uPAR-positive podocyturia, while CD80 correlates with podocyturia. Glomerulosclerosis (S1) at the time of biopsy is associated with higher uP/C, lower renal function, increased uPAR-positive podocyturia, and CD80 excretion, and is independent of M1. In IgAN, uPAR may participate in podocyte detachment.</description><subject>Original Paper</subject><issn>1664-5529</issn><issn>1664-5529</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><recordid>eNptkU1r3DAQhkVpaUKSQ--lCHppoG4l-Uu-FJbNNjGEbSjJWcjyeFeNLTmSnGR_Tv9pFTY1KfSk0byP3hnNIPSOki-U5tVXQkhWppzzV-iQFkWW5DmrXr-ID9CJ978iRgpCU169RQeMF6zISnaIftcG15sFXsO4dXaUYbv7jM97O4CbeutVD8567XHt8cJ7q7QM0OIHHba4NsqB9PF647SRboeXZ5zg1WNMB20NluZJsrdR9JBc70bAV730gzZ2AwYvVND3MliHf4KCMQbJVawVk5GzrVW7MDktj9GbTvYeTp7PI3TzfXW9vEguf5zXy8VlojKWhaQo05ZmPKt41ZWSdXkKFXCpWsJk2SrWtLQhhNKSc1oW0PC0Ik3RpKVqWZdVKj1C3_a-49QM0CowwclejE4P8W_CSi3-VYzeio29F3kcPynSaPDp2cDZuwl8EIP2CvpeGrCTF7SilJE4-jyip3tUxel6B91chhLxtFUxbzWyH172NZN_dxiB93vgVroNuBmY33_8r7xer_aEGNsu_QO3rrVj</recordid><startdate>20170516</startdate><enddate>20170516</enddate><creator>Trimarchi, Hernán</creator><creator>Canzonieri, Romina</creator><creator>Schiel, Amalia</creator><creator>Costales-Collaguazo, Cristian</creator><creator>Stern, Aníbal</creator><creator>Paulero, Matías</creator><creator>Rengel, Tatiana</creator><creator>Andrews, José</creator><creator>Iotti, Alejandro</creator><creator>Forrester, Mariano</creator><creator>Lombi, Fernando</creator><creator>Pomeranz, Vanesa</creator><creator>Iriarte, Romina</creator><creator>Muryan, Alexis</creator><creator>Zotta, Elsa</creator><general>S. 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According to the Oxford classification of IgA nephropathy (IgAN), the S1 lesion describes glomerulosclerosis. Urokinase-type plasminogen activator receptor (uPAR) participates in podocyte attachment, while CD80 increases in glomerulosclerosis. We measured uPAR-positive urinary podocytes and urinary CD80 (uCD80) in controls and in IgAN subjects with M1E0S0T0 and M1E0S1T0 Oxford scores to assess a potential association between podocyturia, inflammation, and glomerulosclerosis. Methods: The groups were as follows: controls (G1), n = 20 and IgAN group (G2), n = 39, subdivided into M1E0S0T0 (G2A), n = 21 and M1E0S1T0 (G2B), n = 18. Among the included variables, we determined uPAR-positive podocytes/gram of urinary creatinine (gUrCr) and uCD80 ng/gUrCr. Biopsies with interstitial fibrosis and tubular atrophy &lt;10% were included. Results: Groups were not different in age and gender; urinary protein-creatinine (uP/C) ratio, Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) equation, uPAR-positive podocytes/gUrCr, and uCD80 were significantly increased in G2 versus G1. G2A and G2B were not different in age, gender, hypertension, and follow-up. G2B displayed significantly higher uP/C, uPAR-positive podocytes, uCD80, and lower CKD-EPI versus G2A. Strong significant correlations were encountered between uCD80 and podocyturia in G2A and G2B. However, when G1 was compared to G2A and G2B separately, the differences with respect to uP/C, uPAR-positive podocytes, and podocyturia were significantly stronger versus G2B than versus G2A. Conclusions: IgAN presents elevated uCD80 excretion and uPAR-positive podocyturia, while CD80 correlates with podocyturia. Glomerulosclerosis (S1) at the time of biopsy is associated with higher uP/C, lower renal function, increased uPAR-positive podocyturia, and CD80 excretion, and is independent of M1. In IgAN, uPAR may participate in podocyte detachment.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>28626472</pmid><doi>10.1159/000473888</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record>
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title In IgA Nephropathy, Glomerulosclerosis Is Associated with Increased Urinary CD80 Excretion and Urokinase-Type Plasminogen Activator Receptor-Positive Podocyturia
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