The efficacy of removable devices to offload and heal neuropathic plantar forefoot ulcers in people with diabetes: a single-blinded multicentre randomised controlled trial.

Non-removable offloading is the 'gold standard' treatment for neuropathic diabetic plantar forefoot ulcers. However, removable offloading is the common 'standard of care'. We compared three removable offloading devices for ulcer healing efficacy. In this multicentre, randomised controlled trial, 60 persons with neuropathic diabetic plantar forefoot ulcers were randomly assigned to wear a custom-made knee-high cast [BTCC (bivalved TCC)], custom-made ankle-high cast shoe or a prefabricated ankle-high forefoot-offloading shoe (FOS). Primary outcome was healing at 12 weeks. Dynamic plantar pressures, daily stride count and treatment adherence were assessed on a randomly selected subset (n = 35). According to intention-to-treat analysis, 58% of patients healed with BTCC [OR 0·77 (95% CI 0·41-1·45) versus FOS], 60% with cast shoe [OR 0·81 (95% CI 0·44-1·49) versus FOS] and 70% with FOS (P = 0·70). Mean ± SD peak pressure in kPa at the ulcer site was 81 ± 55 for BTCC, 176 ± 80 for cast shoe and 107 ± 52 for FOS (P = 0·005); stride count was 4150 ± 1626, 3514 ± 1380 and 4447 ± 3190, respectively (P = 0·71); percentage of 2-week intervals that patients wore the device <50% of time was 17·3%, 5·2% and 4·9%, respectively. Non-significant differences in healing efficacy between the three devices suggest that, when non-removable offloading is contraindicated or not available, each can be used for plantar forefoot ulcer offloading. Efficacy is lower than previously found for non-removable offloading maybe because suboptimal adherence and high stride count expose the patient to high repetitive stresses. These factors should be carefully considered in decision making regarding ulcer treatment.

The association of chronic kidney disease and dialysis treatment with foot ulceration and major amputation.

OBJECTIVE: The objective of this study was to investigate the risk of chronic kidney disease (CKD) stage 4-5 and dialysis treatment on incidence of foot ulceration and major lower extremity amputation in comparison to CKD stage 3. METHODS: In this retrospective study, all individuals who visited our hospital between 2006 and 2012 because of CKD stages 3 to 5 or dialysis treatment were included. Medical records were reviewed for incidence of foot ulceration and major amputation. The time from CKD 3, CKD 4-5, and dialysis treatment until first foot ulceration and first major lower extremity amputation was calculated and analyzed by Kaplan-Meier curves and multivariate Cox proportional hazards model. Diabetes mellitus, peripheral arterial disease, peripheral neuropathy, and foot deformities were included for potential confounding. RESULTS: A total of 669 individuals were included: 539 in CKD 3, 540 in CKD 4-5, and 259 in dialysis treatment (individuals could progress from one group to the next). Unadjusted foot ulcer incidence rates per 1000 patients per year were 12 for CKD 3, 47 for CKD 4-5, and 104 for dialysis (P < .001). In multivariate analyses, the hazard ratio for incidence of foot ulceration was 4.0 (95% confidence interval [CI], 2.6-6.3) in CKD 4-5 and 7.6 (95% CI, 4.8-12.1) in dialysis treatment compared with CKD 3. Hazard ratios for incidence of major amputation were 9.5 (95% CI, 2.1-43.0) and 15 (95% CI, 3.3-71.0), respectively. CONCLUSIONS: CKD 4-5 and dialysis treatment are independent risk factors for foot ulceration and major amputation compared with CKD 3. Maximum effort is needed in daily clinical practice to prevent foot ulcers and their devastating consequences in all individuals with CKD 4-5 or dialysis treatment.

Fatal endotracheal tube obstruction due to the ball valve effect.

In patients suffering from pulmonary haemorrhage, or in patients who recently received a tracheostomy, acute occlusion of the endotracheal tube due to a blood clot is a rare, but well-known complication. Acute and complete occlusion of the tube is easily recognisable. There are various methods of removing the obstructive clot, such as using a bronchoscope with forceps, topical thrombolysis, saline lavage and suctioning. There are no guidelines concerning preventive routine bronchoscopic lavage. When there is a partial obstruction of the endotracheal tube, ventilation is possible, although high inspiratory pressures are necessary. If the clot functions as a ball valve ventil, raised intrathoracic pressure will cause right-sided heart failure or tension pneumothorax. It is important to recognise a partially obstructed tube in time and remove the obstruction.

Distal renal tubular acidosis with multiorgan autoimmunity: a case report.

A 61-year-old woman with a history of pernicious anemia presented with progressive muscle weakness and dysarthria. Hypokalemic paralysis (serum potassium, 1.4 mEq/L) due to distal renal tubular acidosis (dRTA) was diagnosed. After excluding several possible causes, dRTA was considered autoimmune. However, the patient did not meet criteria for any of the autoimmune disorders classically associated with dRTA. She had very high antibody titers against parietal cells, intrinsic factor, and thyroid peroxidase (despite normal thyroid function). The patient consented to a kidney biopsy, and acid-base transporters, anion exchanger type 1 (AE1), and pendrin were undetectable by immunofluorescence. Indirect immunofluorescence detected diminished abundance of AE1- and pendrin-expressing intercalated cells in the kidney, as well as staining by the patient's serum of normal human intercalated cells and parietal cells expressing the adenosine triphosphatase hydrogen/potassium pump (H(+)/K(+)-ATPase) in normal human gastric mucosa. The dRTA likely is caused by circulating autoantibodies against intercalated cells, with possible cross-reactivity against structures containing gastric H(+)/K(+)-ATPase. This case demonstrates that in patients with dRTA without a classic autoimmune disorder, autoimmunity may still be the underlying cause. The mechanisms involved in autoantibody development and how dRTA can be caused by highly specific autoantibodies against intercalated cells have yet to be determined.

Effects of sodium restriction and hydrochlorothiazide on RAAS blockade efficacy in diabetic nephropathy: a randomised clinical trial.

BACKGROUND: Reduction of dietary sodium intake or diuretic treatment increases renin-angiotensin-aldosterone system (RAAS) blockade efficacy in non-diabetic nephropathy. We aimed to investigate the effect of sodium restriction and the diuretic hydrochlorothiazide, separately and in combination, added to RAAS blockade on residual albuminuria in patients with type 2 diabetic nephropathy. METHODS: In this multicentre, double-blind, placebo-controlled, crossover randomised trial, we included patients with type 2 diabetic nephropathy. Main entry criteria were microalbuminaria or macroalbuminuria, and creatinine clearance of 30 mL/min or higher with less than 6 mL/min decline in the previous year. We tested the separate and combined effects of sodium restriction (dietary counselling in the outpatient setting) and hydrochlorothiazide (50 mg daily), added to standardised maximal angiotensin-converting enzyme (ACE) inhibition (lisinopril 40 mg daily), on albuminuria (primary endpoint). Patients were given hydrochlorothiazide (50 mg per day) or placebo during four treatment periods of 6 weeks. Both treatments were combined with regular sodium diet or sodium restriction (target sodium intake 50 mmol Na(+) per day). The 6-week treatment periods were done consecutively in a random order. Patients were randomised in blocks of two patients. The trial was analysed by intention to treat. The trial is registered with TrialRegister.nl, number 2366. FINDINGS: Of 89 eligible patients, 45 were included in the study. Both sodium restriction and hydrochlorothiazide significantly reduced albuminuria, irrespective of treatment sequence. Residual geometric mean albuminuria with baseline treatment was 711 mg per day (95% CI 485-1043); it was significantly reduced by sodium restriction (393 mg per day [258-599], p=0·0002), by hydrochlorothiazide (434 mg per day [306-618], p=0·0003), and to the greatest extent by their combination (306 mg per day [203-461], p<0·0001). Orthostatic complaints were present in two patients (4%) during baseline treatment, five (11%) during addition of sodium restriction, five (11%) during hydrochlorothiazide treatment, and 12 (27%) during combination treatment. No serious adverse events occurred. INTERPRETATION: We conclude that sodium restriction is an effective non-pharmacological intervention to increase RAAS blockade efficacy in type 2 diabetic nephropathy. FUNDING: None.

Test characteristics of the aldosterone-to-renin ratio as a screening test for primary aldosteronism.

BACKGROUND: The aldosterone-to-renin ratio (ARR) is a widely used screening test for primary aldosteronism. Current guidelines recommend a cut-off value of 91  pmol/mU. Studies on its sensitivity, specificity, reproducibility and the role of medication have been conflicting. We prospectively assessed the test characteristics of the ARR and the effect of combination antihypertensive treatment. METHODS: In 178 patients with persistent hypertension despite the use of at least two antihypertensives, plasma renin and aldosterone were assessed twice within an interval of 4 weeks. All patients underwent an intravenous salt loading test. A posttest plasma aldosterone exceeding 235  pmol/l was considered diagnostic for primary aldosteronism. ARR was repeated after 4 weeks of standardized treatment with a calcium channel blocker and/or α-adrenergic-receptor blocker. RESULTS: The prevalence of primary aldosteronism was 15.2%. The median ARR was 35.0 (interquartile range 16.2-82.0) in primary aldosteronism versus 7.1 (2.2-17.5) pmol/mU in essential hypertensive patients (P < 0.001). Under random medication, the ARR had 22.2% sensitivity and 98.7% specificity. On standardized treatment, the ARR rose from 9.6 (2.5-24.8) to 21.4 (10.8-52.1) (P < 0.001). Multivariate regression showed that angiotensin-converting enzyme (ACE)-inhibitors and angiotensin II-receptor blockers were responsible for the lower ARR during random treatment. The area under the receiver operating characteristic curve was, however, similar under random and standardized treatment (84 vs. 86%, respectively, P = 0.314). Bland-Altman plots showed an almost five-fold difference in ARR values taken under the same conditions. CONCLUSION: ARR sensitivity for primary aldosteronism is low when the recommended cut-off is used. Reproducibility is also poor, stressing the need for alternative screening tests.

Determinants of blood pressure reduction by eplerenone in uncontrolled hypertension.

BACKGROUND: Add-on therapy with aldosterone receptor antagonists has been reported to lower blood pressure (BP) in patients with uncontrolled hypertension. We assessed potential predictors of this response. METHODS: In essential hypertensive patients with uncontrolled BP, despite the use of at least two antihypertensives, plasma renin and aldosterone concentrations and the transtubular potassium gradient (TTKG) were measured. Patients were treated with eplerenone 50 mg daily on top of their own medication. The office and ambulatory BP response and biochemical changes were evaluated after 1 week and 3 months of treatment and 6 weeks after discontinuation. Potential predictors for the change in 24-h ambulatory BP were tested in a multivariate regression model. RESULTS: One hundred and seventeen patients with a mean age of 50.5 ± 6.6 years were included. Office BP decreased from 149/91 to 142/87 mmHg (P < 0.001) and ambulatory BP from 141/87 to 132/83 mmHg after 3 months of treatment (P < 0.001). Six weeks after discontinuation of eplerenone, office and ambulatory BP measurements returned to baseline values. Treatment resulted in a small rise in serum potassium and creatinine, and a small decrease in the TTKG. In a multivariate model, neither renin, aldosterone, or their ratio, nor the TTKG predicted the BP response. Only baseline ambulatory SBP predicted the BP response, whereas the presence of left ventricular hypertrophy was associated with a smaller BP reduction. CONCLUSION: Add-on therapy with eplerenone effectively lowers BP in patients with difficult-to-treat primary hypertension. This effect is unrelated to circulating renin-angiotensin-aldosterone system activity and renal mineralocorticoid receptor activity as assessed by the TTKG.

Moderate dietary sodium restriction added to angiotensin converting enzyme inhibition compared with dual blockade in lowering proteinuria and blood pressure: randomised controlled trial.

OBJECTIVE: To compare the effects on proteinuria and blood pressure of addition of dietary sodium restriction or angiotensin receptor blockade at maximum dose, or their combination, in patients with non-diabetic nephropathy receiving background treatment with angiotensin converting enzyme (ACE) inhibition at maximum dose. DESIGN: Multicentre crossover randomised controlled trial. SETTING: Outpatient clinics in the Netherlands. PARTICIPANTS: 52 patients with non-diabetic nephropathy. INTERVENTIONS: All patients were treated during four 6 week periods, in random order, with angiotensin receptor blockade (valsartan 320 mg/day) or placebo, each combined with, consecutively, a low sodium diet (target 50 mmol Na(+)/day) and a regular sodium diet (target 200 mmol Na(+)/day), with a background of ACE inhibition (lisinopril 40 mg/day) during the entire study. The drug interventions were double blind; the dietary interventions were open label. MAIN OUTCOME MEASURES: The primary outcome measure was proteinuria; the secondary outcome measure was blood pressure. RESULTS: Mean urinary sodium excretion, a measure of dietary sodium intake, was 106 (SE 5) mmol Na(+)/day during a low sodium diet and 184 (6) mmol Na(+)/day during a regular sodium diet (P<0.001). Geometric mean residual proteinuria was 1.68 (95% confidence interval 1.31 to 2.14) g/day during ACE inhibition plus a regular sodium diet. Addition of angiotensin receptor blockade to ACE inhibition reduced proteinuria to 1.44 (1.07 to 1.93) g/day (P=0.003), addition of a low sodium diet reduced it to 0.85 (0.66 to 1.10) g/day (P<0.001), and addition of angiotensin receptor blockade plus a low sodium diet reduced it to 0.67 (0.50 to 0.91) g/day (P<0.001). The reduction of proteinuria by the addition of a low sodium diet to ACE inhibition (51%, 95% confidence interval 43% to 58%) was significantly larger (P<0.001) than the reduction of proteinuria by the addition of angiotensin receptor blockade to ACE inhibition (21%, (8% to 32%) and was comparable (P=0.009, not significant after Bonferroni correction) to the reduction of proteinuria by the addition of both angiotensin receptor blockade and a low sodium diet to ACE inhibition (62%, 53% to 70%). Mean systolic blood pressure was 134 (3) mm Hg during ACE inhibition plus a regular sodium diet. Mean systolic blood pressure was not significantly altered by the addition of angiotensin receptor blockade (131 (3) mm Hg; P=0.12) but was reduced by the addition of a low sodium diet (123 (2) mm Hg; P<0.001) and angiotensin receptor blockade plus a low sodium diet (121 (3) mm Hg; P<0.001) to ACE inhibition. The reduction of systolic blood pressure by the addition of a low sodium diet (7% (SE 1%)) was significantly larger (P=0.003) than the reduction of systolic blood pressure by the addition of angiotensin receptor blockade (2% (1)) and was similar (P=0.14) to the reduction of systolic blood pressure by the addition of both angiotensin receptor blockade and low sodium diet (9% (1)), to ACE inhibition. CONCLUSIONS: Dietary sodium restriction to a level recommended in guidelines was more effective than dual blockade for reduction of proteinuria and blood pressure in non-diabetic nephropathy. The findings support the combined endeavours of patients and health professionals to reduce sodium intake. Trial registration Netherlands Trial Register NTR675.

Continuous ambulatory peritoneal dialysis after intra-abdominally placed synthetic mesh for ventral hernia repair.

BACKGROUND: We present a unique experience with a patient who had undergone continuous ambulatory peritoneal dialysis (CAPD) after laparoscopic repair of ventral incisional hernia (LRVIH) with an expanded polytetrafluoroethylene (e-PTFE) mesh (DualMesh(®); WL Gore) and who later suffered from multiple episodes of CAPD-related peritonitis without any signs of mesh infection. METHODS: A 48-year-old man with an open abdominal aortic reconstruction in 1994 for occlusive arterial disease presented with an incisional ventral hernia. He underwent LRVIH using an e-PTFE mesh of 30×20 cm. RESULTS: Postoperatively, he developed renal failure. For various reasons, the only therapeutic option was CAPD. A CAPD-catheter was implanted via laparoscopy, taking care not to compromise the mesh that was completely covered with neoperitoneum. After 3 months of uneventful CAPD, he developed a bacterial peritonitis. Antibiotic treatment failed and the CAPD-catheter was removed. The mesh was left in place and the patient recovered. Later on another CAPD-catheter was implanted via laparoscopy and used for 10 months. Again he developed peritonitis from which he recovered after catheter removal. Mesh was left in place and remained uninfected, probably protected from intra-abdominal bacteria by the neoperitoneum. CONCLUSIONS: The risk of secondary infection of an intra-abdominal mesh seems to diminish largely after neoperitonealization of the mesh. CAPD seems possible in a patient with an intra-abdominal mesh when it is covered with neoperitoneum.

Effect of the urotensin receptor antagonist palosuran in hypertensive patients with type 2 diabetic nephropathy.

The urotensin system has been hypothesized to play an important role in the pathophysiology of diabetic nephropathy. In this multicenter, randomized, double-blind, placebo-controlled, 2-period crossover study, the effects of the urotensin receptor antagonist palosuran on urinary albumin excretion and blood pressure in hypertensive patients with type 2 diabetic nephropathy treated with a single blocker of the renin-angiotensin-aldosterone system were assessed. Patients with 24-hour albuminuria >0.5 and <3.0 g, systolic blood pressure >135 and <170 mm Hg, and/or diastolic blood pressure >85 and <110 mm Hg received both palosuran 125 mg BID and placebo for 4 weeks each. Fifty-four patients (20% women; mean age: 61.6 years, blood pressure: 155/84 mm Hg, and albuminuria: 1016 mg per 24 hours) were included in the per-protocol analysis. Palosuran did not affect albuminuria, blood pressure, glomerular filtration rate, or renal plasma flow significantly. These results question whether urotensin receptor antagonism represents a new treatment strategy in this high-risk patient population.

Prevention of acute kidney injury and protection of renal function in the intensive care unit. Expert opinion of the Working Group for Nephrology, ESICM.

BACKGROUND: Acute renal failure on the intensive care unit is associated with significant mortality and morbidity. OBJECTIVES: To determine recommendations for the prevention of acute kidney injury (AKI), focusing on the role of potential preventative maneuvers including volume expansion, diuretics, use of inotropes, vasopressors/vasodilators, hormonal interventions, nutrition, and extracorporeal techniques. METHOD: A systematic search of the literature was performed for studies using these potential protective agents in adult patients at risk for acute renal failure/kidney injury between 1966 and 2009. The following clinical conditions were considered: major surgery, critical illness, sepsis, shock, and use of potentially nephrotoxic drugs and radiocontrast media. Where possible the following endpoints were extracted: creatinine clearance, glomerular filtration rate, increase in serum creatinine, urine output, and markers of tubular injury. Clinical endpoints included the need for renal replacement therapy, length of stay, and mortality. Studies are graded according to the international Grades of Recommendation, Assessment, Development, and Evaluation (GRADE) group system. CONCLUSIONS AND RECOMMENDATIONS: Several measures are recommended, though none carries grade 1A. We recommend prompt resuscitation of the circulation with special attention to providing adequate hydration whilst avoiding high-molecular-weight hydroxy-ethyl starch (HES) preparations, maintaining adequate blood pressure using vasopressors in vasodilatory shock. We suggest specific vasodilators [corrected] under strict hemodynamic control, sodium bicarbonate for emergency procedures administering contrast media, and periprocedural hemofiltration in severe chronic renal insufficiency undergoing coronary intervention. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00134-009-1678-y) contains supplementary material, which is available to authorized users.

Stent placement in patients with atherosclerotic renal artery stenosis and impaired renal function: a randomized trial.

BACKGROUND: Little is known about the efficacy and safety of renal artery stenting in patients with atherosclerotic renal artery stenosis (ARAS) and impaired renal function. OBJECTIVE: To determine the efficacy and safety of stent placement in patients with ARAS and impaired renal function. DESIGN: Randomized clinical trial. Randomization was centralized and computer generated, and allocation was assigned by e-mail. Patients, providers, and persons who assessed outcomes were not blinded to treatment assignment. SETTING: 10 European medical centers. PARTICIPANTS: 140 patients with creatinine clearance less than 80 mL/min per 1.73 m(2) and ARAS of 50% or greater. INTERVENTION: Stent placement and medical treatment (64 patients) or medical treatment only (76 patients). Medical treatment consisted of antihypertensive treatment, a statin, and aspirin. MEASUREMENTS: The primary end point was a 20% or greater decrease in creatinine clearance. Secondary end points included safety and cardiovascular morbidity and mortality. RESULTS: Forty-six of 64 patients assigned to stent placement had the procedure. Ten of the 64 patients (16%) in the stent placement group and 16 patients (22%) in the medication group reached the primary end point (hazard ratio, 0.73 [95% CI, 0.33 to 1.61]). Serious complications occurred in the stent group, including 2 procedure-related deaths (3%), 1 late death secondary to an infected hematoma, and 1 patient who required dialysis secondary to cholesterol embolism. The groups did not differ for other secondary end points. LIMITATION: Many patients were falsely identified as having renal artery stenosis greater than 50% by noninvasive imaging and did not ultimately require stenting. CONCLUSION: Stent placement with medical treatment had no clear effect on progression of impaired renal function but led to a small number of significant procedure-related complications. The study findings favor a conservative approach to patients with ARAS, focused on cardiovascular risk factor management and avoiding stenting.

Selective cyclooxygenase-2 (COX-2) inhibition reduces proteinuria in renal patients.

BACKGROUND: Renoprotection is predicted by the antiproteinuric efficacy of a pharmacological agent. Non-steroidal anti-inflammatory drugs (NSAIDs) interfering non-selectively in the prostaglandin system have strong antiproteinuric potency without reduction of systemic blood pressure. The effect of the selective COX-2 inhibitor rofecoxib in proteinuric patients is unknown, granted recently reported detrimental effects in non-renal patients. Short-term effects of rofecoxib on proteinuria and blood pressure as compared to NSAID and RAAS blockade were studied. METHODS: Sixteen stable patients [mean proteinuria 4.4 g/ day; MAP 103 mmHg)] were included after a wash-out period. Hydrochlorothiazide 12.5 mg QD was given throughout. Additional blood pressure control was ensured by non-RAAS blocking antihypertensive agents. Patients received rofecoxib 25 mg QD, 50 mg QD and indomethacin 75 mg BID in randomized order for 4 weeks. Thereafter, a subset of the included patients (n = 11) received lisinopril 40 mg QD for 6 weeks preceded by a wash-out period. RESULTS: Rofecoxib exerted a dose-dependent antiproteinuric effect. As compared to rofecoxib 25 and 50 mg, indomethacin was more effective [-18, -28 versus -49% (n = 16; P < 0.05)]. As compared to rofecoxib 50 mg, lisinopril was more effective [-21 versus -51% (n = 11; P < 0.05)]. No significant blood pressure changes were observed after rofecoxib and indomethacin, whereas lisinopril had a significant antihypertensive effect. CONCLUSION: Selective COX-2 inhibition reduces proteinuria without reduction of systemic blood pressure, pointing towards a specific renal effect, and may serve as a novel non-hypotensive adjunct antiproteinuric treatment.

Atherosclerotic renovascular disease and renal impairment: can we predict the effect of intervention?

Atherosclerotic renal artery stenosis (ARAS) is associated with hypertension, ischemic nephropathy, and high cardiovascular risk. We review the data on revascularization of the renal artery by percutaneous transluminal renal angioplasty (PTRA) and pharmacological therapy. In patients with severe ARAS and poorly controlled hypertension, PTRA can improve blood pressure control. In patients with rapid renal function loss and severe ARAS, PTRA can improve short-term renal function, but there is no evidence for long-term renoprotection. Recent evidence indicates that ARAS, and incidental renal artery stenosis, considerably increases cardiovascular risk, independent of blood pressure, renal function, and prevalent risk factors. This suggests that revascularization might potentially improve overall prognosis, but no data are available currently. The high cardiovascular risk warrants aggressive pharmacological treatment to prevent progression of the generalized vascular disorder. Ongoing trials will show whether revascularization has added, long-term effects on blood pressure, renal function, and cardiovascular prognosis.

Incidental renal artery stenosis is an independent predictor of mortality in patients with peripheral vascular disease.

In patients with peripheral vascular disease (PVD), mortality is high and renal artery stenosis (RAS) is a frequent incidental finding. RAS carries a high risk for mortality, but whether incidentally discovered RAS is a risk factor for mortality is unknown. The prognostic impact of incidental RAS for mortality was studied in 550 consecutive patients who underwent intra-arterial digital subtraction angiography for PVD in a single center between 1997 and 2000. In 491 patients (336 men, 155 women; mean follow-up 3.8 +/- 1.9 yr), the renal arteries were visualized and follow-up data were available. RAS (diameter reduction > 50%) was present in 26% of the patients. Mortality in the RAS group was 59 versus 28% in the non-RAS group (odds ratio 3.8; 95% confidence interval 2.5 to 5.7; P < 0.0001). Diabetes, previous myocardial infarction, history of PVD, stroke, and hypertension were more frequent in the RAS group; age was higher and GFR was lower in the RAS group. Therefore, RAS was associated with elevated mortality and increased prevalence of cardiovascular risk factors. Cox regression analysis showed that RAS was an independent predictor for mortality (P = 0.005), along with age, diabetes, smoking, previous myocardial infarction, history of PVD, and stroke. In patients who were evaluated for PVD by digital subtraction angiography, mortality was high. Incidental RAS was a frequent finding and an independent predictor for mortality. Whether RAS is a marker for or, alternatively, a mediator of the poor prognosis and whether prognosis can be improved by specific intervention should be the subject of future prospective studies.

Long-term effects of arterial stenting on kidney function for patients with ostial atherosclerotic renal artery stenosis and renal insufficiency.

It is uncertain whether renal artery stent placement in patients with atherosclerotic renovascular renal failure can prevent further deterioration of renal function. Therefore, the effects of renal artery stent placement, followed by patency surveillance, were prospectively studied in 63 patients with ostial atherosclerotic renal artery stenosis and renal dysfunction (i.e., serum creatinine concentrations of >120 micromol/L (median serum creatinine concentration, 171 micromol/L; serum creatinine concentration range, 121 to 650 micromol/L). Pre-stent renal (dys) function was stable for 28 patients and declining for 35 patients (defined as a serum creatinine concentration increase of > or =20% in 12 mo). The median follow-up period was 23 mo (interquartile range, 13 to 29 mo). Angioplasty to treat restenosis was performed in 12 cases. Five patients reached end-stage renal failure within 6 mo, and this was related to stent placement in two cases. Two other patients died or were lost to follow-up monitoring within 6 mo, with stable renal function. For the remaining 56 patients, the treatment had no effect on serum creatinine levels if function had previously been stable; if function had been declining, median serum creatinine concentrations improved in the first 1 yr [from 182 micromol/L (135 to 270 micromol/L ) to 154 micromol/L (127 to 225 micromol/L ); P < 0.05] and remained stable during further follow-up monitoring. In conclusion, stent placement, followed by patency surveillance, to treat ostial atherosclerotic renal artery stenosis can stabilize declining renal function. For patients with stable renal dysfunction, the usefulness is less clear. The possible advantages must be weighed against the risk of renal failure advancement with stent placement.