The 2023 Society for Vascular Surgery, American Venous Forum, and American Vein and Lymphatic Society clinical practice guidelines for the management of varicose veins of the lower extremities. Part II: Endorsed by the Society of Interventional Radiology and the Society for Vascular Medicine.

The Society for Vascular Surgery, the American Venous Forum, and the American Vein and Lymphatic Society recently published Part I of the 2022 clinical practice guidelines on varicose veins. Recommendations were based on the latest scientific evidence researched following an independent systematic review and meta-analysis of five critical issues affecting the management of patients with lower extremity varicose veins, using the patients, interventions, comparators, and outcome system to answer critical questions. Part I discussed the role of duplex ultrasound scanning in the evaluation of varicose veins and treatment of superficial truncal reflux. Part II focuses on evidence supporting the prevention and management of varicose vein patients with compression, on treatment with drugs and nutritional supplements, on evaluation and treatment of varicose tributaries, on superficial venous aneurysms, and on the management of complications of varicose veins and their treatment. All guidelines were based on systematic reviews, and they were graded according to the level of evidence and the strength of recommendations, using the GRADE method. All ungraded Consensus Statements were supported by an extensive literature review and the unanimous agreement of an expert, multidisciplinary panel. Ungraded Good Practice Statements are recommendations that are supported only by indirect evidence. The topic, however, is usually noncontroversial and agreed upon by most stakeholders. The Implementation Remarks contain technical information that supports the implementation of specific recommendations. This comprehensive document includes a list of all recommendations (Parts I-II), ungraded consensus statements, implementation remarks, and best practice statements to aid practitioners with appropriate, up-to-date management of patients with lower extremity varicose veins.

The 2022 Society for Vascular Surgery, American Venous Forum, and American Vein and Lymphatic Society clinical practice guidelines for the management of varicose veins of the lower extremities. Part I. Duplex Scanning and Treatment of Superficial Truncal Reflux: Endorsed by the Society for Vascular Medicine and the International Union of Phlebology.

The Society for Vascular Surgery, American Venous Forum, and American Vein and Lymphatic Society collaborated to update the 2011 Society for Vascular Surgery/American Venous Forum clinical practice guidelines and provide new evidence-based recommendations on critical issues affecting the care of patients with varicose veins. Each recommendation is based on a recent, independent systematic review and meta-analysis of the diagnostic tests and treatments options for patients with lower extremity varicose veins. Part I of the guidelines includes evidence-based recommendations for the evaluation of patients with CEAP (Clinical Class, Etiology, Anatomy, Pathology) class 2 varicose vein using duplex ultrasound scanning and other diagnostic tests, open surgical treatment (ligation and stripping) vs endovenous ablation techniques, thermal vs nonthermal ablation of the superficial truncal veins, and management of incompetent perforating veins in CEAP class 2 disease. We have also made recommendations on the concomitant vs staged treatment of varicose tributaries using phlebectomy or liquid or foam sclerotherapy (with physician-compounded foam or commercially prepared polidocanol endovenous microfoam) for patients undergoing ablation of incompetent superficial truncal veins.

Preserved function of late-outgrowth endothelial cells in medically treated hypertensive patients under well-controlled conditions.

Endothelial progenitor cells (EPCs) participate in renal repair, but their number and function may be impaired by exposure to cardiovascular risk factors. The number of circulating EPCs is decreased in essential and renovascular hypertensive patients, but the effects of hypertension on EPC function are incompletely understood. We hypothesized that EPC function was preserved under well-controlled conditions in treated hypertensive patients. Patients with atherosclerotic renal artery stenosis (ARAS; n=22) or essential hypertension (n=24) were studied during controlled sodium intake and antihypertensive regimen. Late-outgrowth EPCs were isolated from the inferior vena cava (IVC) and renal vein blood of ARAS and essential hypertension patients and a peripheral vein of matched normotensive controls (n=18). The angiogenic function of EPCs was assessed in vitro, and multidetector computed tomography was used to measure single-kidney hemodynamics and function in ARAS and essential hypertension patients. Inflammatory biomarkers and EPC homing signal levels and renal release were calculated. Inferior vena cava and renal vein-obtained EPC function were similar in ARAS and essential hypertension patients and comparable to that in normal controls (tube length, 171.86±16.846, 191.09±14.222, 174.925±19.774 µm, respectively). Function of renal vein-obtained EPCs directly correlated with stenotic kidney glomerular filtration rate, EPC homing factors, and anti-inflammatory mediator levels in ARAS patients. Therefore, EPC function was relatively preserved in ARAS patients, although it directly correlated with renal function. Adequate EPC function supports the feasibility of using autologous EPCs as a therapeutic option in essential and renovascular hypertensive patients. Homing signals and inflammatory mediators may potentially regulate EPC angiogenic function.

Validity of International Classification of Diseases, Ninth Revision, Clinical Modification codes for estimating the prevalence of venous ulcer.

BACKGROUND: The American Venous Forum issued a call to reduce the prevalence of venous ulcers (VUs) by 50% in 10 years. The objectives of this study were to determine the validity of the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) codes for VU and to estimate the prevalence of VU in a well-defined geographic population (Olmsted County, Minn). METHODS: Rochester Epidemiology Project resources and 18 VU ICD-9-CM codes were used to identify residents with possible VUs during the 2-year period 2010-2011 (n = 1551). The complete medical records in the community were reviewed for a 15% random sample (n = 227) of these residents, and on the basis of prespecified criteria, patients were categorized as a VU or non-VU case. Continuous and categorical variables were compared between groups by the two-sample t-test and χ(2) test. RESULTS: Ninety-three patients (41%) had active or healed VUs, 83 had non-VUs, and 51 never had ulcers but had stasis skin changes or skin infection. ICD-9-CM code 454.0 best identified VU cases (sensitivity, 24%; specificity, 100%). VU patients were older and heavier and more frequently had bilateral ulcers. On the basis of the random sample review, an estimated 635 patients had healed or active VUs during the 2-year period of the study. The prevalence of VUs in the Olmsted County population was estimated to be 210 per 100,000 person-years, with VU incidence (newly diagnosed ulcers) of 85 per 100,000 person-years. CONCLUSIONS: ICD-9-CM VU codes operated poorly for VU identification. VU surveillance for estimating trends in incidence and prevalence of VUs will require better methods. The estimated prevalence of VUs in Olmsted County is 210 per 100,000 person-years. New ulcers developed each year in 85 of 100,000 people, an incidence that seems to be higher than in the previous epidemiologic study in this population.

Blood oxygen level-dependent (BOLD) MRI analysis in atherosclerotic renal artery stenosis.

PURPOSE OF REVIEW: Blood oxygen level-dependent MRI (BOLD MRI) is a noninvasive technique for evaluating kidney tissue oxygenation that requires no contrast exposure, with the potential to allow functional assessment in patients with atherosclerotic renal artery stenosis. Normal cortical-to-medulla oxygenation gradients are preserved in many patients treated for several years with medical antihypertensive therapy without restoring renal blood flow. The current review is of particular interest as new methods have been applied to the analyses of BOLD MRI, opening the perspective of its wider utilization in clinical practice. RECENT FINDINGS: Recent findings show that more severe vascular compromise ultimately overwhelms renal adaptive changes, leading to overt cortical hypoxia and expansion of medullary hypoxic zones. 'Fractional kidney hypoxia' method of analysis, developed as an alternative method of BOLD MRI analysis, avoids the assumption of discrete cortical and medullary values and decreases the bias related to operator selection of regions of interests. SUMMARY: We believe that thoughtful application and analysis of BOLD MRI can provide critical insights into changes in renal function prior to the onset of irreversible renal injury and may identify patients most likely to gain from measures to reverse or repair disorders of tissue oxygenation.

Increased circulating inflammatory endothelial cells in blacks with essential hypertension.

Morbidity and mortality attributable to hypertension are higher in black essential hypertensive (EH) compared with white EH patients, possibly related to differential effects on vascular injury and repair. Although circulating endothelial progenitor cells (EPCs) preserve endothelial integrity, inflammatory endothelial cells (IECs) detach from sites of injury and represent markers of vascular damage. We hypothesized that blood levels of IECs and inflammatory markers would be higher in black EH compared with white EH patients. Inferior vena cava and renal vein levels of CD34+/KDR+ (EPC) and VAP-1+ (IEC) cells were measured by fluorescence-activated cell sorting in white EH and black EH patients under fixed sodium intake and blockade of the renin-angiotensin system, and compared with systemic levels in normotensive control subjects (n=19 each). Renal vein and inferior vena cava levels of inflammatory cytokines and EPC homing factors were measured by Luminex. Blood pressure, serum creatinine, lipids, and antihypertensive medications did not differ between white and black EH patients, and EPC levels were decreased in both. Circulating IEC levels were elevated in black EH patients, and inversely correlated with EPC levels (R(2)=0.58; P=0.0001). Systemic levels of inflammatory cytokines and EPC homing factors were higher in black EH compared with white EH patients, and correlated directly with IECs. Renal vein inflammatory cytokines, EPCs, and IECs did not differ from their circulating levels. Most IECs expressed endothelial markers, fewer expressed progenitor cell markers, but none showed lymphocyte or phagocytic cell markers. Thus, increased release of cytokines and IECs in black EH patients may impair EPC reparative capacity and aggravate vascular damage, and accelerate hypertension-related complications.

TGF expression and macrophage accumulation in atherosclerotic renal artery stenosis.

BACKGROUND AND OBJECTIVES: Atherosclerotic renal artery stenosis (ARAS) reduces renal blood flow and is a potential cause of chronic kidney injury, yet little is known regarding inflammatory pathways in this disorder in human participants. This study aimed to examine the hypothesis that reduced renal blood flow (RBF) in ARAS would be associated with tissue TGF-ß activation and inflammatory cell accumulation. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: This cross-sectional study of ARAS of varying severity compared transjugular biopsy specimens in patients with ARAS (n=12, recruited between 2008 and 2012) with tissue from healthy kidney donors (n=15) and nephrectomy specimens from individuals with total vascular occlusion (n=65). ARAS patients were studied under controlled conditions to measure RBF by multidetector computed tomography and tissue oxygenation by blood oxygen level-dependent magnetic resonance imaging. RESULTS: Compared with the nonstenotic contralateral kidneys, RBF was reduced in poststenotic kidneys (242±149 versus 365+174 ml/min; P<0.01) as was single-kidney GFR (28±17 versus 41±19 ml/min; P<0.01), whereas cortical and medullary oxygenation were relatively preserved. Tissue TGF-ß immunoreactivity was higher in ARAS patients compared with those with both normal kidneys and those with total occlusion (mean score 2.4±0.7 versus 1.5+1.1 in the nephrectomy group and versus 0±0 in donors; P<0.01). By contrast, the number of CD68+ macrophages was higher with greater disease severity (from 2.2±2.7 in normal to 22.4±18 cells/high-power field in nephrectomy samples; P<0.001). CONCLUSIONS: The results of this study indicate robust stimulation of TGF-ß associated with macrophage infiltration within the human kidney with vascular occlusive disease.

Inflammatory and injury signals released from the post-stenotic human kidney.

AIMS: The mechanisms mediating kidney injury and repair in humans with atherosclerotic renal artery stenosis (ARAS) remain poorly understood. We hypothesized that the stenotic kidney releases inflammatory mediators and recruits progenitor cells to promote regeneration. METHODS AND RESULTS: Essential hypertensive (EH) and ARAS patients (n=24 each) were studied during controlled sodium intake and antihypertensive treatment. Inferior vena cava (IVC) and renal vein (RV) levels of CD34+/KDR+ progenitor cells, cell adhesion molecules, inflammatory biomarkers, progenitor cell homing signals, and pro-angiogenic factors were measured in EH and ARAS, and their gradient and net release compared with systemic levels in matched normotensive controls (n= 24). Blood pressure in ARAS was similar to EH, but the glomerular filtration rate was lower. Renal vein levels of soluble E-Selectin, vascular cell adhesion molecule-1, and several inflammatory markers were higher in the stenotic kidney RV vs. normal and EH RV (P < 0.05), and their net release increased. Similarly, stem-cell homing factor levels increased in the stenotic kidney RV. Systemic CD34+/KDR+ progenitor cell levels were lower in both EH and ARAS and correlated with cytokine levels. Moreover, CD34+/KDR+ progenitor cells developed a negative gradient across the ARAS kidney, suggesting progenitor cell retention. The non-stenotic kidney also showed signs of inflammatory processes, which were more subtle than in the stenotic kidney. CONCLUSION: Renal vein blood from post-stenotic human kidneys has multiple markers reflecting active inflammation that portends kidney injury and reduced function. CD34+/KDR+ progenitor cells sequestered within these kidneys may participate in reparative processes. These inflammation-related pathways and limited circulating progenitor cells may serve as novel therapeutic targets to repair the stenotic kidney.

Chronic renovascular hypertension is associated with elevated levels of neutrophil gelatinase-associated lipocalin.

BACKGROUND: Renovascular hypertension (RVH) is characterized by chronic inflammation of the stenotic kidney and progressive renal dysfunction. Neutrophil gelatinase-associated lipocalin (NGAL), an acute phase protein induced in inflammatory conditions and ischemia, is a novel biomarker for acute kidney injury. We hypothesized that chronic RVH would be associated with increased renal and circulating NGAL levels. METHODS: We prospectively measured renal vein and inferior vena cava (IVC) levels of NGAL and inflammatory cytokines in essential hypertensive (EH) and RVH patients, during constant sodium intake and anti-hypertensive regimens, and compared them with systemic levels in age-matched normotensive subjects (n = 22 each). In addition, we measured urinary NGAL and kidney injury molecule (KIM)-1 in all patients. RESULTS: Blood pressure, serum creatinine, estimated glomerular filtration rate (eGFR), lipid panels and medications were similar in RVH and EH. Systemic, stenotic and contralateral renal vein levels of NGAL were all similarly elevated in RVH versus normal hypertension and EH (P < 0.05), as were renal vein levels of inflammatory markers like tumor necrosis factor-α. Furthermore, renal vein NGAL levels inversely correlated with eGFR, and directly with renal vein (but not systemic) levels of inflammatory markers. Urinary levels of NGAL and KIM-1 were elevated in both EH and RVH, as were systemic levels of C-reactive protein. CONCLUSIONS: Chronic RVH is associated with elevated NGAL levels, likely due to ongoing kidney and systemic inflammation and ischemia. These findings may also imply the occurrence of the inflammation process in chronic RVH, which might contribute to the poorer outcomes of RVH compared with EH patients.

Association of filtered sodium load with medullary volumes and medullary hypoxia in hypertensive African Americans as compared with whites.

BACKGROUND: African Americans develop hypertension earlier with more target manifestations than whites despite having a higher glomerular filtration rate (GFR) for any level of serum creatinine. STUDY DESIGN & PARTICIPANTS: This study tested the hypothesis that increased GFR and sodium reabsorption in African Americans is associated with increased metabolic work and medullary hypoxia in 49 nondiabetic patients with essential hypertension (29 whites and 20 African Americans) following a constant-sodium diet (150 mEq/d) and renin-angiotensin system blockade. PREDICTORS: Ethnicity, age, measured GFR, sodium excretion, and body mass index. OUTCOMES: We examined cortical and medullary volumes and blood flows using multidetector computed tomography and intrarenal deoxyhemoglobin (R2*) using blood oxygen level-dependent magnetic resonance. RESULTS: Blood pressure and sodium excretion were similar, whereas African Americans were more obese and had higher iothalamate GFRs. Renal cortical volumes did not differ, but medullary volumes adjusted for body size and age were higher in African Americans (32.3 ± 11.2 vs 25.1 ± 7.4 cm(3)/m(2) body surface area; P < 0.001). Sodium reabsorption and blood flows were higher in African Americans. Basal cortical deoxyhemoglobin values were similar between ethnic groups, whereas medullary R2* was higher in African Americans (39.7 ± 5.1 vs 36.3 ± 6.5/s; P = 0.02), but decreased to levels similar to whites after furosemide treatment. Levels of the circulating isoprostane prostaglandin F(2α) were higher in African Americans and daily urinary prostaglandin F(2α) excretion in African Americans correlated directly with renal blood flow (R = 0.71; P < 0.01). LIMITATIONS: Studies were limited to treated volunteers with normal kidney function without knowledge of prior nutrient intake. CONCLUSIONS: These data show for the first time that increased sodium reabsorption in obese African American patients with hypertension was associated with enlarged medullary volumes, functional hypoxia related to solute reabsorption, and a direct relationship between blood flows and urinary isoprostane levels. Our results support a model of increased oxygen consumption and oxidative stress in African Americans that may accelerate hypertension and target-organ injury compared with white patients with essential hypertension.

Blood oxygen level-dependent magnetic resonance imaging identifies cortical hypoxia in severe renovascular disease.

Atherosclerotic renal artery stenosis has a range of manifestations depending on the severity of vascular occlusion. The aim of this study was to examine whether exceeding the limits of adaptation to reduced blood flow ultimately leads to tissue hypoxia, as determined by blood oxygen level dependent MRI. We compared 3 groups of hypertensive patients, 24 with essential hypertension, 13 with "moderate" (Doppler velocities 200-384 cm/s), and 17 with "severe" atherosclerotic renal artery stenosis (ARAS; velocities >384 cm/s and loss of functional renal tissue). Cortical and medullary blood flows and volumes were determined by multidetector computed tomography. Poststenotic kidney size and blood flow were reduced with ARAS, and tissue perfusion fell in the most severe lesions. Tissue medullary deoxyhemoglobin, as reflected by R2* values, was higher as compared with the cortex for all of the groups and did not differ between subjects with renal artery lesions and essential hypertension. By contrast, cortical R2* levels were elevated for severe ARAS (21.6±9.4 per second) as compared with either essential hypertension (17.8±2.3 per second; P<0.01) or moderate ARAS (15.7±2.1 per second; P<0.01). Changes in medullary R2* after furosemide administration tended to be blunted in severe ARAS as compared with unaffected (contralateral) kidneys. These results demonstrate that severe vascular occlusion overwhelms the capacity of the kidney to adapt to reduced blood flow, manifest as overt cortical hypoxia as measured by blood oxygen level-dependent MRI. The level of cortical hypoxia is out of proportion to the medulla and may provide a marker to identify irreversible parenchymal injury.

Blood oxygen level-dependent (BOLD) MRI in renovascular hypertension.

Establishing whether large vessel occlusive disease threatens tissue oxygenation and viability in the post-stenotic kidney is difficult for clinicians. Development of blood oxygen level-dependent (BOLD) MRI methods can allow functional evaluation of regional differences in deoxyhemoglobin levels within the kidney without requiring contrast. The complex renal circulation normally provides a gradient of oxygenation from a highly vascular cortex to much reduced levels in the deep sections of medulla, dependent upon adjustments in renal afferent arterioles, oxygen consumption related to solute transport, and arteriovenous shunting related to the juxtaposition of descending and ascending vasa recta. Studies with BOLD imaging have identified adaptation to substantial reductions in renal blood flow, volume, and glomerular filtration rate in post-stenotic kidneys that preserves medullary and cortical oxygenation during medical therapy. However, extreme vascular compromise overwhelms these adaptive changes and leads to cortical hypoxia and microvascular injury.

The care of patients with varicose veins and associated chronic venous diseases: clinical practice guidelines of the Society for Vascular Surgery and the American Venous Forum.

The Society for Vascular Surgery (SVS) and the American Venous Forum (AVF) have developed clinical practice guidelines for the care of patients with varicose veins of the lower limbs and pelvis. The document also includes recommendations on the management of superficial and perforating vein incompetence in patients with associated, more advanced chronic venous diseases (CVDs), including edema, skin changes, or venous ulcers. Recommendations of the Venous Guideline Committee are based on the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) system as strong (GRADE 1) if the benefits clearly outweigh the risks, burden, and costs. The suggestions are weak (GRADE 2) if the benefits are closely balanced with risks and burden. The level of available evidence to support the evaluation or treatment can be of high (A), medium (B), or low or very low (C) quality. The key recommendations of these guidelines are: We recommend that in patients with varicose veins or more severe CVD, a complete history and detailed physical examination are complemented by duplex ultrasound scanning of the deep and superficial veins (GRADE 1A). We recommend that the CEAP classification is used for patients with CVD (GRADE 1A) and that the revised Venous Clinical Severity Score is used to assess treatment outcome (GRADE 1B). We suggest compression therapy for patients with symptomatic varicose veins (GRADE 2C) but recommend against compression therapy as the primary treatment if the patient is a candidate for saphenous vein ablation (GRADE 1B). We recommend compression therapy as the primary treatment to aid healing of venous ulceration (GRADE 1B). To decrease the recurrence of venous ulcers, we recommend ablation of the incompetent superficial veins in addition to compression therapy (GRADE 1A). For treatment of the incompetent great saphenous vein (GSV), we recommend endovenous thermal ablation (radiofrequency or laser) rather than high ligation and inversion stripping of the saphenous vein to the level of the knee (GRADE 1B). We recommend phlebectomy or sclerotherapy to treat varicose tributaries (GRADE 1B) and suggest foam sclerotherapy as an option for the treatment of the incompetent saphenous vein (GRADE 2C). We recommend against selective treatment of perforating vein incompetence in patients with simple varicose veins (CEAP class C(2); GRADE 1B), but we suggest treatment of pathologic perforating veins (outward flow duration ≥500 ms, vein diameter ≥3.5 mm) located underneath healed or active ulcers (CEAP class C(5)-C(6); GRADE 2B). We suggest treatment of pelvic congestion syndrome and pelvic varices with coil embolization, plugs, or transcatheter sclerotherapy, used alone or together (GRADE 2B).

Preserved oxygenation despite reduced blood flow in poststenotic kidneys in human atherosclerotic renal artery stenosis.

Atherosclerotic renal artery stenosis reduces blood flow and perfusion pressures to the poststenotic kidney producing renovascular hypertension and threatening glomerular filtration rate. Little is known regarding regional tissue oxygenation in human renovascular disease that develops slowly. We compared stenotic and contralateral kidneys regarding volume, tissue perfusion, blood flow measured by multidetector computed tomography, and blood oxygen level-dependent magnetic resonance values in the cortex and medulla in 14 patients with unilateral stenosis (mean: 71% by quantitative computed tomography) and in 14 essential hypertensive patients during 150 mEq/d of sodium intake and renin-angiotensin blockade. Stenotic kidney volume was reduced compared with the contralateral kidney (118.6+/-9.9 versus 155.4+/-13.7 mL; P<0.01), as was total blood flow (269.7+/-42.2 versus 383.7+/-49; P=0.02), mainly because of reduced cortical volume. Tissue perfusion was similar but lower than essential hypertension (1.5 versus 1.2 mL/min per milliliter; P<0.05). Blood oxygen level-dependent MR at 3 T confirmed elevated R2* values (a measure of deoxyhemoglobin) in deep medullary regions in all 3 sets of kidneys (38.9+/-0.7 versus cortex 17.8+/-0.36 s(-1); P<0.0001). Despite reduced blood flow, R2* values did not differ between atherosclerotic and essential hypertensive kidneys, although furosemide-suppressible fall in medullary R2* was reduced in stenotic kidneys (5.7+/-1.8 versus 9.4+/-1.9 s(-1); P<0.05). Renal venous oxygen levels from the stenotic kidney were higher than those from essential hypertensives (65.1+/-2.2 versus 58.1+/-1.2; P=0.006). These data indicate that, although stenosis reduced blood flow and volume, cortical and medullary oxygenation was preserved under these conditions.

Comparison of 1.5 and 3 T BOLD MR to study oxygenation of kidney cortex and medulla in human renovascular disease.

OBJECTIVES: Imaging of the kidney using blood oxygen level dependent MR presents a major opportunity to examine differences in tissue oxygenation within the cortex and medulla applicable to human disease. We sought to define the differences between regions within kidneys and to optimize selection of regions of interest for study with 1.5 and 3 Tesla systems. MATERIALS AND METHODS: Studies in 38 subjects were performed under baseline conditions and after administration of furosemide intravenously to examine changes in R2* as a result of suppressing oxygen consumption related to medullary tubular solute transport. These studies were carried out in patients with atherosclerotic renal artery stenosis (n = 24 kidneys) or essential hypertension or nonstenotic kidneys (n = 39). All patients but one were treated with agents to block the renin angiotensin system (ACE inhibitors or angiotensin receptor blockers). For each kidney, 3 levels (upper pole, hilum, and lower pole) were examined, including 3 individual segments (anterior, lateral, and posterior). RESULTS: Low basal R2* levels in kidney cortex (12.06 +/- 0.84 s(-1)) at 1.5 Tesla reflected robust blood flow and oxygenation and agreed closely with values obtained at 3.0 Tesla (13.62 +/- 0.56 s(-1), NS). Coefficients of variation ranged between 15% and 20% between segments and levels at both field strengths. By contrast, inner medullary R2* levels were higher at 3 T (31.66 +/- 0.74 s(-1)) as compared with 1.5 T (22.19 +/- 1.52 s(-1), P < 0.01). Medullary R2* values fell after furosemide administration reflecting reduced deoxyhemoglobin levels associated with blocked energy-dependent transport. The fall in medullary R2* at 3.0 Tesla (-12.61 +/- 0.97 s(-1)) was greater than observed at 1.5 T (-6.07 +/- 1.38 s(-1), P < 0.05). Cortical R2* levels remained low after furosemide and did not vary with field strength. Correlations between measurements of defined cortical and medullary regions of interest within kidneys were greater at each sampling level and segment at 3.0 T as compared to 1.5 T. For patients studied with 3.0 T, furosemide administration induced a lesser fall in R2* in poststenotic kidneys at 3.0 T (-10.61 +/- 1.61 s(-1)) versus nonstenotic kidneys (-13.21 +/- 0.72 s(-1), P < 0.05). This difference was not evident in comparisons made at 1.5 T. The magnitude of furosemide-suppressible oxygen consumption at 3.0 T (-43%) corresponded more closely with reported experimental differences observed during direct measurement with tissue electrodes (45%-50%) than changes measured at 1.5 T. CONCLUSION: These results indicate that blood oxygen level dependent MR measurements at high field strength can better distinguish discrete cortical and inner medullary regions of the kidney and approximate measured differences in oxygen tension. Maneuvers that reduce oxygen consumption related to tubular solute transport allow functional evaluation of the interstitial compartment as a function of tissue oxygenation. Impaired response to alterations in oxygen consumption can be detected at 3 T more effectively than at 1.5 T and may provide real-time tools to examine developing parenchymal injury associated with impaired oxygenation.

Evidence on efficacy of treatments of venous ulcers and on prevention of ulcer recurrence.

Venous ulcers affect almost 1 million people in the United States. Delayed healing and frequent recurrence result in pain, disability, decreased quality of life, and loss of working days for the patients. Compression therapy is the most effective treatment of ulcers, but compliance with conservative treatment is important, and recurrence must be prevented by treating the underlying ambulatory venous hypertension. Evidence from prospective randomized trials confirm that ulcer recurrence is decreased with superficial vein surgery. Evidence is also increasing about the superiority of endovenous interventions, such as laser or radiofrequency ablation, over the classic open surgical treatment of high ligation, division, and stripping of the saphenous vein. Well-conducted randomized trials are still needed to provide grade A evidence to justify treatment of incompetent perforating veins. Treatment of proximal venous occlusion is important, and venous stents have been effective and durable. Open surgery is only considered today for iliac or iliocaval venous obstruction if endovascular treatment is not possible or has already failed. Open surgery for deep venous incompetence is recommended in centers of excellence, although evidence to support its effectiveness is of low quality.