Impact of metabolic syndrome on the outcomes of percutaneous renal angioplasty and stenting
Article Outline
Background
Endovascular therapy for symptomatic atherosclerotic renal artery stenosis (ARAS) is common and effective in the well-selected patient. Hypertension is a common indication for intervention and a major component of metabolic syndrome (MetS). The impact of MetS on outcomes after percutaneous renal intervention is unknown.
Methods
We performed a retrospective analysis of records from patients who underwent endovascular intervention for ARAS and were followed by duplex ultrasound between January 1990 and January 2008. MetS was defined as the presence of ≥3 of the following criteria: Blood pressure ≥140 mm Hg/≥90 mm Hg; triglycerides ≥150 mg/dL; high-density lipoprotein ≤50 mg/dL for women and ≤40 mg/dL for men; fasting blood glucose ≥110 mg/dL; or body mass index ≥30 kg/m2. The average follow-up period was 3.3 years. Clinical benefit defined as freedom from renal-related morbidity (increase in persistent creatinine >20% of baseline, progression to hemodialysis, death from renal-related causes) or freedom from recurrent hypertension, anatomic patency, restenosis, and patient survival were measured.
Results
Five hundred ninety-two renal artery interventions were performed in 427 patients. Fifty-two percent were identified as having MetS. Patients with MetS were more often female (35% vs 50%, NoMetS vs MetS). There were no significant differences in presenting symptoms. There was no peri-operative mortality and equivalent morbidity (6% vs 7%, NoMetS vs MetS). Patients with MetS had equivalent survival and cumulative patency. However, the MetS group had a lower five-year freedom from restenosis (87±2% vs 69±9%, NoMetS vs MetS; P < .01) and lower five-year retained clinical benefit (71±8% vs 45±8%, NoMetS vs MetS; P < .01) with a higher number progressing to hemodialysis (3% vs 13%, NoMetS vs MetS; P < .01). Individually, the components of MetS did not influence outcomes. Statin therapy did not influence outcomes.
Conclusion
MetS is associated with markedly reduced renal clinical benefit and increased progression to hemodialysis following endovascular intervention for atherosclerotic renal artery stenosis. MetS is thus a risk factor for poor long-term outcomes following renal interventions.
Endovascular therapy for symptomatic atherosclerotic renal artery stenosis has increased in frequency and is effective in controlling blood pressure and reversing declining renal function in the well-selected patient.1 The greatest efficacy appears to be in the hypertensive patient with a distinct lesion or the patient with rapidly decreasing estimated glomerular filtration rate and no evidence of parenchymal damage.1, 2 Metabolic syndrome (MetS) is a condition manifested by hypertension, obesity, and a prediabetic state (high fasting blood glucose, high triglycerides, and low high-density lipoproteins), is rapidly increasing in prevalence3 and is an emerging risk factor for cardiovascular morbidity and mortality.4 It is known that the presence of MetS is a marker for progression of chronic renal insufficiency.5 MetS is associated with a larger coronary infarct size, severe heart failure, and higher overall in-hospital complications, including acute renal failure.6, 7 MetS has also been demonstrated to amplify vascular wall thickness and stiffness8 and create an overall pro-thrombotic state.9 Patients with MetS exhibit impaired fibrinolysis through increased plasminogen activator-1 levels compared with those without MetS.10 Prior studies have shown that the presence of MetS can be correlated with increased carotid intima-media thickness in both men11 and women,12 that peripheral arterial disease will be present in 23% of the patients, and that female patients with the combination of MetS and peripheral arterial disease are more likely to have a trend toward kidney dysfunction.13 We have recently demonstrated that the presence of MetS is a risk factor for stroke following carotid intervention (endarterectomy or stent).14 The purpose of this study is to examine the impact of MetS on outcomes after percutaneous renal intervention, which is often used in the setting of poorly controlled hypertension and decreasing renal function. The hypothesis we wish to test is that the presence of MetS is associated with poor renal outcomes after percutaneous intervention.
Methods
Study design
We performed a retrospective analysis of records from patients who underwent percutaneous transluminal renal artery angioplasty for symptomatic atherosclerotic renal artery stenosis of the main renal artery between January 1990 and December 2008. MetS was defined as previously described.15 We substituted a body mass index (BMI) score ≥30.0 as a positive score instead of an abdominal circumference >102 cm or >88 cm for male or female patients, respectively.14 Indications for intervention were poorly controlled hypertension (diastolic BP >90 mm Hg on >3 antihypertensive medications) and/or with elevated creatinine (≥1.5 mg/dL). For each patient, demographics, existing comorbid conditions, and risk factors for atherosclerosis were identified. Freedom from recurrent hypertension, retained clinical benefit defined as freedom from renal-related morbidity (increase in persistent creatinine >20% of baseline, progression to hemodialysis, death from renal-related causes), and factors influencing these parameters were measured. Average follow-up was 3.3 years (range, 1-14 years). Data utilization fell under the category of secondary use of pre-existing data as defined by the Institutional Review Board (IRB) and the Health Insurance Portability and Accountability Act (HIPAA).
Treatment algorithm
Patients with hypertension or elevated creatinine underwent a diagnostic study to identify the presence of renal artery stenosis. This study consisted of standard angiography, magnetic resonance angiography, renal isotope scan, or duplex ultrasound. Duplex ultrasound criteria to identify renal artery stenosis have been previously described.16, 17, 18 In the presence of clinical criteria defined by Rundback et al19 and a ≥60% stenosis on ultrasound or magnetic resonance angiography or a positive renal scan, angiography was performed. The majority of these interventions were transfemoral, and no distal protection devices were used. Patients not categorized into the clinical criteria referenced were managed medically. Occluded renal arteries and nonfunctioning kidneys were not treated. Patients with creatinine >1.5 mg/mL were hydrated overnight with normal saline, and those treated within the last 5 years received mucomyst 600 mg twice a day orally 24 hours preoperatively and 48 hours postoperatively. Patients were followed at 6-month intervals after the procedure. Blood pressure, serum creatinine, and number of antihypertensive medications were identified during these intervals. Each patient had at least one duplex ultrasound within 6 months of the procedure and an ultrasound every 6 months thereafter to assess patency. If the duplex ultrasound showed ≥60% stenosis and the patient had recurrent symptoms, angiography was performed, and restenosis was treated if the arterial diameter was decreased by ≥50%.
Definitions
Coronary artery disease was defined as a history of angina pectoris, myocardial infarction, congestive heart disease, or prior coronary artery revascularizations. Cerebrovascular disease included a history of stroke, transient ischemic attack, or carotid artery revascularization. Hypercholesterolemia was defined as fasting cholesterol >200 mg/dL. Diabetes was defined as a fasting plasma glucose >110 mg/dL or an HbA1c >7%. Diabetics were characterized as IDDM (insulin-dependent diabetes mellitus) or NIDDM (non-insulin-dependent diabetes mellitus). Hypertension was defined as diastolic blood pressure greater than 90 mm Hg on >3 antihypertensive medications. An elevated creatinine level was defined as ≥1.5 mg/dL on two consecutive values during a three-month period. Chronic renal insufficiency was defined as a persistent serum creatinine >1.5 mg/dL for greater than 6 months. eGFR was defined as 186.3 ∗ serum creatinine−1.154 ∗ age−0.203 ∗ 0.742 (if female) ∗ 1.212 (if African American). The baseline serum creatinine was the value recorded closest to the procedure. Patients were considered to have a “nonfunctioning kidney” if any two of the following local criteria used at our institution over the time of the study were met: (1) a duplex ultrasound scan identified a pole-to-pole length of less than 9 cm with no renal flow in the main renal artery and parenchymal peak systolic velocity <10 cm/s; (2) surgically or congenitally absent kidney; (3) no visible nephrogram on contrast arteriogram. A normal contralateral kidney was considered a kidney without evidence of >50% renal artery stenosis and not fulfilling criteria for a “nonfunctioning kidney”. Renal resistive index was defined from duplex imaging as 1-[EDV/PSV]*100. Nephrosclerosis was defined as grade 1: Normal intrarenal vessels, orderly progression of branching patterns (no pruning), normal nephrogram with distinct corticomedullary junction; grade 2: ectasia of arcuate and distal interlobular arteries, peripheral pruning, reduced arterial volume with normal renal mass, normal nephrogram; grade 3: marked ectasia extending centrally, total pruning with abrupt interlobar artery terminations, marked reduced arterial volume with decreased renal mass, faint absent nephrogram. An endoluminal procedural success was a residual stenosis of <30%; failures were residual stenosis ≥30%, by angiographic measurement, including lesions unable to be dilated or crossed and occlusion within 30 days. A death within 30 days of the procedure was considered procedure-related. Acute functional renal injury was defined as a persistent increase in the serum creatinine of ≥0.5 mg/dL at 1 month after the procedure. Acute anatomic renal injury was defined renal artery dissection, perforation, acute occlusion, renal parenchymal infarction, or renal parenchymal perforation. Access site complication was defined as hematoma, pseudoaneurysms, arteriovenous fistula, or a vessel injury requiring either percutaneous or open intervention. Systemic complications were any new cardiac pulmonary infectious or non-renal systemic complication that required intervention or halted discharge within 24 hours of the procedure. Response in the hypertensive patient was defined as follows: “cured” patients were normotensive (diastolic blood pressure <90 mm Hg and systolic blood pressure <140 mm Hg) without medications; “improved” patients were normotensive (diastolic blood pressure <90 mm Hg and/or systolic blood pressure <140 mm Hg) on the same (or reduced) number of medications or had a diastolic blood pressure 15 mm Hg below baseline with the same or reduced number of medications. “No effect” patients had no change or an inability to meet these criteria for cure or improvement and were considered a treatment failure. Early renal function responses to angioplasty were defined as follows: “cured” renal function required a serum creatinine concentration <1.5 mg/dL; “improvement” in renal function required a >20% reduction in the serum creatinine concentration; “stable” renal function required a <20% increase or reduction in the serum creatinine concentration; “deterioration” in renal function required a >20% increase in the serum creatinine concentration.19 Stable renal function and deterioration were considered treatment failures. Renal-related morbidity was defined as a persistent increase in creatinine >20% of baseline, progression to hemodialysis, death from renal-related causes.19
Statistical analysis
We performed our analysis on an “intention-to-treat” basis. Measured values are reported as percentages or means ± one standard deviation. Mann-Whitney tests were used to test the difference between means. Fischer's or Chi-squared tests were performed to test the significance between proportions in each group. Survival and clinical benefit rates are calculated using life table analysis and reported using the SVS criteria. Standard errors are reported in actuarial analyses. The log rank test was used to determine differences between life tables. Non-parametric testing or Χ2 were used to analyze individual variables. Cox proportional hazards models were employed for time-dependent outcomes by preprocedural variables (demographic and comorbidities as one set and renal anatomic and function variables as a second set) and periprocedural variables. Analyses were performed using JMP software version 7.0 (SAS Institute, Cary North Carolina, USA).
Results
Patient population
Five hundred ninety-two renal artery interventions were performed in 427 patients. Over the 18 year period, the number of percutaneous interventions did rise, and annual volume was maintained over the last 5 years. Fifty-two percent were identified as having MetS. Patients with MetS were more often female (35% vs 50%, NoMetS vs MetS). There were no significant differences in presenting symptoms with the majority in both groups presenting with hypertension (Table I). More patients with MetS carried a diagnosis of diabetes and hyperlipidemia but were less likely to have a smoking history (Table I). Fifty-six percent of NoMetS patients and 83% of MetS patients received statins. Other measured comorbidities were equivalent. There was no significant difference in the distribution of stage of chronic kidney disease, mean creatinine concentration, or mean eGFR between the groups. However, the size, nephrosclerosis grade, and resistive index of the ipsilateral kidneys were significantly different between the patients with or without MetS (Table II). In contrast, the size of the kidney, nephrosclerosis grade, and resistive index of the contralateral kidneys were not different between the patients with or without MetS (Table II). The anatomy of the contralateral kidney was equivalent with regard to the presence of disease and functionality (Table II).
Table I. Patients characteristics, presenting symptoms and comorbidities
| No MetS | MetS | P value | |
|---|---|---|---|
| Demographics | |||
 Patients | 205 | 222 | – |
| Kidneys treated | 282 | 310 | – |
| Male | 65% | 50% | .04 |
| Average age (mean ± SD, years) | 70±11 | 70±9 | >.99 |
| Symptoms | |||
| Hypertension | 60% | 58% | .88 |
| Elevated creatinine | 12% | 10% | .82 |
| Hypertension with elevated creatinine | 28% | 32% | .64 |
| Comorbidities | |||
| Smoking history | 84% | 64% | .002 |
| Coronary artery disease | 48% | 61% | .08 |
| Congestive heart failure | 33% | 31% | .87 |
| Diabetes mellitus | 12% | 47% | .0001 |
| Hyperlipidemia | 51% | 85% | .0001 |
| Cerebrovascular | 24% | 27% | .74 |
Table II. Kidney disease, creatinine levels, eGFR, and ipsilateral and contralateral hemodynamic and anatomy parameters
| No MetS | MetS | P value | |
|---|---|---|---|
| Kidney disease stage | |||
| 1 | 2% | 5% | .17 |
| 2 | 15% | 17% | |
| 3 | 54% | 54% | |
| 4 | 21% | 19% | |
| 5 | 8% | 5% | |
| Functional parameters | |||
| Creatinine (mg/dL) | 1.7±1.1 | 1.7±1.0 | >.99 |
| Mean eGFR mL/min/1.73 m2 | 52±28 | 48±22 | .052 |
| eGFR <30 mL/min/1.73 m2 | 17% | 22% | – |
| eGFR 30-60 mL/min/1.73 m2 | 54% | 54% | .19 |
| eGFR >60 mL/min/1.73 m2 | 29% | 24% | – |
| Ipsilateral kidney anatomy | |||
| Kidney size | 10.2±1.4 | 10.4±1.3 | <.0001 |
| Resistive index | 0.81±0.09 | 0.77±0.18 | .0008 |
| Mean nephrosclerosis grade | 1.32±0.51 | 1.33±0.51 | .0044 |
| Grade 1 | 70% | 68% | .0005 |
| Grade 2 | 28% | 30% | |
| Grade 3 | 2% | 2% | |
| Contralateral kidney anatomy | |||
| Normal | 53% | 55% | .27 |
| Stenosis (>60%) | 33% | 26% | |
| Non-functioning | 12% | 15% | |
| Surgically absent | 2% | 3% | |
| Contralateral kidney parameters | |||
| Kidney size | 9.8±1.4 | 9.9±1.4 | >.99 |
| Resistive index | 0.78±0.08 | 0.77±0.15 | .32 |
| Mean nephrosclerosis grade | 1.47±0.71 | 1.44±0.64 | .59 |
Immediate outcomes (<3 months)
There was no perioperative mortality and equivalent morbidity (6% vs 7%, NoMetS vs MetS). The categories of morbidity were similar between the two groups (Table III). Technical success was equivalent between the two groups. Those in the NoMetS group had significantly more predilations than the MetS group (Table III). However, there was no difference in the preoperative degree of stenosis between the groups. Stent placement occurred significantly more frequently in the MetS group (Table III). Importantly, similar numbers of contralateral stenoses were treated (Table III). Fifty percent of the NoMetS patients and 47% of the MetS patients demonstrated “improved” or “cured” hypertension within 3 months of intervention (Table IV). Twenty-six percent of the NoMetS patients and 7% of the MetS patients demonstrated “improved” or “cured” renal function within 3 months of intervention (Table IV). A similar proportion of patients in both groups demonstrated no change in renal function (Table IV). Equivalent numbers in both groups showed postprocedural functional deterioration (Table IV).
Table III. Interventions
| No MetS | MetS | P value | |
|---|---|---|---|
| Interventions | |||
| Angioplasty | 54% | 48% | .15 |
| Predilation | 38% | 28% | .01 |
| Stent placement | 71% | 80% | .01 |
| Contralateral intervention | 33% | 37% | .29 |
| Complications | |||
| Acute functional injury | 20% | 18% | .98 |
| Anatomic injury | 4% | 2% | .15 |
| Access site | 7% | 10% | .21 |
| Systemic | 7% | 9% | .39 |
Table IV. Outcomes
| No MetS | MetS | P value | |
|---|---|---|---|
| Immediate hypertension outcomes | |||
| Deterioration | 1% | 0% | .74 |
| No change | 49% | 53% | |
| Improved | 45% | 42% | |
| Cured | 5% | 5% | |
| Long term hypertension outcomes | |||
| Deterioration | 6% | 10% | .29 |
| No change | 94% | 90% | |
| Immediate renal outcomes | |||
| Deterioration | 18% | 19% | .025 |
| No change | 63% | 75% | |
| Improved | 22% | 8% | |
| Cured | 4% | 1% | |
| Long term renal outcomes | |||
| Increase in creatinine | 9% | 14% | .27 |
| Progression to hemodialysis | 3% | 13% | .009 |
| Death from renal cause | 1% | 4% | .17 |
There were no factors that distinguished those patients who had cure or improved benefit and those who had deterioration in the No MetS or MetS groups.
Outcomes (>3 months)
Patient survival was equivalent between the two groups at five years (survival 67% ± 4% vs 67% ± 4%, NoMetS vs MetS) but diverged by 10 years, with survival being 46% ± 7% vs 34% ± 8% for NoMetS and MetS groups, respectively (Fig, A). Survival in MetS was influenced by eGFR <30 mL (Relative Risk [RR] = 2.01, 1.07-3.95; P = .03). There was no significant difference in the distribution of DM between those that died and those that survived (Fisher's exact test two-sided P = .154). Cumulative patency was equivalent between the 2 groups, but the freedom from restenosis in the MetS group was significantly lower by life table analysis within 3 years and continued to diverge thereafter (87% ± 2% vs 69% ± 9% at 5 years, NoMetS vs MetS; P < .01) (Fig, B and C). A greater number of reinterventions were performed to maintain patency in the MetS group. Smoking (RR = 1.42, P = .02) and an immediate increase in creatinine (RR = 1.58, 1.08-2.25; P = .017) influenced restenosis in MetS. There was no difference in the postoperative degree of stenosis between the groups, and the final technical result did not influence the development of restenosis. The presence of diabetes, the presence of hyperlipidemia, placement of a stent, or statin administration did not influence restenosis rates. While freedom from recurrent hypertension was not significant at 5 years, the MetS group did show a lower freedom from recurrent hypertension in the long term (Table IV and Fig, D). When renal-related morbidity was examined, the MetS group performed significantly worse within three years and continued to diverge as follow up continued (retained clinical benefit at five years, 71% ± 8% vs 45% ± 8%, NoMetS vs MetS; P < .01) (Fig, E). The principal reason for this divergence was a progression to dialysis (3% vs 13%, NoMetS vs MetS; P = .009) (Table IV). Smoking (RR = 1.54, P = .004) and increasing age (RR = 1.25, P = .001) influenced freedom from renal-related morbidity. The presence of diabetes, the presence of hyperlipidemia, placement of a stent, or statin administration had no influence on the freedom from renal-related morbidity in the MetS group. No parameter of renal function or anatomy influenced freedom from renal-related morbidity in the MetS group. No individual characteristic of MetS independently influenced patency, restenosis, or functional outcomes.
Fig.
(A) Survival: Kaplan-Meier analysis of survival of the patients with and without MetS. (B) Patency: Kaplan-Meier analysis of cumulative vessel patency with and without MetS. (C) Restenosis: Kaplan-Meier analysis of freedom from restenosis of the patients with and without MetS. (D) Hypertension: Kaplan-Meier analysis of freedom from recurrent hypertension of the patients with and without MetS. (E) Renal-related morbidity: Kaplan-Meier analysis of freedom from renal-related morbidity (persistent increase in creatinine >20% of baseline, progression to hemodialysis, death from renal-related causes) of the patients with and without MetS. The number at risk at each time interval is shown below each figure. Values are mean ± standard error of the mean. Standard errors exceeding 10% are not shown.
When controlled for gender, diabetes, or hyperlidemia, the effect of the presence of MetS is maintained. There was no significant difference in outcomes between the first 9 years and the last 9 years of the study.
Discussion
General
This is the first study to examine MetS in patients undergoing renal intervention. The current study demonstrates that MetS is present in over 50% of patients presenting for renal intervention and that it is more common in females and is associated with significantly poor markers of renal perfusion before intervention. Perioperative events are not impacted by MetS, but MetS does adversely affect the long-term anatomic and functional renal outcomes.
MetS
Identification of the MetS allows clinicians to move away from a strategy based on management of a single risk factor to one that focuses on a constellation of synergistic risk factors.20 However, there are multiple definitions of MetS,15, 21, 22, 23, 24, 25 and several substitute abdominal obesity with a BMI >30 kg/m2. Due to the retrospective design of our study, we could not obtain the abdominal circumference of each individual patient, as it is not routinely determined, and thus used the BMI as a surrogate for waist circumference. Most of the basic components of the MetS, namely type 2 diabetes mellitus, hypertension, obesity, or low high-density lipoprotein cholesterol levels, apart from being major risk factors for cardiovascular disease, have been also associated with an increased risk of chronic kidney disease. Insulin resistance and compensatory hyperinsulinemia are independently associated with an increased prevalence of chronic kidney disease.26 Multiple observational studies have consistently shown that increased BMI as well as insulin resistance and increased fasting insulin levels are associated with chronic kidney disease, even after adjustment for related disorders.26 Obesity may promote intracellular lipid accumulation in the kidney.27 Prevalence of a BMI of at least 35 kg/m2 among incident dialysis patients has increased by 64% over the past decade, and if trends continue, 20% of all patients will initiate dialysis with this degree of obesity. Weight loss improves glomerular hemodynamics in morbidly obese adults and may retard progression of chronic kidney disease. In contrast, once a patient reaches end-stage renal disease, the degree of adiposity correlates with survival, and weight loss may not necessarily be beneficial.28
Patients
In this cohort of patients presenting with symptomatic renal artery disease, we found MetS was highly prevalent (52%) and was more common in females. It has been demonstrated that MetS is present at an equivalent level in patients presenting with lower extremity disease.29 Well-established indicators of increased cardiovascular risk such as low ankle-brachial index (ABI) and increased C-reactive protein (CRP) levels also cluster with MetS.29 The degree of peripheral arterial disease clinical manifestations was not related to MetS score (ie, the number of criteria of MetS present).30 We did observe that patients with MetS and ipsilateral renal artery disease had anatomic markers of more distal renal disease, while the contralateral kidneys were normal. This may suggest that significant renal artery atherosclerosis and MetS act synergistically. A similar observation was made by Wei et al, where they noted that female patients with MetS and lower extremity atherosclerosis were more likely to have developed kidney dysfunction.13 We did see more female patients in the MetS group, but gender did not emerge as a significant co-factor during our analysis. Renal artery stenosis is an independent predictor of mortality. At 7 years, 73% of patients with untreated renal artery stenosis are dead.31 The 7-year actuarial mortality in this study for patients with MetS was 47% and without MetS was 42%, which is better than the historically reported data for untreated disease. Similar to the current study, immediate and long-term post procedure creatinine deterioration and dialysis dependency have been associated with increased mortality.16, 17, 18 The presence of MetS did appear to alter the survival after renal intervention.
Anatomic outcomes
While technical success was equal in both groups, there was a greater use of stents in the MetS group, which may have reflected more significant disease. Regardless of the modality chosen to intervene (angioplasty or stenting), cumulative patency was equivalent between the patients with and without MetS. However, the freedom from restenosis in the MetS group was significantly lower by life table analysis within 3 years and continued to diverge thereafter. This restenosis was not mirrored by an increase in ipsilateral reintervention rates. It is possible that the increased restenosis rate was an artifact induced by the increased use of stents in the MetS group. In-stent velocities on duplex imaging are considered elevated compared with nonstented vessels. Similarly, target lesion revascularization in the coronary circulation is not influenced by the presence of MetS.32, 33 Major and minor morbidity in this study was also equivalent. This is also the case in the coronary32, 33 and carotid circulations following intervention.14
Functional outcomes
Functional outcomes remain the primary goal of renal interventions. There is significant controversy as to whether intervention is superior to best medical therapy. The most significant finding in this study is the markedly poor freedom from renal-related morbidity in MetS. The response in the hypertensive was an equivalent in both groups. Twenty-six percent of the NoMetS patients and 7% of the MetS patients demonstrated “improved” or “cured” renal function within 3 months of intervention. This difference in improvement likely reflects the preexisting anatomic and parenchymal parameters we noted in the ipsilateral kidney pre-intervention. During long-term follow up, despite normal mean eGFR and distribution of chronic kidney disease, more patients demonstrated progression to hemodialysis in the MetS group. MetS appears to be a risk factor for chronic kidney disease, likely due to the combination of dys-glycemia and high blood pressure.5 Ispilateral kidneys in the MetS group showed a decrease in length, resistive index, and nephrosclerosis grade compared with those in the NoMetS group, suggesting parenchymal deterioration. However, the contralateral kidneys were equivalent between the two groups, suggesting that MetS on its own was unlikely to have induced the changes in parenchymal parameters.
Conclusion
MetS is prevalent among patients undergoing renal angioplasty and stenting. MetS is associated with markedly reduced renal clinical benefit and increased progression to hemodialysis following endovascular intervention for atherosclerotic renal artery stenosis. MetS is thus a risk factor for poor long-term outcomes following renal interventions.
Author contributions
The authors thank Daynene Vykoukal, PhD, for critical reading of the manuscript.
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Competition of interest: none.
The editors and reviewers of this article have no relevant financial relationships to disclose per the JVS policy that requires reviewers to decline review of any manuscript for which they may have a competition of interest.
PII: S0741-5214(09)01930-2
doi:10.1016/j.jvs.2009.09.042
© 2010 Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved.
