Impact Of Renal Artery Stenosis Research Articles

The prevalence and impact of renal artery stenosis in patients undergoing TAVI

The prevalence and impact of renal artery stenosis in patients undergoing TAVI

Impact of renal artery stenosis on acute kidney injury and outcomes after heart failure hospitalization

BackgroundRenal artery stenosis (RAS) is known to co-exist with heart failure (HF), however the impact of RAS on rates of acute kidney injury during an acute HF hospitalization, and adverse events after acute HF hospitalizations has not been well studied. MethodsWe performed a retrospective cohort study of subjects hospitalized for acute HF at a tertiary academic care center. We identified subjects who had a renal artery duplex ultrasound or other diagnostic study for RAS to categorize heart failure subjects as RAS+ or RAS-. AKI was defined as a rise from admission to peak creatinine of >0.3 mg/dL or >1.5 fold. In-hospital outcomes including rates of AKI were ascertained. Adverse outcomes over a two-year follow up period were also ascertained. ResultsA total of 93 subjects with acute HF hospitalization met the inclusion criteria and were enrolled in this study; 27 (29%) were identified as RAS+. At admission, subjects with RAS had higher rates of diabetes and prior PCI. During the HF hospitalization, subjects with RAS were more likely to develop AKI. No significant differences were identified in baseline or hospital medication use among subjects with versus without RAS. Importantly, the rate of ACE-I/ARB use was low in both groups and no significant difference in ACE-I/ARB use was demonstrated. Subjects with RAS had higher rates of recurrent HF hospitalization during the follow-up period. ConclusionsRAS is prevalent among subjects with acute HF, associated with higher rates of AKI during HF hospitalization, and associated with higher rates of recurrent HF hospitalization during follow-up.

Renal Ultrasound (and Doppler Sonography) in Hypertension: An Update.

Ultrasound (US) allows the non-invasive evaluation of morphological changes of kidney structure (by means of B-Mode) and patterns of renal and extrarenal vascularization (by means of color-Doppler and contrast-enhanced US). In hypertensive subjects it offers a relevant contribution to the diagnosis of early renal damage, acute or chronic nephropathies and nephrovascular disease. However, morphological changes are often detected late and non-specific and in recent years evidence has increased regarding the clinical relevance of renal resistive index (RRI) for the study of vascular and renal parenchymal renal abnormalities. RRI is measured by Doppler sonography in an intrarenal artery, as the difference between the peak systolic and end-diastolic blood velocities divided by the peak systolic velocity. At first RRI was proved to be a marker of renal disease onset and progression; later the influence of systemic vascular properties on RRI was shown and authors claimed its use as an independent predictor of cardiovascular risk rather than of renal damage. Indeed, renal vascular resistance is only one of several renal (vascular compliance, interstitial and venous pressure), and extrarenal (heart rate, pulse pressure) determinants that concur to determine RRI individual values but not the most important one. The clinical relevance of RRI measurement as a surrogate endpoint of specific renal damage or/and as surrogate endpoint of atherosclerotic diffuse vascular damage is still debated.To summarize, from the literature: (a) In hypertensives with normal renal function and no albuminuria, especially in younger people, RRI is an early marker of renal damage that is especially useful when hypertension and diabetes concur in the same subjects. In these subjects RRI could improve current clinical scores used to stratify early renal damage. In older subjects RRI increases in accordance with the increase in systemic vascular stiffness and, because of this close relationship, RRI is also a marker of systemic atherosclerotic burden and the role of renal determinants can weaken. The clinical relevance was not specifically investigated. (b) In transplant kidney and in chronic renal disease high (>0.80) RRI values can independently predict renal failure. The recent claim that systemic (pulse pressure) rather than renal hemodynamic determinants sustain this predictive role of RRI, does not significantly reduce this predictive role of RRI. (c) Doppler ultrasound allows diagnosis and grading of renal stenosis in both fibromuscolar dysplastic and atherosclerotic diseases. Moreover, by RRI assay Doppler ultrasound can indirectly measure the hemodynamic impact of renal artery stenosis on the homolateral kidney, by virtue of the stenosis-related decrease in pulse pressure. However, in elderly subjects with atherosclerotic renal artery stenosis coexisting renal diseases can independently increase RRI by the augmentation in renal vascular stiffness and tubulo-interstitial pressure and hidden changes due to renal artery stenosis.

The internist and the renal resistive index: truths and doubts.

The renal resistive index (RRI) is measured by Doppler sonography in an intrarenal artery, and is the difference between the peak systolic and end-diastolic blood velocities divided by the peak systolic velocity. The RRI is used for the study of vascular and renal parenchymal renal abnormalities, but growing evidence indicates that it is also a dynamic marker of systemic vascular properties. Renal vascular resistance is only one of several renal (vascular compliance, interstitial and venous pressure), and extrarenal (heart rate, aortic stiffness, pulse pressure) determinants that combine to determine the RRI values, and not the most important one. RRI cannot always be considered a specific marker of renal disease. To summarize from the literature: (1) hydronephrosis, abdominal hypertension, renal vein thrombosis and acute kidney injury are all associated with an acute increase in interstitial and venous pressure that determine RRI values. In all these conditions, RRI is a reliable marker of the severity of renal damage. (2) The hemodynamic impact of renal artery stenosis can be assayed by the RRI decrease in the homolateral kidney by virtue of decreasing pulse pressure. However, renal diseases that often coexist, increase renal vascular stiffness and hide the hemodynamic effect of renal stenosis. (3) In transplant kidney and in chronic renal disease, high RRI values (>0.80) can independently predict renal and clinical outcomes, but systemic (pulse pressure) rather than renal hemodynamic determinants sustain the predictive role of RRI. (4) Higher RRI detects target renal organ damage in hypertension and diabetes when renal function is still preserved, as a marker of systemic atherosclerotic burden. Is this the fact? We attempt to answer.

The Impact of Renal Artery Stenosis on Outcomes After Open-Heart Surgery

The aim of this study was to assess the impact of atherosclerotic renal artery stenosis (ARAS) on outcomes after open-heart surgery (OHS). Acute kidney injury after OHS portends significant morbidity and mortality. Data from all adult patients undergoing OHS from January 2000 to April 2010 who underwent renal duplex ultrasound were prospectively collected. ARAS was severe (60% to 99% stenosis) if peak systolic velocity was >200cm/s. The associations between ARAS and post-operative reduction in glomerular filtration rate (GFR), need for renal replacement therapy, length of stay, and overall short-term and long-term mortality (up to 8 years) were tested using multivariate time-to-event adjusted analysis. A total of 714 patients were evaluated, with a mean age of 67 ± 12 years (63% men) and a mean GFR of 52±25.9ml/min/1.73 m(2). A total of 206 (29%) had ARAS; of these, 79% (n= 163) had unilateral and 21% (n=43)had bilateral ARAS. ARAS was associated with peripheral artery disease (p= 0.004) and lower high-density lipoprotein levels (p= 0.04). Patients with advanced age (p= 0.01) and descending aorta grafting (p= 0.004) had significant post-operative reductions in GFR. Adjusted models showed a nonsignificant trend between ARAS and reduction inGFR (p= 0.09). ARAS was not associated with need for renal replacement therapy (p= 0.4), longer length of stay(p=0.7), or mortality (p= 0.7), but low pre-operative GFR was a strong predictor of long-term mortality. ARAS does not appear to be associated with post-operative change in GFR, need for hemodialysis, longer length of stay, or mortality in patients undergoing OHS.

Comprehensive Renal Artery Stenosis Management by Nephrology: A More Selective Approach

The impact of renal artery stenosis (RAS) and resulting ischemic nephropathy on kidney function has been well described. Based on several recent randomized, multicenter trials that revealed limitations to the utility of nonselective renal artery intervention, the general nephrology community has recently taken a conservative stance on this disease state. The purpose of this report is to summarize some recent contributions to our understanding of renal artery stenosis, which may cast RAS intervention in a new light.

Critical review of indications for renal artery stenting: Do randomized trials give the answer?

Significant renal artery stenosis (RAS) is a well accepted cause of deterioration of arterial hypertension and of renal insufficiency. Just recently, more interest has been focused on the impact of RAS on structural heart disease and patient survival. Technical improvements of diagnostic and interventional endovascular tools have lead to a more widespread use of endoluminal renal artery revascularization and extension of the indications for this type of therapy during the past 2 decades. Since the first renal artery angioplasties performed by Felix Mahler and Andreas Grüntzig, numerous single centre studies have reported the beneficial effect of percutaneous transluminal renal angioplasty, and since the early 1990's stenting of renal artery stenosis caused either by atherosclerosis or fibromuscular dysplasia. However, none of the so far published or presented randomized controlled trials (RCT) could prove a beneficial outcome of RAS revascularization compared with medical management. As a result of these negative trials including the recently presented ASTRAL trial, referrals to endovascular renal artery revascularization went down and moreover, reimbursement of these procedures became a matter of debate. This article summarizes the background and the limitations of the so far published and still ongoing controlled trials. Moreover, we discuss why well-designed registries might give important insight on the impact of endovascular revascularization of hemodynamically relevant atherosclerotic RAS.

Clinical Outcome in Patients With Peripheral Artery Disease and Renal Artery Stenosis

There is controversy on the influence of renal artery stenosis on outcome in patients with peripheral artery disease. The 12-month impact of renal artery stenosis on declining renal function, control of hypertension, and incidence of major cardiovascular events in 100 consecutive patients undergoing angiography for peripheral artery disease was evaluated. A total of 60 patients had renal artery stenosis: 32 mild, 16 moderate, and 12 severe stenosis. There were no significant differences in either the decline of renal function (2.7 +/- 18% vs 0.9 +/- 16%), control of hypertension (139 +/- 16 vs 139 +/- 22 mm Hg) or number of antihypertensive drugs (1.8 +/- 1.0 vs 1.6 +/- 0.8). Patients with renal artery stenosis had an increased incidence of major cardiovascular events (odds ratio: 2.3; 95% confidence interval: 1.03-5.4), but on multivariate analysis its influence disappeared. Patients with peripheral artery disease having renal artery stenosis had similar decline of renal function and control of hypertension. They had an increased incidence of major cardiovascular events, but it may be explained by the confounding effect of additional variables.

Prevalence and Outcome of Renal Artery Stenosis in Atherosclerotic Patients with Renal Dysfunction.

We investigated the prevalence of renal artery disease and outcome in a cohort of atherosclerotic patients with renal dysfunction. We studied 44 consecutive patients who were older than 50 years of age, who had renal dysfunction and in whom one or more of the following atherosclerotic diseases was confirmed: cerebral infarction, coronary artery disease or peripheral vascular disease. Renal artery stenosis was assessed by gadolinium-enhanced magnetic-resonance angiography. Patients who were treated medically were prospectively followed up in our outpatient clinic and the impact of renal artery stenosis on survival was evaluated. Renal artery stenosis was found in 22 (50%) of the 44 patients. Difference in kidney length and carotid artery stenosis were identified as independent predictors of renal artery stenosis. Among the patients who were treated medically (n=42), rates of mortality were 4.4, 12.7 and 18.1 per 100 patient-years in those without renal artery stenosis, those with unilateral renal artery stenosis and those with bilateral renal artery stenosis, respectively. The mortality and renal survival curves were significantly different among these three groups. These findings indicate that renal artery stenosis is common in patients with renal dysfunction and concomitant cardiovascular disease, especially in those with carotid artery stenosis, and that a substantial difference in the length of kidneys may be a predictor of renovascular disease. Patients with renal dysfunction resulting from renal artery stenosis are at risk of death from cardiovascular disease and end-stage renal failure.

Severity of renal vascular disease predicts mortality in patients undergoing coronary angiography

Renal artery stenosis (RAS) is a relatively uncommon but potentially reversible cause of renal failure. In a previous report, we demonstrated that the presence of RAS is independently associated with mortality in a group of patients undergoing coronary angiography. Our current study expands on this cohort, investigating the effect of the severity of RAS on all-cause mortality. A total of 3987 patients underwent abdominal aortography immediately following coronary angiography. For the purpose of survival analysis, significant RAS was defined as > or =75% narrowing in the luminal diameter. Significant RAS was present in 4.8% of patients studied and was bilateral in 0.8%. Factors associated with the presence of RAS included female gender, older age, hypertension, congestive heart failure, elevated serum creatinine, and congestive heart failure. The four-year unadjusted survivals for patients with and without significant RAS were 57 and 89%, respectively (P < 0.001). Using the Cox proportional hazards model, the factors independently associated with decreased survival were the presence of RAS, increased age, the severity of coronary artery disease, the presence of comorbid disease, reduced ejection fraction, symptoms of congestive cardiac failure, and the mode of treatment of coronary artery disease. In the multivariate model, the presence of RAS conferred a hazard ratio of 2.01 (95% CI, 1.51 to 2.67, P < 0.001). We demonstrated an incremental effect on mortality according to the severity of RAS at baseline. Four-year adjusted survival for patients with 50%, 75%, and > or =95% stenosis was 70%, 68%, and 48%, respectively. In addition, bilateral disease was associated with four-year survival of 47% as compared with 59% for patients with unilateral disease (P < 0.001). The impact of RAS on survival remained robust regardless of the manner of treatment of coronary artery disease [that is, medical, percutaneous transluminal coronary angioplasty (PTCA), or coronary artery bypass graft (CABG)]. In this patient population, the presence of RAS is a strong independent predictor of mortality. Increasing severity of RAS has an incremental effect on survival probability.