Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

Suppression of the Nitric Oxide Pathway in Metastatic Renal Cell Carcinoma Patients Receiving Vascular Endothelial Growth Factor–Signaling Inhibitors

Suppression of the Nitric Oxide Pathway in Metastatic Renal Cell Carcinoma Patients Receiving... Angiogenesis Inhibitors and Hypertension Suppression of the Nitric Oxide Pathway in Metastatic Renal Cell Carcinoma Patients Receiving Vascular Endothelial Growth Factor–Signaling Inhibitors Emily S. Robinson, Eliyahu V. Khankin, Toni K. Choueiri, Mallika S. Dhawan, Miranda J. Rogers, S. Ananth Karumanchi, Benjamin D. Humphreys Abstract—Therapies that target the vascular endothelial growth factor (VEGF) pathway cause hypertension, but the mechanism remains unknown. This cross-sectional study tested the hypothesis that VEGF inhibition causes hypertension by suppressing VEGF-mediated vasodilatory pathways. Urine was collected from 80 patients with metastatic renal cell carcinoma from 2002 to 2009, 40 at baseline and 40 while on VEGF inhibitors. Measured urinary biomarkers include albumin, metabolites of the nitric oxide (NO) pathway and its downstream effector cGMP, and prostaglandin pathway biomarkers prostaglandin E2, 6-keto prostaglandin F1, and cAMP, all normalized to urinary creatinine. The mean age in both groups was 61.8 years, 76% were men, and urinary albumin was higher in patients receiving VEGF inhibitors (median: 18.4 versus 4.6 mg/g; P0.009). cGMP/creatinine was suppressed in patients on VEGF inhibitors (0.28 versus 0.39 pmol/g; P0.01), with a trend toward suppression of nitrate/creatinine (0.46 versus 0.62 mol/mg; P0.09). Both comparisons were strengthened when patients on bevacizumab were excluded, and only those http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Hypertension Wolters Kluwer Health

Suppression of the Nitric Oxide Pathway in Metastatic Renal Cell Carcinoma Patients Receiving Vascular Endothelial Growth Factor–Signaling Inhibitors

Hypertension , Volume 56 (6) – Dec 1, 2010

Loading next page...
 
/lp/wolters-kluwer-health/suppression-of-the-nitric-oxide-pathway-in-metastatic-renal-cell-9T400SGEkt

References (44)

ISSN
0194-911X
eISSN
1524-4563
DOI
10.1161/HYPERTENSIONAHA.110.160481
pmid
20956731
Publisher site
See Article on Publisher Site

Abstract

Angiogenesis Inhibitors and Hypertension Suppression of the Nitric Oxide Pathway in Metastatic Renal Cell Carcinoma Patients Receiving Vascular Endothelial Growth Factor–Signaling Inhibitors Emily S. Robinson, Eliyahu V. Khankin, Toni K. Choueiri, Mallika S. Dhawan, Miranda J. Rogers, S. Ananth Karumanchi, Benjamin D. Humphreys Abstract—Therapies that target the vascular endothelial growth factor (VEGF) pathway cause hypertension, but the mechanism remains unknown. This cross-sectional study tested the hypothesis that VEGF inhibition causes hypertension by suppressing VEGF-mediated vasodilatory pathways. Urine was collected from 80 patients with metastatic renal cell carcinoma from 2002 to 2009, 40 at baseline and 40 while on VEGF inhibitors. Measured urinary biomarkers include albumin, metabolites of the nitric oxide (NO) pathway and its downstream effector cGMP, and prostaglandin pathway biomarkers prostaglandin E2, 6-keto prostaglandin F1, and cAMP, all normalized to urinary creatinine. The mean age in both groups was 61.8 years, 76% were men, and urinary albumin was higher in patients receiving VEGF inhibitors (median: 18.4 versus 4.6 mg/g; P0.009). cGMP/creatinine was suppressed in patients on VEGF inhibitors (0.28 versus 0.39 pmol/g; P0.01), with a trend toward suppression of nitrate/creatinine (0.46 versus 0.62 mol/mg; P0.09). Both comparisons were strengthened when patients on bevacizumab were excluded, and only those

Journal

HypertensionWolters Kluwer Health

Published: Dec 1, 2010

There are no references for this article.