Prevalence of renal artery stenosis in subjects with type 2 diabetes and coexistent hypertension.

Valabhji, Jonathan; Robinson, Sam; Poulter, C; Robinson, A. C. J.; Chen, Kong; Henzen, Christoph; Gedroyc, W.; Feher, Michael; Elkeles, R. S.

doi:10.2337/diacare.23.4.539

Cited by 56 publications

(29 citation statements)

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“…We performed systematic RA in consecutive AMI patients, regardless of other risk factors suggesting RAS (severe hypertension, PAD, or abdominal bruits). Data showed concordant values of RAS prevalence in AMI (16.6%) to those reported in well‐recognized risk groups (suspected renovascular hypertension5, 30—14.1%, hypertension and diabetes mellitus31—17.1%, chronic CAD5, 32, 33—9.1% to 10.8%) but lower values than in patients with chronic heart failure34—54.1%, aortic abdominal aneurysm35—38%, end‐stage renal disease36—40.8%. Differences between reports are driven by inclusion of patients with different stages of atheromatous disease and inflammation.…”

Section: Discussionsupporting

confidence: 64%

Atherosclerotic Renal Artery Stenosis Prevalence and Correlations in Acute Myocardial Infarction Patients Undergoing Primary Percutaneous Coronary Interventions: Data From Nonrandomized Single‐Center Study (REN‐ACS)—A Single Center, Prospective, Observational Study

Burlacu¹,

Siriopol

Voroneanu

et al. 2015

JAHA

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BackgroundWe are the first to evaluate the prevalence of renal artery stenosis (RAS) in consecutive patients with acute myocardial infarction (AMI) referred for primary percutaneous coronary intervention from a single tertiary center. As a novelty, we assessed hydration and metabolic status and measured arterial stiffness. We elaborated a predicting model for RAS in AMI.Methods and ResultsOne hundred and eighty‐one patients with AMI underwent concomitantly primary percutaneous coronary intervention and renal angiography. We obtained data on demographics, medical history, cardiovascular risk factors, echocardiography, Killip class, and blood tests. In the first 24 hours post–primary percutaneous coronary intervention, we assessed bioimpedance through Body Composition Monitoring® and arterial stiffness through pulsed‐wave velocity, SphygmoCor®. Significant RAS (>50% lumen narrowing, RAS+) was present in 16.6% patients. In the RAS+ group we recorded significantly higher stiffness, CRUSADE score and dehydration, and more women with higher prevalence of multivascular coronary artery disease and heart failure. In our multivariate models, variables independently associated with RAS+ were previous percutaneous coronary intervention, low estimated glomerular filtration rate, multivascular coronary artery disease, and total/extracellular body water. These models had good specificity and low sensitivity.ConclusionsWe observed that RAS+ AMI patients have a particular hydration, metabolic, and endothelial profile that could generate more future major adverse cardiac events. Hence, renal angiography in AMI should be considered in specific subsets of patients.Clinical Trial Registration URL: https://www.clinicaltrials.gov/. Unique identifier: NCT02388139.

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Section: Discussionsupporting

confidence: 64%

Atherosclerotic Renal Artery Stenosis Prevalence and Correlations in Acute Myocardial Infarction Patients Undergoing Primary Percutaneous Coronary Interventions: Data From Nonrandomized Single‐Center Study (REN‐ACS)—A Single Center, Prospective, Observational Study

Burlacu¹,

Siriopol

Voroneanu

et al. 2015

JAHA

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“…2 The complexity of the management of RVH raises a pressing need for an in vivo imaging technique that cannot only demonstrate reduced blood flow to the organ but also detect and monitor renal ischemia at the molecular level. [3][4][5][6] Magnetic resonance (MR) angiography (MRA) and computed tomography angiography are oriented toward depicting anatomy rather than tissue injury. 7,8 Radionuclide captopril renography has not been widely accepted 9 because of its limited accuracy in the presence of bilateral disease 10 or therapy with ACE inhibitors.…”

mentioning

confidence: 99%

Positron-Emission Tomography Imaging of the Angiotensin II Subtype 1 Receptor in Swine Renal Artery Stenosis

Xia¹,

Seckin²,

Xiang³

et al. 2008

Hypertension

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Abstract-The angiotensin II subtype 1 receptor (AT 1 R) has been linked to the development and progression of renovascular hypertension. In this study we applied a pig model of renovascular hypertension to investigate the AT 1 R in vivo with positron-emission tomography (PET) and in vitro with quantitative autoradiography. AT 1 R PET measurements were performed with the radioligand [ 11 C]KR31173 in 11 control pigs and in 13 pigs with hemodynamically significant renal artery stenosis; 4 were treated with lisinopril for 2 weeks before PET imaging. The radioligand impulse response function was calculated by deconvolution analysis of the renal time-activity curves. Key Words: positron-emission tomography Ⅲ angiotensin AT 1 receptor Ⅲ swine Ⅲ animal models Ⅲ renovascular hypertension R enovascular hypertension is the most common type of secondary hypertension that occurs in 2 to 4 million people in the United States. The renin-angiotensin system and its component, the angiotensin II subtype 1 receptor (AT 1 R), have been tightly linked to the development and progression of renovascular hypertension (RVH), but experimental mechanistic evidence for regulation of the AT 1 R has not been established in vivo. Antagonists against the angiotensin-converting enzyme (ACE; ACE inhibitors) or the AT 1 R (angiotensin receptor blockers) continue to play a key role in the therapy of renal hypertension and other kidney diseases. 1 Both drugs represent a "doubleedged sword," because they may deactivate regulatory effects of the renin-angiotensin system and the AT 1 R and trigger irreversible renal damage. 2 The complexity of the management of RVH raises a pressing need for an in vivo imaging technique that cannot only demonstrate reduced blood flow to the organ but also detect and monitor renal ischemia at the molecular level. [3][4][5][6] Magnetic resonance (MR) angiography (MRA) and computed tomography angiography are oriented toward depicting anatomy rather than tissue injury. 7,8 Radionuclide captopril renography has not been widely accepted 9 because of its limited accuracy in the presence of bilateral disease 10 or therapy with ACE inhibitors. 11 Inhibiting the activity of the AT 1 R with angiotensin receptor blockers or ACE inhibitors, on the other hand, is widely adapted by clinicians to protect the kidney from renal injury. [12][13][14][15][16] Probing molecular changes is expected to assist diagnosis and support prediction and evaluation of treatment success. We have identified the AT 1 R as a significant molecular imaging target because of its intricate involvement in the many aspects of renal physiology and pathology, [17][18][19] particularly in acute, subacute, and chronic complications of renal ischemia. 20,21 The AT 1 R is a key injury response protein because its continuing activation leads to stimulation of the extracellular matrix, 22 collagen deposition, glomerular remodeling, 23 inflammation, 24 apoptosis, 25 generation of oxygen species, and cell cycle arrest. 26 To this end, our group has synthesized several ...

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“…6 ACEIs/ARBs may prevent nephropathy progression in diabetes, and are recommended for diabetic hypertension 4,6 although the majority require additional anti-hypertensive agents. However, hypertension in type 2 diabetes may be associated with renal vascular disease in 17% of cases, 26 which may explain the reported 16% discontinuation rate of these agents due to progressive renal dysfunction in a treat-to-target clinical study. 27 Effective CVD reduction will follow efforts to lower both systolic and diastolic blood pressure by a tailored individual approach, including use of ACEIs/ARBs.…”

Section: Studies Of Fixed Doses Of Ace Inhibitors (Aceis) Angiotensimentioning

confidence: 95%

Drug therapy for prevention of cardiovascular disease – should surrogate measures be abandoned?

Winocour

2005

Clinical Medicine

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-It has been suggested that the most effective method of reducing cardiovascular disease (CVD) is to define overall CVD risk and apply fixed doses of anti-hypertensive, hypolipidaemic and anti-platelet therapies, using the evidence base from clinical outcome studies. Such studies have examined large numbers of patients with a wide representation of subgroups and demonstrated equivalent benefits in all subsets. In so doing, there may be over-interpretation of the data leading to large-scale applicability of the findings to individuals who were not genuinely represented in the study populations. Most lipid-lowering studies have been unable to consider the possibility that optimal correction of dyslipidaemia would have been more effective than the use of a fixed dose of statins. Studies of angiotensinconverting enzyme (ACE) inhibitors and angiotensin receptor blockade have produced contradictory findings regarding unique non-hypotensive beneficial CVD effects, and suboptimal control of mild hypertension was a frequent finding in the study populations. Scrutiny of concomitant therapy in studies that focus on a particular issue such as LDL (low-density lipoprotein) cholesterol or blood pressure supports the notion that benefits from the agent may be attenuated by other drugs. Widespread application of fixed doses of all these agents to at-risk cases will increase the incidence of inappropriate use and side effects. Clinical experience with modulators of the renin-angiotensin system in hypertensive diabetic renal disease confirms reduced efficacy, and more frequent deterioration of renal function than observed in clinical trials. Measurement of individual biomedical CVD risk factors along with overall risk estimation should continue to be the mainstay of clinical practice. This will allow appropriate case selection for different agents, optimisation of dosage or better assessment of compliance where treatment is less efficacious, and monitoring for adverse effects of therapy. Pragmatic individualisation of care should remain the basis for treating asymptomatic CVD risk factors. KEY WORDS: anti-platelet therapy, cardiovascular disease, diabetes, dyslipidaemia, hypertension, statinsDefining and treating total cardiovascular disease (CVD) risk through assessment of several individual risk factors is more effective in reducing CVD than treating levels of single risk markers in isolation, 1 as they operate in a synergistic fashion. 2 There are conflicting approaches regarding drug therapy, as individuals can be selected on the basis of estimated risk and treated with fixed doses of therapies where there is an evidence base, or by dose titration to biomedical targets, based on individual levels of risk factors, co-morbidity and concurrent therapy. All patients with coronary heart disease (CHD) or an equivalent risk of future CVD events could potentially be treated with fixed doss of angiotensinconverting enzyme (ACE) inhibitors, β-blockers, statins and aspirin, assuming no contraindications. 1 Alternatively, risk p...

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Prevalence of renal artery stenosis in subjects with type 2 diabetes and coexistent hypertension.

Abstract: RAS is common in hypertensive type 2 diabetic subjects. The presence of a femoral bruit is a useful predictive clinical marker. The captopril test is not useful in predicting the hemodynamic significance of RAS in this patient group.

Cited by 56 publications

References 0 publications

Atherosclerotic Renal Artery Stenosis Prevalence and Correlations in Acute Myocardial Infarction Patients Undergoing Primary Percutaneous Coronary Interventions: Data From Nonrandomized Single‐Center Study (REN‐ACS)—A Single Center, Prospective, Observational Study

Atherosclerotic Renal Artery Stenosis Prevalence and Correlations in Acute Myocardial Infarction Patients Undergoing Primary Percutaneous Coronary Interventions: Data From Nonrandomized Single‐Center Study (REN‐ACS)—A Single Center, Prospective, Observational Study

Positron-Emission Tomography Imaging of the Angiotensin II Subtype 1 Receptor in Swine Renal Artery Stenosis

Drug therapy for prevention of cardiovascular disease – should surrogate measures be abandoned?

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