The relationship between albuminuria, MCP-1/CCL2, and interstitial macrophages in chronic kidney disease
Glomerular-derived proteins may activate tubular cells to express the macrophage-directed chemokine monocyte chemoattractant protein-1 (MCP-1/CCL2). Macrophages at interstitial sites have a central role in directing renal scarring. We have prospectively assessed the relationship between albuminuria,...
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Veröffentlicht in: | Kidney international 2006-04, Vol.69 (7), p.1189-1197 |
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description | Glomerular-derived proteins may activate tubular cells to express the macrophage-directed chemokine monocyte chemoattractant protein-1 (MCP-1/CCL2). Macrophages at interstitial sites have a central role in directing renal scarring. We have prospectively assessed the relationship between albuminuria, urinary MCP-1/CCL2, interstitial macrophage infiltration, in situ damage, and clinical outcomes in a large group of patients with chronic kidney disease. We studied 215 patients and quantified albumin–creatinine ratio (ACR), urinary MCP-1/CCL2, interstitial macrophage numbers, and in situ damage. ACR correlated with urinary MCP-1/CCL2 (correlation 0.499; P |
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Macrophages at interstitial sites have a central role in directing renal scarring. We have prospectively assessed the relationship between albuminuria, urinary MCP-1/CCL2, interstitial macrophage infiltration, in situ damage, and clinical outcomes in a large group of patients with chronic kidney disease. We studied 215 patients and quantified albumin–creatinine ratio (ACR), urinary MCP-1/CCL2, interstitial macrophage numbers, and in situ damage. ACR correlated with urinary MCP-1/CCL2 (correlation 0.499; P<0.001), interstitial macrophage numbers (correlation 0.481; P<0.001), and index of chronic damage (correlation 0.363; P<0.001). Macrophage numbers closely correlated with in situ damage (correlation 0.755; P<0.001). By multivariate analysis ACR, urinary MCP-1/CCL2, and interstitial macrophage numbers were interdependent. By Kaplan–Meier survival analysis albuminuria, urinary MCP-1/CCL2, interstitial macrophages, and chronic damage predict the outcome. ACR, macrophage numbers, chronic damage, and creatinine independently predicted renal survival. The association of ACR with other variables was strongest in patients with less advanced disease states. There is a close association between albuminuria, urinary MCP-1/CCL2, and interstitial macrophage infiltration with in situ damage and clinical outcomes. These findings support the hypothesis that albuminuria triggers tubular MCP-1/CCL2 expression with subsequent macrophage infiltration. These processes may represent the dominant pathway for the progression of renal injury before the establishment of advanced renal scarring</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1038/sj.ki.5000212</identifier><identifier>PMID: 16609683</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Albuminuria ; Biological and medical sciences ; Cell Count ; Chemokine CCL2 - genetics ; Chemokine CCL2 - urine ; Chronic Disease ; chronic kidney disease ; Disease Progression ; Humans ; Immunoglobulin A - analysis ; Immunoglobulin G - analysis ; Immunoglobulin M - analysis ; Immunohistochemistry ; Kidney Diseases - immunology ; Kidney Diseases - physiopathology ; Kidney Diseases - urine ; Kidneys ; macrophages ; Macrophages - pathology ; Macrophages - physiology ; MCP-1/CCL2 ; Medical sciences ; Nephrology. Urinary tract diseases ; Urinary system involvement in other diseases. Miscellaneous ; Urinary tract. Prostate gland</subject><ispartof>Kidney international, 2006-04, Vol.69 (7), p.1189-1197</ispartof><rights>2006 International Society of Nephrology</rights><rights>2006 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Apr 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c555t-21b9d53e2ce0347496d6c75eb7b8906f6cb9a693ac6e9f84ff7b208c447485663</citedby><cites>FETCH-LOGICAL-c555t-21b9d53e2ce0347496d6c75eb7b8906f6cb9a693ac6e9f84ff7b208c447485663</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/210110115?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,64385,64387,64389,72469</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17923912$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16609683$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Eardley, K.S.</creatorcontrib><creatorcontrib>Zehnder, D.</creatorcontrib><creatorcontrib>Quinkler, M.</creatorcontrib><creatorcontrib>Lepenies, J.</creatorcontrib><creatorcontrib>Bates, R.L.</creatorcontrib><creatorcontrib>Savage, C.O.</creatorcontrib><creatorcontrib>Howie, A.J.</creatorcontrib><creatorcontrib>Adu, D.</creatorcontrib><creatorcontrib>Cockwell, P.</creatorcontrib><title>The relationship between albuminuria, MCP-1/CCL2, and interstitial macrophages in chronic kidney disease</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>Glomerular-derived proteins may activate tubular cells to express the macrophage-directed chemokine monocyte chemoattractant protein-1 (MCP-1/CCL2). Macrophages at interstitial sites have a central role in directing renal scarring. We have prospectively assessed the relationship between albuminuria, urinary MCP-1/CCL2, interstitial macrophage infiltration, in situ damage, and clinical outcomes in a large group of patients with chronic kidney disease. We studied 215 patients and quantified albumin–creatinine ratio (ACR), urinary MCP-1/CCL2, interstitial macrophage numbers, and in situ damage. ACR correlated with urinary MCP-1/CCL2 (correlation 0.499; P<0.001), interstitial macrophage numbers (correlation 0.481; P<0.001), and index of chronic damage (correlation 0.363; P<0.001). Macrophage numbers closely correlated with in situ damage (correlation 0.755; P<0.001). By multivariate analysis ACR, urinary MCP-1/CCL2, and interstitial macrophage numbers were interdependent. By Kaplan–Meier survival analysis albuminuria, urinary MCP-1/CCL2, interstitial macrophages, and chronic damage predict the outcome. ACR, macrophage numbers, chronic damage, and creatinine independently predicted renal survival. The association of ACR with other variables was strongest in patients with less advanced disease states. There is a close association between albuminuria, urinary MCP-1/CCL2, and interstitial macrophage infiltration with in situ damage and clinical outcomes. These findings support the hypothesis that albuminuria triggers tubular MCP-1/CCL2 expression with subsequent macrophage infiltration. These processes may represent the dominant pathway for the progression of renal injury before the establishment of advanced renal scarring</description><subject>Albuminuria</subject><subject>Biological and medical sciences</subject><subject>Cell Count</subject><subject>Chemokine CCL2 - genetics</subject><subject>Chemokine CCL2 - urine</subject><subject>Chronic Disease</subject><subject>chronic kidney disease</subject><subject>Disease Progression</subject><subject>Humans</subject><subject>Immunoglobulin A - analysis</subject><subject>Immunoglobulin G - analysis</subject><subject>Immunoglobulin M - analysis</subject><subject>Immunohistochemistry</subject><subject>Kidney Diseases - immunology</subject><subject>Kidney Diseases - physiopathology</subject><subject>Kidney Diseases - urine</subject><subject>Kidneys</subject><subject>macrophages</subject><subject>Macrophages - pathology</subject><subject>Macrophages - physiology</subject><subject>MCP-1/CCL2</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Urinary system involvement in other diseases. Miscellaneous</subject><subject>Urinary tract. 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Urinary tract diseases</topic><topic>Urinary system involvement in other diseases. Miscellaneous</topic><topic>Urinary tract. Prostate gland</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Eardley, K.S.</creatorcontrib><creatorcontrib>Zehnder, D.</creatorcontrib><creatorcontrib>Quinkler, M.</creatorcontrib><creatorcontrib>Lepenies, J.</creatorcontrib><creatorcontrib>Bates, R.L.</creatorcontrib><creatorcontrib>Savage, C.O.</creatorcontrib><creatorcontrib>Howie, A.J.</creatorcontrib><creatorcontrib>Adu, D.</creatorcontrib><creatorcontrib>Cockwell, P.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</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>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>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Eardley, K.S.</au><au>Zehnder, D.</au><au>Quinkler, M.</au><au>Lepenies, J.</au><au>Bates, R.L.</au><au>Savage, C.O.</au><au>Howie, A.J.</au><au>Adu, D.</au><au>Cockwell, P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The relationship between albuminuria, MCP-1/CCL2, and interstitial macrophages in chronic kidney disease</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2006-04-01</date><risdate>2006</risdate><volume>69</volume><issue>7</issue><spage>1189</spage><epage>1197</epage><pages>1189-1197</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>Glomerular-derived proteins may activate tubular cells to express the macrophage-directed chemokine monocyte chemoattractant protein-1 (MCP-1/CCL2). Macrophages at interstitial sites have a central role in directing renal scarring. We have prospectively assessed the relationship between albuminuria, urinary MCP-1/CCL2, interstitial macrophage infiltration, in situ damage, and clinical outcomes in a large group of patients with chronic kidney disease. We studied 215 patients and quantified albumin–creatinine ratio (ACR), urinary MCP-1/CCL2, interstitial macrophage numbers, and in situ damage. ACR correlated with urinary MCP-1/CCL2 (correlation 0.499; P<0.001), interstitial macrophage numbers (correlation 0.481; P<0.001), and index of chronic damage (correlation 0.363; P<0.001). Macrophage numbers closely correlated with in situ damage (correlation 0.755; P<0.001). By multivariate analysis ACR, urinary MCP-1/CCL2, and interstitial macrophage numbers were interdependent. By Kaplan–Meier survival analysis albuminuria, urinary MCP-1/CCL2, interstitial macrophages, and chronic damage predict the outcome. ACR, macrophage numbers, chronic damage, and creatinine independently predicted renal survival. The association of ACR with other variables was strongest in patients with less advanced disease states. There is a close association between albuminuria, urinary MCP-1/CCL2, and interstitial macrophage infiltration with in situ damage and clinical outcomes. These findings support the hypothesis that albuminuria triggers tubular MCP-1/CCL2 expression with subsequent macrophage infiltration. These processes may represent the dominant pathway for the progression of renal injury before the establishment of advanced renal scarring</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>16609683</pmid><doi>10.1038/sj.ki.5000212</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Albuminuria Biological and medical sciences Cell Count Chemokine CCL2 - genetics Chemokine CCL2 - urine Chronic Disease chronic kidney disease Disease Progression Humans Immunoglobulin A - analysis Immunoglobulin G - analysis Immunoglobulin M - analysis Immunohistochemistry Kidney Diseases - immunology Kidney Diseases - physiopathology Kidney Diseases - urine Kidneys macrophages Macrophages - pathology Macrophages - physiology MCP-1/CCL2 Medical sciences Nephrology. Urinary tract diseases Urinary system involvement in other diseases. Miscellaneous Urinary tract. Prostate gland |
title | The relationship between albuminuria, MCP-1/CCL2, and interstitial macrophages in chronic kidney disease |
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