Key result
Renal artery stenosis was independently associated with elevated plasma marinobufagenin levels, which were partially reversed by stenting (0.77±0.06 nmol/L at baseline to 0.61±0.05 nmol/L at 1 month).
Why the study?
Does renal artery revascularization by stenting reduce plasma marinobufagenin levels in patients with renal artery stenosis?
Observational
Does renal artery revascularization by stenting reduce plasma marinobufagenin levels in patients with renal artery stenosis?
Renal artery stenosis is associated with elevated marinobufagenin levels, which are partially reversed by renal artery stenting, suggesting renal ischemia drives the release of this cardiotonic steroid in humans.
Supports marinobufagenin as ischemia marker in renal artery stenosis; hypothesis-generating and does not support practice change without randomized data.
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.
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Tian et al. (2010) conducted an observational in Renal artery stenosis. Renal artery stenosis vs. Non-RAS controls and healthy individuals was evaluated on Plasma marinobufagenin levels. Renal artery stenosis was independently associated with elevated plasma marinobufagenin levels, which were partially reversed by stenting (0.77±0.06 nmol/L at baseline to 0.61±0.05 nmol/L at 1 month).
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