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Nephrotoxicity: Role and significance of renal biomarkers in the early detection of acute renal injury
Nephrotoxicity is defining as rapid deterioration in the kidney function due to toxic effect of medications and chemicals. There are various forms, and some drugs may affect renal function in more than one way. Nephrotoxins are substances displaying nephrotoxicity. Different mechanisms lead to nephr...
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Published in: | Journal of advanced pharmaceutical technology and research 2019-07, Vol.10 (3), p.95-99 |
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creator | Al-Naimi, Marwa Rasheed, Huda Hussien, Nawar Al-Kuraishy, Hayder Al-Gareeb, Ali |
description | Nephrotoxicity is defining as rapid deterioration in the kidney function due to toxic effect of medications and chemicals. There are various forms, and some drugs may affect renal function in more than one way. Nephrotoxins are substances displaying nephrotoxicity. Different mechanisms lead to nephrotoxicity, including renal tubular toxicity, inflammation, glomerular damage, crystal nephropathy, and thrombotic microangiopathy. The traditional markers of nephrotoxicity and renal dysfunction are blood urea and serum creatinine which are regarded as low sensitive in the detection of early renal damage. Thus, the detection of the initial renal injures required new biomarkers which are more sensitive and highly specific that gives an insight into the site of underlying renal damage. Kidney injury molecule-1, Cystatin C, and neutrophil gelatinase-associated lipocalin sera levels are more sensitive than blood urea and serum creatinine in the detection of acute kidney injury during nephrotoxicity. |
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There are various forms, and some drugs may affect renal function in more than one way. Nephrotoxins are substances displaying nephrotoxicity. Different mechanisms lead to nephrotoxicity, including renal tubular toxicity, inflammation, glomerular damage, crystal nephropathy, and thrombotic microangiopathy. The traditional markers of nephrotoxicity and renal dysfunction are blood urea and serum creatinine which are regarded as low sensitive in the detection of early renal damage. Thus, the detection of the initial renal injures required new biomarkers which are more sensitive and highly specific that gives an insight into the site of underlying renal damage. Kidney injury molecule-1, Cystatin C, and neutrophil gelatinase-associated lipocalin sera levels are more sensitive than blood urea and serum creatinine in the detection of acute kidney injury during nephrotoxicity.</description><identifier>ISSN: 2231-4040</identifier><identifier>EISSN: 0976-2094</identifier><identifier>DOI: 10.4103/japtr.JAPTR_336_18</identifier><identifier>PMID: 31334089</identifier><language>eng</language><publisher>India: Wolters Kluwer India Pvt. Ltd</publisher><subject>Adefovir dipivoxil ; Angiotensin II ; Biological markers ; Biomarkers ; Creatinine ; Cystatin C ; Cytotoxicity ; Drug dosages ; Gelatinase ; glomerular damage ; Heart failure ; Homeostasis ; Kidney diseases ; Kidneys ; Lipocalin ; Metabolites ; Nephropathy ; nephrotoxicity ; Nonsteroidal anti-inflammatory drugs ; Pamidronate ; Patients ; Prevention ; Proteins ; Renal function ; Review ; Thrombotic microangiopathy ; Toxicity ; Urea ; Urine ; Valsartan</subject><ispartof>Journal of advanced pharmaceutical technology and research, 2019-07, Vol.10 (3), p.95-99</ispartof><rights>COPYRIGHT 2019 Medknow Publications and Media Pvt. Ltd.</rights><rights>2019. This work is published under https://creativecommons.org/licenses/by-nc-sa/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Copyright: © 2019 Journal of Advanced Pharmaceutical Technology & Research 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c623o-67e30746d0b3d01c4e49e2cce317537210bdb0a16b6b41a9413d74c6651794633</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6621352/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6621352/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,886,27926,27927,53793,53795</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31334089$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Al-Naimi, Marwa</creatorcontrib><creatorcontrib>Rasheed, Huda</creatorcontrib><creatorcontrib>Hussien, Nawar</creatorcontrib><creatorcontrib>Al-Kuraishy, Hayder</creatorcontrib><creatorcontrib>Al-Gareeb, Ali</creatorcontrib><title>Nephrotoxicity: Role and significance of renal biomarkers in the early detection of acute renal injury</title><title>Journal of advanced pharmaceutical technology and research</title><addtitle>J Adv Pharm Technol Res</addtitle><description>Nephrotoxicity is defining as rapid deterioration in the kidney function due to toxic effect of medications and chemicals. There are various forms, and some drugs may affect renal function in more than one way. Nephrotoxins are substances displaying nephrotoxicity. Different mechanisms lead to nephrotoxicity, including renal tubular toxicity, inflammation, glomerular damage, crystal nephropathy, and thrombotic microangiopathy. The traditional markers of nephrotoxicity and renal dysfunction are blood urea and serum creatinine which are regarded as low sensitive in the detection of early renal damage. Thus, the detection of the initial renal injures required new biomarkers which are more sensitive and highly specific that gives an insight into the site of underlying renal damage. Kidney injury molecule-1, Cystatin C, and neutrophil gelatinase-associated lipocalin sera levels are more sensitive than blood urea and serum creatinine in the detection of acute kidney injury during nephrotoxicity.</description><subject>Adefovir dipivoxil</subject><subject>Angiotensin II</subject><subject>Biological markers</subject><subject>Biomarkers</subject><subject>Creatinine</subject><subject>Cystatin C</subject><subject>Cytotoxicity</subject><subject>Drug dosages</subject><subject>Gelatinase</subject><subject>glomerular damage</subject><subject>Heart failure</subject><subject>Homeostasis</subject><subject>Kidney diseases</subject><subject>Kidneys</subject><subject>Lipocalin</subject><subject>Metabolites</subject><subject>Nephropathy</subject><subject>nephrotoxicity</subject><subject>Nonsteroidal anti-inflammatory drugs</subject><subject>Pamidronate</subject><subject>Patients</subject><subject>Prevention</subject><subject>Proteins</subject><subject>Renal function</subject><subject>Review</subject><subject>Thrombotic microangiopathy</subject><subject>Toxicity</subject><subject>Urea</subject><subject>Urine</subject><subject>Valsartan</subject><issn>2231-4040</issn><issn>0976-2094</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNp9kl1v0zAUhi0EYlXZH-ACReKGmxR_J-ECqapgDE2ApnFtOc5J6za1i-NQ-u_nrl21IkR8Ecl-zmOfoxeh1wRPOMHs_VJvYph8nf64u1WMSUXKZ2iEq0LmFFf8ORpRykjOMccX6LLvlzh9rKIFFS_RBSOMcVxWI9R-g80i-Oj_WGPj7kN26zvItGuy3s6dba3RzkDm2yyA011WW7_WYQWhz6zL4gIy0KHbZQ1EMNF6t0e1GSIcC6xbDmH3Cr1oddfD5fE_Rj8_f7qbfclvvl9dz6Y3uZGU-VwWwHDBZYNr1mBiOPAKqDHASCFYQQmumxprImtZc6IrTlhTcCOlIEXFJWNjdH3wNl4v1SbY9Nid8tqqhw0f5kqHaE0HqhQaalaThpEyKYRmJPkETcM0JScmuT4eXJuhXkNjwMWguzPp-YmzCzX3v5WUlLAkGqN3R0Hwvwboo1rb3kDXaQd-6BWlktN0IxUJffsXuvRDSPPbU6IsqeCpvRM116kB61qf7jV7qZqKilIiJa8SNfkHlVYDa2u8g9am_bMCeigwwfd9gPbUI8FqHzb1EDb1NGyp6M3T6ZxKHqOVgNkB2PouprysumELQSV25fz2P2pVCfWYSnYPyM7niQ</recordid><startdate>20190701</startdate><enddate>20190701</enddate><creator>Al-Naimi, Marwa</creator><creator>Rasheed, Huda</creator><creator>Hussien, Nawar</creator><creator>Al-Kuraishy, Hayder</creator><creator>Al-Gareeb, Ali</creator><general>Wolters Kluwer India Pvt. 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There are various forms, and some drugs may affect renal function in more than one way. Nephrotoxins are substances displaying nephrotoxicity. Different mechanisms lead to nephrotoxicity, including renal tubular toxicity, inflammation, glomerular damage, crystal nephropathy, and thrombotic microangiopathy. The traditional markers of nephrotoxicity and renal dysfunction are blood urea and serum creatinine which are regarded as low sensitive in the detection of early renal damage. Thus, the detection of the initial renal injures required new biomarkers which are more sensitive and highly specific that gives an insight into the site of underlying renal damage. Kidney injury molecule-1, Cystatin C, and neutrophil gelatinase-associated lipocalin sera levels are more sensitive than blood urea and serum creatinine in the detection of acute kidney injury during nephrotoxicity.</abstract><cop>India</cop><pub>Wolters Kluwer India Pvt. 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subjects | Adefovir dipivoxil Angiotensin II Biological markers Biomarkers Creatinine Cystatin C Cytotoxicity Drug dosages Gelatinase glomerular damage Heart failure Homeostasis Kidney diseases Kidneys Lipocalin Metabolites Nephropathy nephrotoxicity Nonsteroidal anti-inflammatory drugs Pamidronate Patients Prevention Proteins Renal function Review Thrombotic microangiopathy Toxicity Urea Urine Valsartan |
title | Nephrotoxicity: Role and significance of renal biomarkers in the early detection of acute renal injury |
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