Journal
HYPERTENSION
Volume 56, Issue 5, Pages 914-919Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/HYPERTENSIONAHA.110.155564
Keywords
renal artery stenosis; hypertension; cardiotonic steroids; marinobufagenin; renal artery stenting
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Funding
- American Heart Association [0980027N]
- National Institute on Aging, National Institutes of Health
- Centocor, Inc
- Cordis Corp
- University of Toledo, Health Sciences Campus, Toledo, Ohio
- National Institutes of Health for the Cardiovascular Outcomes in Renal Atherosclerotic Lesions Study [5U01HL071556-06]
- Cordis Corp for RESIST
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Cardiotonic steroids, including marinobufagenin, are a group of new steroid hormones found in plasma and urine of patients with congestive heart failure, myocardial infarction, and chronic renal failure. In animal studies, partial nephrectomy induces marinobufagenin elevation, cardiac hypertrophy, and fibrosis. The objective of this study is to test the effect of renal ischemia on marinobufagenin levels in humans with renal artery stenosis (RAS). To test this, plasma marinobufagenin levels were measured in patients with RAS of the Prospective Randomized Study Comparing Renal Artery Stenting With or Without Distal Protection, non-RAS patient controls who were scheduled for coronary angiography, and normal healthy individuals. Marinobufagenin levels were significantly higher in patients with RAS compared with those of the other 2 groups. Multivariate analysis shows that occurrence of RAS is independently related to marinobufagenin levels. In addition, renal artery revascularization by stenting partially reversed marinobufagenin levels in the patients with RAS (0.77 +/- 0.06 nmol/L at baseline; 0.66 +/- 0.06 nmol/L at 24 hours; and 0.61 +/- 0.05 nmol/L at 1 month). In conclusion, we have found that marinobufagenin levels are increased in patients with RAS, whereas reversal of renal ischemia by stenting treatment reduces marinobufagenin levels. These results suggest that RAS-induced renal ischemia may be a major cause of marinobufagenin release. (Hypertension. 2010;56:914-919.)
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