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10.1152/ajprenal.00682.2014 http://scihub22266oqcxt.onion/10.1152/ajprenal.00682.2014 C4556889!4556889!26084933     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Renal+Physiol 2015 ; 309 (5): F406-13 Nephropedia Template TP {{tp|p=26084933|t=2015. Molecular phenotyping of clinical AKI with novel urinary biomarkers |pdf=|usr=}}{{26084933}} gab.com Text Molecular phenotyping of clinical AKI with novel urinary biomarkers JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26084933 #FOAvip Acute kidney injury (AKI) is a common hospital complication. There are no effective treatments to minimize kidney injury or limit associated morbidity and mortality. Currently, serum creatinine and urine output remain the gold standard used clinically in the diagnosis of AKI. Several novel biomarkers can diagnose AKI earlier than elevations of serum creatinine and changes in urine output. Recent long-term observational studies have elucidated a subgroup of patients who have positive biomarkers of AKI but do not meet criteria for AKI by serum creatinine or urine output, termed subclinical AKI. These patients with subclinical AKI have increased risk of both short- and long-term mortality. In this review, we will highlight the implications of what these patients may represent and the need for better phenotyping of AKI by etiology, severity of injury, and ability to recover. We will discuss two AKI biomarkers, neutrophil gelatinase-associated lipocalin (NGAL) and breast regression protein-39 (BRP-39)/YKL-40, that exemplify the need to characterize the complexity of the biological meaning behind the biomarker, beyond elevated levels reporting on tissue injury. Ultimately, careful phenotyping of AKI will lead to identification of therapeutic targets and appropriate patient populations for clinical trials. Twit Text FOAVip Molecular phenotyping of clinical AKI with novel urinary biomarkers ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26084933 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26084933 #FOAvip English Wikipedia <ref>{{Cite pmid|26084933}}</ref> Molecular phenotyping of clinical AKI with novel urinary biomarkers #MMPMID26084933 Huen SC; Parikh CR Am J Physiol Renal Physiol 2015[Sep]; 309 (5): F406-13 PMID26084933show ga Acute kidney injury (AKI) is a common hospital complication. There are no effective treatments to minimize kidney injury or limit associated morbidity and mortality. Currently, serum creatinine and urine output remain the gold standard used clinically in the diagnosis of AKI. Several novel biomarkers can diagnose AKI earlier than elevations of serum creatinine and changes in urine output. Recent long-term observational studies have elucidated a subgroup of patients who have positive biomarkers of AKI but do not meet criteria for AKI by serum creatinine or urine output, termed subclinical AKI. These patients with subclinical AKI have increased risk of both short- and long-term mortality. In this review, we will highlight the implications of what these patients may represent and the need for better phenotyping of AKI by etiology, severity of injury, and ability to recover. We will discuss two AKI biomarkers, neutrophil gelatinase-associated lipocalin (NGAL) and breast regression protein-39 (BRP-39)/YKL-40, that exemplify the need to characterize the complexity of the biological meaning behind the biomarker, beyond elevated levels reporting on tissue injury. Ultimately, careful phenotyping of AKI will lead to identification of therapeutic targets and appropriate patient populations for clinical trials. äMolecular phenotyping of clinical AKI with novel urinary biomarkers (epmc).pdf DeepDyve Pubget Overpricing