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10.1111/bcp.12282 http://scihub22266oqcxt.onion/10.1111/bcp.12282 C4093920!4093920!24219059     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Br+J+Clin+Pharmacol 2014 ; 77 (6): 947-57 Nephropedia Template TP {{tp|p=24219059|t=2014. Urinary kidney biomarkers for early detection of nephrotoxicity in clinical drug development |pdf=|usr=}}{{24219059}} gab.com Text Urinary kidney biomarkers for early detection of nephrotoxicity in clinical drug development JO: Br J Clin Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=24219059 #FOAvip Early detection of drug-induced kidney injury is vital in drug development. Generally accepted biomarkers such as creatinine and blood urea nitrogen (BUN) lack sensitivity and early injury responses are missed. Many new biomarkers to detect nephrotoxicity for pre-clinical utilization have been described and their use is adopted in regulatory guidelines. However, guidance on appropriate biomarkers for clinical trials is minimal. We provide an overview of potentially useful kidney biomarkers that can be used in clinical trials. This includes guidance to select biomarkers suitable to capture specific characteristics of the (expected) kidney injury. We conclude that measurement of urinary kidney injury marker-1 (KIM-1) serves many purposes and is often an appropriate choice. Cystatin C captures effects on glomerular filtration rate (GFR), but this marker should preferably be combined with more specific markers to localize the origin of the observed effect. Untoward effects on tubules can be captured relatively well with several markers. Direct detection of glomerular injury is currently impossible since specific biomarkers are lacking. Indirect assessment of toxic effects on glomeruli is possible by using carefully selected panels of other injury markers. We conclude that it is possible to obtain appropriate information on nephrotoxicity in clinical drug development by using carefully selected panels of injury markers and suggest that identification and validation of specific glomerular biomarkers could be of great value. Twit Text FOAVip Urinary kidney biomarkers for early detection of nephrotoxicity in clinical drug development ????Br J Clin Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=24219059 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24219059 #FOAvip English Wikipedia <ref>{{Cite pmid|24219059}}</ref> Urinary kidney biomarkers for early detection of nephrotoxicity in clinical drug development #MMPMID24219059 van Meer L; Moerland M; Cohen AF; Burggraaf J Br J Clin Pharmacol 2014[Jun]; 77 (6): 947-57 PMID24219059show ga Early detection of drug-induced kidney injury is vital in drug development. Generally accepted biomarkers such as creatinine and blood urea nitrogen (BUN) lack sensitivity and early injury responses are missed. Many new biomarkers to detect nephrotoxicity for pre-clinical utilization have been described and their use is adopted in regulatory guidelines. However, guidance on appropriate biomarkers for clinical trials is minimal. We provide an overview of potentially useful kidney biomarkers that can be used in clinical trials. This includes guidance to select biomarkers suitable to capture specific characteristics of the (expected) kidney injury. We conclude that measurement of urinary kidney injury marker-1 (KIM-1) serves many purposes and is often an appropriate choice. Cystatin C captures effects on glomerular filtration rate (GFR), but this marker should preferably be combined with more specific markers to localize the origin of the observed effect. Untoward effects on tubules can be captured relatively well with several markers. Direct detection of glomerular injury is currently impossible since specific biomarkers are lacking. Indirect assessment of toxic effects on glomeruli is possible by using carefully selected panels of other injury markers. We conclude that it is possible to obtain appropriate information on nephrotoxicity in clinical drug development by using carefully selected panels of injury markers and suggest that identification and validation of specific glomerular biomarkers could be of great value. äUrinary kidney biomarkers for early detection of nephrotoxicity in cli(epmc).pdf DeepDyve Pubget Overpricing