Carvounis and colleagues prospectively compared FEUrea with FENa during 102 episodes of AKI [ARF] due to prerenal azotemia or ATN. They divided the patients into 3 groups: those with prerenal azotemia (n=50), those with prerenal azotemia treated with diuretics (n=27) and those with ATN (n=25).
Bottom-line: low FEUrea (less than 35%) is a more sensitive and specific index than FENa in differentiating between ARF due to prerenal azotemia and that due to ATN, especially if diuretics have been administered. There are on-line calculators for FEUrea on the internet.
(ps: Nate Hellman had a nice post on FENa in the Renal Fellow Network that is worth looking at also).
Hi Dr Singh
ReplyDeleteI agree that FE Urea is quite useful, especially when a patient has recently received loop diuretics. However, I am not totally convinced about the evidenc. Two other studies did not report results as impressive as the initial report you have quoted (http://www.ncbi.nlm.nih.gov/pubmed/19887835 and http://www.ncbi.nlm.nih.gov/pubmed/17900456). Secondly, I call reading that sepsis may interfere with urea transport and hence in these cases of AKI, the FE Urea may not be as useful as FE NA (as reported in Http://www.ncbi.nlm.nih.gov/pubmed/21794161).
Your thoughts would be appreciated.
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Lovastatin combined cholangiocarcinoma cell line QBC939 KRN633 on biological behavior of
ReplyDeleteObjective To study the lovastatin (Lovastatin) combined with vascular endothelial growth factor receptor tyrosine kinase inhibitor (KRN633) on human cholangiocarcinoma cell line QBC939 growth, migration, apoptosis, and other biological behavior.
Methods tetrazolium salt (MTT) assay the role of various drug concentrations 24 h, 48 h, 72 h after cell proliferation; inverted microscope morphological changes; cell apoptosis was detected by flow cytometry; experimental observation of cell migration cell scratch the ability to change; RT-PCR assay before and after drug myeloid leukemia -1 (Mcl-1), a serine / threonine protein kinase B (Akt), tumor necrosis factor-related apoptosis-inducing ligand body (TRAIL), vascular endothelial growth factor (VEGF) expression.
Results lovastatin, KRN633 QBC939 significantly inhibited cell proliferation (P <0.01) in a concentration - time-dependent, lovastatin joint KRN633 synergistic inhibitory effect (F = 8.85, P <0.05). Drugs can be observed QBC939 cells showed morphological changes of apoptosis; flow cytometry showed that apoptosis was significantly increased (37.5 ± 1.92%, 32.14 ± 1.30% vs. 11.23 ± 1.26%, F = 250.04, P <0.01). Combination group cells 24 h, 48 h average migration rate slowed down (respectively 1.21 ± 0.68 and 1.52 ± 0.19, P <0.05). Proliferation, apoptosis, migration-related genes Mcl-1, Akt, VEGF mRNA expression was significantly lower than the control group (P <0.05).
Conclusion Lovastatin inhibits cholangiocarcinoma cell proliferation, migration and induce apoptosis, combined with KRN633 synergistic inhibitory effect.
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