Abstract
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.
Highlights
Renal artery stenosis (RAS) is defined as narrowing of the main or branch renal arteries
RAS is associated with a critical decrease in the perfusion pressure of the kidneys that triggers the activation of the renin-angiotensin-aldosterone system (RAAS) with two possible consequences: the occurrence of renovascular hypertension and the development of ischemic nephropathy-defined as a reduction in glomerular filtration rate (GFR) in patients with hemodynamically significant renovascular disease affecting the entire functional renal parenchyma
We considered such indicators to be: hypertension started before age of 30, or after the age of 55, accelerated/malignant/difficult to control hypertension, unexplained renal dysfunction, unexplained atrophic kidney, size discrepancy between kidneys of greater than 1.5 cm, development of new azotemia or worsening renal function after administration of an Angiotensin converting enzyme inhibitor (ACEI) or an Angiotensin II receptor blocker (ARB), systemic atherosclerotic disease, unexplained congestive heart failure, and sudden and unexplained pulmonary edema [29,30]
Summary
Renal artery stenosis (RAS) is defined as narrowing of the main or branch renal arteries. RAS is associated with a critical decrease in the perfusion pressure of the kidneys that triggers the activation of the renin-angiotensin-aldosterone system (RAAS) with two possible consequences: the occurrence of renovascular hypertension and the development of ischemic nephropathy-defined as a reduction in glomerular filtration rate (GFR) in patients with hemodynamically significant renovascular disease affecting the entire functional renal parenchyma This condition has been defined as plasma creatinine concentrations higher than 1.5 mg/dl [3,4,5,6,7].
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