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Renal Artery Stenosis and Acute Pulmonary Edema-A Possible Correlation beyond Pickering Syndrome

Roxana Oana Darabont, Alexandru Dan Corlan, Dragos Vinereanu,

Journal of Clinical & Experimental Cardiology 6:6-6, 2015


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.

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