|Darabont Roxana Oana1*, Corlan Alexandru Dan2, Vinereanu Dragos1|
|1University of Medicine and Pharmacy “Carol Davila”, Internal Medicine and Cardiology Department at University Emergency Hospital, Bucharest, Romania|
|2Cardiology Department at University Emergency Hospital, Bucharest, Romania|
|Corresponding Author :||Darabont Roxana Oana
University of Medicine and Pharmacy
Internal Medicine and Cardiology
Department at University Emergency Hospital
Fax: + 40-21-3180576
E-mail: [email protected]
|Received April 30, 2015; Accepted June 26, 2015; Published June 29, 2015|
|Citation: Darabont RO, Corlan AD, Vinereanu D (2015) Renal Artery Stenosis and Acute Pulmonary Edema-A Possible Correlation beyond Pickering Syndrome. J Clin Exp Cardiolog 6:377. doi:10.4172/2155-9880.1000377|
|Copyright: ©2015 Darabont RO, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.|
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Objectives: The association of renal artery stenosis (RAS) with acute pulmonary edema (APE) is considered specific for bilateral or solitary functioning kidney (SFK) RAS. We aimed to check if APE is also associated with unilateral RAS when both kidneys are functional.
Method: A series of 189 patients with uncontrolled hypertension were investigated for RAS suspicion by duplex ultrasonography. Clinical criteria considered in current guidelines as predictors of RAS were recorded and analysed.
Results: Potentially hemodynamically significant RAS (≥ 50%) was identified in 29% of cases (55/189): unilateral in 35 cases (group A), bilateral or on SFK in 20 cases (group B). The remaining 134 were designated controls (group C). Age, blood pressure and gender did not differ between groups. The presence of acute pulmonary edema was higher in both groups of patients with RAS (23%-group A (p<0.01) and 20%-group B vs 8% in control group). The prevalence of azotemia and of azotemia under angiotensin converting enzyme inhibitors or angiotensin II receptor blockers were significantly higher in group B (p<0.01 vs. group A, p<0.00001 vs. control). Linear discriminant analysis based on: age, gender, abdominal bruit, vascular disease, renal dysfunction and azotemia under angiotensin converting inhibitors or angiotensin II receptor blockers, had an accuracy of 0.70 for unilateral RAS, 0.85 for bilateral/SFK RAS, and 0.77 for both. This accuracy was not improved when adding APE as a predictive variable.
Conclusions: In a series of hypertensive patients evaluated for renovascular disease the prevalence of APE is higher in patients with RAS. We have found a significant association of RAS with APE for unilateral RAS. This association, little emphasized until present, might contribute to the clarification of the flash pulmonary edema mechanisms beyond those related to bilateral/SFK RAS.