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Glomerular nephrotoxicity of aminoglycosides
Aminoglycoside antibiotics are the most commonly used antibiotics worldwide in the treatment of Gram-negative bacterial infections. However, aminoglycosides induce nephrotoxicity in 10–20% of therapeutic courses. Aminoglycoside-induced nephrotoxicity is characterized by slow rises in serum creatinin...
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| Published in: | Toxicology and applied pharmacology 2007-08, Vol.223 (1), p.86-98 |
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| cites | cdi_FETCH-LOGICAL-c443t-b56ce3d78a9d2c206b5ed5d9ab31d4d37beacac2c6e67d269ae219a59d66aa0d3 |
| container_end_page | 98 |
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| container_title | Toxicology and applied pharmacology |
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| creator | Martínez-Salgado, Carlos López-Hernández, Francisco J. López-Novoa, José M. |
| description | Aminoglycoside antibiotics are the most commonly used antibiotics worldwide in the treatment of Gram-negative bacterial infections. However, aminoglycosides induce nephrotoxicity in 10–20% of therapeutic courses. Aminoglycoside-induced nephrotoxicity is characterized by slow rises in serum creatinine, tubular necrosis and marked decreases in glomerular filtration rate and in the ultrafiltration coefficient. Regulation of the ultrafiltration coefficient depends on the activity of intraglomerular mesangial cells. The mechanisms responsible for tubular nephrotoxicity of aminoglycosides have been intensively reviewed previously, but glomerular toxicity has received less attention. The purpose of this review is to critically assess the published literature regarding the toxic mechanisms of action of aminoglycosides on renal glomeruli and mesangial cells. The main goal of this review is to provide an actualized and mechanistic vision of pathways involved in glomerular toxic effects of aminoglycosides. |
| doi_str_mv | 10.1016/j.taap.2007.05.004 |
| format | article |
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However, aminoglycosides induce nephrotoxicity in 10–20% of therapeutic courses. Aminoglycoside-induced nephrotoxicity is characterized by slow rises in serum creatinine, tubular necrosis and marked decreases in glomerular filtration rate and in the ultrafiltration coefficient. Regulation of the ultrafiltration coefficient depends on the activity of intraglomerular mesangial cells. The mechanisms responsible for tubular nephrotoxicity of aminoglycosides have been intensively reviewed previously, but glomerular toxicity has received less attention. The purpose of this review is to critically assess the published literature regarding the toxic mechanisms of action of aminoglycosides on renal glomeruli and mesangial cells. The main goal of this review is to provide an actualized and mechanistic vision of pathways involved in glomerular toxic effects of aminoglycosides.</description><identifier>ISSN: 0041-008X</identifier><identifier>EISSN: 1096-0333</identifier><identifier>DOI: 10.1016/j.taap.2007.05.004</identifier><identifier>PMID: 17602717</identifier><identifier>CODEN: TXAPA9</identifier><language>eng</language><publisher>San Diego, CA: Elsevier Inc</publisher><subject>60 APPLIED LIFE SCIENCES ; Aminoglycosides ; Aminoglycosides - adverse effects ; Animals ; Anti-Bacterial Agents - adverse effects ; ANTIBIOTICS ; Apoptosis ; Apoptosis - drug effects ; Biological and medical sciences ; CELL PROLIFERATION ; CREATININE ; GENE REGULATION ; Gentamicin ; Gentamicins - adverse effects ; Glomerular Filtration Rate ; Glomerular toxicity ; GLOMERULI ; Humans ; Kidney Diseases - chemically induced ; Kidney Diseases - metabolism ; Kidney Diseases - pathology ; Medical sciences ; Mesangial cells ; Mesangial Cells - drug effects ; Mesangial Cells - pathology ; NECROSIS ; Platelet-activating factor ; Proliferation ; REVIEWS ; TOXICITY ; Toxicology ; ULTRAFILTRATION</subject><ispartof>Toxicology and applied pharmacology, 2007-08, Vol.223 (1), p.86-98</ispartof><rights>2007 Elsevier Inc.</rights><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c443t-b56ce3d78a9d2c206b5ed5d9ab31d4d37beacac2c6e67d269ae219a59d66aa0d3</citedby><cites>FETCH-LOGICAL-c443t-b56ce3d78a9d2c206b5ed5d9ab31d4d37beacac2c6e67d269ae219a59d66aa0d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27922,27923</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19018765$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17602717$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/21077783$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Martínez-Salgado, Carlos</creatorcontrib><creatorcontrib>López-Hernández, Francisco J.</creatorcontrib><creatorcontrib>López-Novoa, José M.</creatorcontrib><title>Glomerular nephrotoxicity of aminoglycosides</title><title>Toxicology and applied pharmacology</title><addtitle>Toxicol Appl Pharmacol</addtitle><description>Aminoglycoside antibiotics are the most commonly used antibiotics worldwide in the treatment of Gram-negative bacterial infections. However, aminoglycosides induce nephrotoxicity in 10–20% of therapeutic courses. Aminoglycoside-induced nephrotoxicity is characterized by slow rises in serum creatinine, tubular necrosis and marked decreases in glomerular filtration rate and in the ultrafiltration coefficient. Regulation of the ultrafiltration coefficient depends on the activity of intraglomerular mesangial cells. The mechanisms responsible for tubular nephrotoxicity of aminoglycosides have been intensively reviewed previously, but glomerular toxicity has received less attention. The purpose of this review is to critically assess the published literature regarding the toxic mechanisms of action of aminoglycosides on renal glomeruli and mesangial cells. The main goal of this review is to provide an actualized and mechanistic vision of pathways involved in glomerular toxic effects of aminoglycosides.</description><subject>60 APPLIED LIFE SCIENCES</subject><subject>Aminoglycosides</subject><subject>Aminoglycosides - adverse effects</subject><subject>Animals</subject><subject>Anti-Bacterial Agents - adverse effects</subject><subject>ANTIBIOTICS</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>CELL PROLIFERATION</subject><subject>CREATININE</subject><subject>GENE REGULATION</subject><subject>Gentamicin</subject><subject>Gentamicins - adverse effects</subject><subject>Glomerular Filtration Rate</subject><subject>Glomerular toxicity</subject><subject>GLOMERULI</subject><subject>Humans</subject><subject>Kidney Diseases - chemically induced</subject><subject>Kidney Diseases - metabolism</subject><subject>Kidney Diseases - pathology</subject><subject>Medical sciences</subject><subject>Mesangial cells</subject><subject>Mesangial Cells - drug effects</subject><subject>Mesangial Cells - pathology</subject><subject>NECROSIS</subject><subject>Platelet-activating factor</subject><subject>Proliferation</subject><subject>REVIEWS</subject><subject>TOXICITY</subject><subject>Toxicology</subject><subject>ULTRAFILTRATION</subject><issn>0041-008X</issn><issn>1096-0333</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><recordid>eNp9kE1r3DAQhkVoSTab_oEeykJpTrUzkmzJglxCSNJAoJcEehNjabbRYltbyVuy_742u5BbTwPD887Hw9hnDiUHrq425Yi4LQWALqEuAaoTtuBgVAFSyg9sMXV4AdD8OmPnOW8AwFQVP2VnXCsQmusF-_7QxZ7SrsO0Gmj7muIY34IL434V1yvswxB_d3sXc_CUL9jHNXaZPh3rkr3c3z3f_iiefj483t48Fa6q5Fi0tXIkvW7QeOEEqLYmX3uDreS-8lK3hA6dcIqU9kIZJMEN1sYrhQheLtnXw9yYx2DzdA25VxeHgdxoBQetdSMn6vJAbVP8s6M82j5kR12HA8VdttzoBoyoJ1AcQJdizonWdptCj2lvOdjZpN3Y2aSdTVqo7eRtCn05Tt-1Pfn3yFHdBHw7ApgdduuEgwv5nTPAG63m7dcHjiZjfwOl-SEaHPmQ5n98DP-74x-w3pGt</recordid><startdate>20070815</startdate><enddate>20070815</enddate><creator>Martínez-Salgado, Carlos</creator><creator>López-Hernández, Francisco J.</creator><creator>López-Novoa, José M.</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</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>7QL</scope><scope>7U7</scope><scope>C1K</scope><scope>OTOTI</scope></search><sort><creationdate>20070815</creationdate><title>Glomerular nephrotoxicity of aminoglycosides</title><author>Martínez-Salgado, Carlos ; López-Hernández, Francisco J. ; López-Novoa, José M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c443t-b56ce3d78a9d2c206b5ed5d9ab31d4d37beacac2c6e67d269ae219a59d66aa0d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>60 APPLIED LIFE SCIENCES</topic><topic>Aminoglycosides</topic><topic>Aminoglycosides - adverse effects</topic><topic>Animals</topic><topic>Anti-Bacterial Agents - adverse effects</topic><topic>ANTIBIOTICS</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>CELL PROLIFERATION</topic><topic>CREATININE</topic><topic>GENE REGULATION</topic><topic>Gentamicin</topic><topic>Gentamicins - adverse effects</topic><topic>Glomerular Filtration Rate</topic><topic>Glomerular toxicity</topic><topic>GLOMERULI</topic><topic>Humans</topic><topic>Kidney Diseases - chemically induced</topic><topic>Kidney Diseases - metabolism</topic><topic>Kidney Diseases - pathology</topic><topic>Medical sciences</topic><topic>Mesangial cells</topic><topic>Mesangial Cells - drug effects</topic><topic>Mesangial Cells - pathology</topic><topic>NECROSIS</topic><topic>Platelet-activating factor</topic><topic>Proliferation</topic><topic>REVIEWS</topic><topic>TOXICITY</topic><topic>Toxicology</topic><topic>ULTRAFILTRATION</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Martínez-Salgado, Carlos</creatorcontrib><creatorcontrib>López-Hernández, Francisco J.</creatorcontrib><creatorcontrib>López-Novoa, José M.</creatorcontrib><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>Bacteriology Abstracts (Microbiology B)</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>OSTI.GOV</collection><jtitle>Toxicology and applied pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Martínez-Salgado, Carlos</au><au>López-Hernández, Francisco J.</au><au>López-Novoa, José M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Glomerular nephrotoxicity of aminoglycosides</atitle><jtitle>Toxicology and applied pharmacology</jtitle><addtitle>Toxicol Appl Pharmacol</addtitle><date>2007-08-15</date><risdate>2007</risdate><volume>223</volume><issue>1</issue><spage>86</spage><epage>98</epage><pages>86-98</pages><issn>0041-008X</issn><eissn>1096-0333</eissn><coden>TXAPA9</coden><abstract>Aminoglycoside antibiotics are the most commonly used antibiotics worldwide in the treatment of Gram-negative bacterial infections. However, aminoglycosides induce nephrotoxicity in 10–20% of therapeutic courses. Aminoglycoside-induced nephrotoxicity is characterized by slow rises in serum creatinine, tubular necrosis and marked decreases in glomerular filtration rate and in the ultrafiltration coefficient. Regulation of the ultrafiltration coefficient depends on the activity of intraglomerular mesangial cells. The mechanisms responsible for tubular nephrotoxicity of aminoglycosides have been intensively reviewed previously, but glomerular toxicity has received less attention. The purpose of this review is to critically assess the published literature regarding the toxic mechanisms of action of aminoglycosides on renal glomeruli and mesangial cells. The main goal of this review is to provide an actualized and mechanistic vision of pathways involved in glomerular toxic effects of aminoglycosides.</abstract><cop>San Diego, CA</cop><pub>Elsevier Inc</pub><pmid>17602717</pmid><doi>10.1016/j.taap.2007.05.004</doi><tpages>13</tpages></addata></record> |
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| language | eng |
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| source | Elsevier |
| subjects | 60 APPLIED LIFE SCIENCES Aminoglycosides Aminoglycosides - adverse effects Animals Anti-Bacterial Agents - adverse effects ANTIBIOTICS Apoptosis Apoptosis - drug effects Biological and medical sciences CELL PROLIFERATION CREATININE GENE REGULATION Gentamicin Gentamicins - adverse effects Glomerular Filtration Rate Glomerular toxicity GLOMERULI Humans Kidney Diseases - chemically induced Kidney Diseases - metabolism Kidney Diseases - pathology Medical sciences Mesangial cells Mesangial Cells - drug effects Mesangial Cells - pathology NECROSIS Platelet-activating factor Proliferation REVIEWS TOXICITY Toxicology ULTRAFILTRATION |
| title | Glomerular nephrotoxicity of aminoglycosides |
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