Drug-Resistant Hypertension
2019; Lippincott Williams & Wilkins; Volume: 73; Issue: 5 Linguagem: Norueguês
10.1161/hypertensionaha.118.12068
ISSN1524-4563
AutoresGiuseppe Maiolino, Peter W. de Leeuw, Daan J.L. van Twist, Giulio Barbiero, Michele Battistel, Garry Jennings, Gian Paolo Rossi,
Tópico(s)Sodium Intake and Health
ResumoHomeHypertensionVol. 73, No. 5Drug-Resistant Hypertension Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessReview ArticlePDF/EPUBDrug-Resistant HypertensionAn Intriguing Case Giuseppe Maiolino, Peter W. de Leeuw, Daan J.L. van Twist, Giulio Barbiero, Michele Battistel, Garry L.R. Jennings and Gian Paolo Rossi Giuseppe MaiolinoGiuseppe Maiolino Correspondence to Giuseppe Maiolino, University of Padua, via Giustiniani 2, Padova 35128, Italy. Email E-mail Address: [email protected] From the Hypertension Unit, Department of Medicine (G.M., G.P.R.), University of Padua, Italy , Peter W. de LeeuwPeter W. de Leeuw Department of Internal Medicine, Cardiovascular Research Institute Maastricht, Maastricht University Medical Centre, the Netherlands (P.W.d.L.) Department of Internal Medicine, Zuyderland Medical Centre, Sittard/Heerlen, the Netherlands (P.W.d.L., D.J.L.v.T.) , Daan J.L. van TwistDaan J.L. van Twist Department of Internal Medicine, Zuyderland Medical Centre, Sittard/Heerlen, the Netherlands (P.W.d.L., D.J.L.v.T.) , Giulio BarbieroGiulio Barbiero Department of Medicine, Institute of Radiology (G.B., M.B.), University of Padua, Italy , Michele BattistelMichele Battistel Department of Medicine, Institute of Radiology (G.B., M.B.), University of Padua, Italy , Garry L.R. JenningsGarry L.R. Jennings Sydney Health Partners, Sydney Medical School, University of Sydney, NSW, Australia (G.L.R.J.). and Gian Paolo RossiGian Paolo Rossi From the Hypertension Unit, Department of Medicine (G.M., G.P.R.), University of Padua, Italy Originally published25 Mar 2019https://doi.org/10.1161/HYPERTENSIONAHA.118.12068Hypertension. 2019;73:920–925Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: March 25, 2019: Ahead of Print Our clinical case has a very long history, lasting over 51 years.PatientThe patient was a 64-year-old lady when she was referred to our unit for the first time in 2006 with a remote history of right nephrectomy. The nephrectomy was performed for massive hydronephrosis and recurrent pyelonephritis when she was 23 years old.She was referred for so-called drug-resistant hypertension while on atenolol and manidipine. She had no symptoms and an unremarkable medical history except for iodine contrast medium allergy and the nephrectomy. A 50% stenosis of the left renal artery had recently been detected at renal Doppler ultrasound.On physical exam, her systolic blood pressure was very high, 211/87 mm Hg. She had a harsh 3/6 ejection bruit at Erb's point, and a systolic-diastolic bruit was heard all over the abdomen.Her blood tests were unremarkable, and in particular, she had normal renal function and serum potassium. Was this truly resistant hypertension? Clearly, it was not. The European Society of Hypertension/European Society of Cardiology guidelines define a patient as having resistant hypertension who is not at target blood pressure on three medications, one of which should be a diuretic, after implementation of appropriate lifestyle measures. The American Heart Association guidelines are more liberal, in that they do not require the lifestyle measures and include a patient as resistant when blood pressure control is achieved with four or more antihypertensive agents.1Her electrocardiogram was unremarkable, but transthoracic echocardiography showed a left ventricular mass index (49 g/m2.7) and relative wall thickness (0.48) increase with a normal left ventricular diastolic volume and ejection fraction, that is, concentric left ventricular hypertrophy. Her urinary albumin excretion was 325 mg/g of creatinine indicating early kidney damage.Discussion: First StepsProf Persu: I would try to check drug adherence. I would not consider angioplasty and stenting at this stage with only a 50% stenosis.Dr Maiolino: As a rule of thumb a stenosis attains hemodynamic relevance when ≥70% or when there is a post-stenotic dilatation. Hence, I definitely agree: angioplasty seems not warranted in this case. Nowadays, we systematically check for adherence to treatment by therapeutic drug monitoring in all patients with so-called resistant hypertension before labeling them as resistant.Prof Kroon: Was this lady a smoker?Dr Maiolino: She was not.Prof Kroon: Did she have peripheral vascular disease or signs of peripheral vascular disease?Dr Maiolino: She did not have other signs of peripheral vascular disease.Prof Kroon: If you put things together, she has only one kidney, she has albuminuria, and high blood pressure, but renal artery stenosis shown on the ultrasound is unlikely to be the cause. She requires further investigation. One kidney renal artery stenosis with high blood pressure is commonly associated with heart failure. Having said that, I wonder what the cause of the bruit was on her heart. You did not mention it on the echocardiogram report. Did you see any aortic valve abnormality?Dr Maiolino: She did not have aortic stenosis. She did have a thickened aortic valve, that is, aortic valve sclerosis, but no stenosis, and she had normal creatinine and estimated glomerular filtration rate.Prof de Leeuw: I have a question in the same line. This patient has a situation similar to the one-kidney, one-clip animal model, and that generally leads to very high blood pressure and deteriorating renal function. However she is very hypertensive, in the face of using atenolol. Did you consider the possibility of a pheochromocytoma?Dr Maiolino: Yes, she was screened for pheochromocytoma. Twenty-four–hour urinary metanephrine excretion was in the normal range.Prof Grossman: Did you do 24-hour blood pressure monitoring to confirm that there is not a white coat effect?Dr Maiolino: We did a 24-hour ambulatory blood pressure monitoring to exclude a white coat effect, and it confirmed systolic hypertension.Prof Bursztyn: What was the size of the left kidney?Dr Maiolino: We will show it later, but it was normal.Prof Bursztyn: You would expect the kidney would be hypertrophied in someone who has had a single kidney for 40 years. Having a normal size kidney suggests to me that there is functional stenosis.Dr Maiolino: This is a reasonable possibility and we followed the same reasoning and went further with the diagnostic studies.Dr Spiering: Did you measure renin and aldosterone under standardized conditions?Dr Maiolino: No, we did not because she was on atenolol, and she had really high systolic blood pressure. We thought that it was dangerous to undertake a washout or to switch therapy to a calcium channel blocker or doxazosin or their combination to screen her. It was our view that screening a patient with drugs like hydrochlorothiazide or angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, which will increase renin, will not give us reliable information in this case.Dr Jennings: We need to move on with the case. This lady has more secrets to reveal, I think.Dr Spiering: On physical examination, were there any signs of volume overload, such as edema or hepatojugular reflux? I ask because if that was the case and you corrected the volume overload, her blood pressure should go down, but her kidney function would deteriorate with this renal stenosis.Dr Maiolino: There were no signs of volume overload; we will show her neck and jugular veins in a movie.S. Ratanjee: This patient is not yet drug resistant because she is currently treated with only two drugs and without a diuretic. Secondly, the best treatment might be an angiotensin-converting enzyme inhibitor. However, before starting an inhibitor of the renin-angiotensin system, a captopril renogram should be considered to assess renal function and whether the stenosis is functional or not. If the captopril renogram demonstrates reduced renal perfusion after captopril, it would support the possibility that the renal artery stenosis is functional and mandate extreme caution in using an ACE inhibitor.Dr Maiolino: I agree.Next Chapter…The attending physician increased the antihypertensive therapy by adding 5 mg of ramipril. However, as he was worried about her renal function because she had only one kidney, with a reported renal artery stenosis, he ordered careful monitoring of the estimated glomerular filtration rate over the weeks after starting the angiotensin-converting enzyme inhibitor and ordered magnetic resonance (MR) angiography of the abdomen.Her blood pressure was adequately controlled thereafter, and her creatinine remained normal on medical therapy. This is why the patient did not attend our clinic for the next three years. She attended for follow-up in 2009. At this visit, she reported verbally that MR angiography had been done at another hospital, but she did not bring it with her. Her left renal artery stenosis was described as unchanged. A computed tomography angiogram was not feasible because of the allergy to the contrast medium.She did not present again for the next two years. In 2011, her blood pressure was high while on the same treatment, including ramipril. Renal Doppler ultrasound showed left renal artery stenosis unchanged at 50% with high resistivity of the left kidney and an arteriovenous fistula involving the right renal artery and the inferior vena cava. A new MR angiogram was arranged as the previous one was unavailable.After MR angiography, which was not provided, she was again lost to follow-up and did not return for five years. In 2016, she still had very high blood pressure on atenolol, lercanidipine, hydrochlorothiazide, amiloride, and valsartan, and physical exam was unchanged.The movie of her neck shows pseudo-Lancisi sign with a visible carotid pulse secondary to her high pulse pressure. (Movie S1 in the online-only Data Supplement).Dr Maiolino: We asked her to bring the Digital Versatile Disc with the images on her next visit. What else would you do?Prof Bursztyn: One possibility is to consider surgery to reconnect the kidney.Dr van Twist: A few years ago, there was a study on the ROX Coupler,2 which involves creating an arteriovenous fistula to reduce blood pressure. This lady has a natural variant of the ROX Coupler. Can you explain why the blood pressure is so high?Dr Maiolino: Excellent comment. Clearly, the arteriovenous fistula was not very successful in lowering blood pressure in this case.Dr van Twist: But why is she hypertensive? I do not understand that.Dr Maiolino: I will address this later when discussing the pathophysiology.Prof Burnier: Her medications included 7 pills a day, if I counted correctly. I would probably bring her to the hospital and give her the drugs under control. In a patient who does not show up for 2 years, then does not show up for another 5 years, the likelihood is that she takes none or very little of what you prescribe; I would check adherence before doing anything else, as any procedure that is considered should be done after making sure that she takes what you prescribe.Dr Maiolino: Yes, I concur, about 50% of so-called resistant hypertensive patients are actually not adherent.Prof Dominiczak: Could I make a technological comment? I am surprised that in your fantastic academic center in Italy, you need to bring your magnetic resonance imaging on a Digital Versatile Disc. I thought that we are progressing with precision medicine and digital radiology across Europe, that these types of investigations are accessible to physician and we do not need to do what is happening in the United States where the patient goes with his radiograph to the doctor because the insurance company would not share. So, could Prof Rossi explain this to me?Prof Rossi: We now have all the radiological examinations available online in our fantastic academic center as you said, and this is no longer an issue. However, this case lasted 51 years. She had the first MR many years before and did not want to come to Padua to have the test because she lived in the eastern part of the Veneto region. She preferred to have her MR angiography done at her local hospital. She did not bring the Digital Versatile Disc until she was pushed to do so.Prof Grossman: Okay, you are excused. On her first visit, her potassium was 3.6 mmol/L, which is a little low, but I did not see electrolytes at the last few visits. What happened to the electrolytes during the follow-up?Dr Maiolino: The blood tests were unremarkable, and they did not change significantly after 2006. It is relevant that the patient was not only on hydrochlorothiazide but also an angiotensin receptor blocker and amiloride, which may increase potassium. Therefore, it is not unexpected that her potassium was within the normal range.Prof Rossi: Can I propose that we move forward and look at the MR angiography because when I saw it, I was shocked.Magnetic resonance imaging Is ViewedThe patient was reevaluated in 2016 while on atenolol and lercanidipine. Valsartan had been withdrawn by her primary care physician for unknown reasons, and the systolic blood pressure was still very high (216/78 mm Hg) with an unchanged physical exam. She brought the images of the MR angiography, which showed a right renal artery stump, 7 mm in diameter, connected through a large arteriovenous fistula involving multiple dilated segments, up to a maximum of 40 mm in diameter, to the inferior vena cava (Figure 1).Download figureDownload PowerPointFigure 1. By magnetic resonance angiography, it is possible to detect the right renal artery stump, 7 mm in diameter (black arrow), connected through a large arteriovenous fistula entailing multiple dilated segments, up to a maximum of 40 mm in diameter (white arrows), to the inferior vena cava (black arrow head). Please note the funneling aorta below the origin of the renal arteries (see text).As already described, the patient underwent a total nephrectomy in 1965. The artichoke technique was used whereby the surgeon clamped the renal artery and the renal vein, ligated them together, and then removed the kidney. This procedure has been abandoned because of the high risk of arteriovenous fistulae.We consulted with the vascular surgeon who gave an unequivocal recommendation to close the arteriovenous fistula because of the high risk of rupture with fatal hemorrhage. However, he felt that surgical closure was a high-risk procedure and suggested that we consult the interventional radiologist, who recommended percutaneous embolization.The patient was admitted in April 2016 for a percutaneous arteriovenous fistula embolization procedure. To allow a better planning of the interventional procedure, the patient was scheduled for computed tomography angiography of the abdominal aorta, as the previous MR was five years old. Because of the contrast medium allergy, the patient had prophylaxis according to guidelines, and an anesthesiologist was present in the computed tomography facility. After the injection of the iodine contrast medium, the patient had an anaphylactic reaction successfully treated with methylprednisolone, chlorpheniramine, and ethylephrine according to guidelines. This was followed by a swift recovery and discharge in good health after one day.Prof Rossi: At this stage, she was understandably very scared as she was now aware of both the high risk of rupture of her arteriovenous fistula and the high risk of the surgical correction. She was also concerned about a new interventional procedure because of her allergy to the contrast medium. She was scheduled again for percutaneous closure procedure, but on this occasion, carbon dioxide was used as contrast medium.She was admitted again in October 2016, with still uncontrolled blood pressure (165/80 mm Hg), on multiple antihypertensive drugs. The arteriovenous embolization procedure was performed in the angiography suite with anesthesiology support under local anesthesia with carbon dioxide as contrast medium.The images of the procedure show the right renal artery and the arteriovenous fistula (Figure 2A; Movie S2). After delivery of the vascular plug Amplatzer device (14 mm) by the interventional radiologist, it is possible to see closure of the arteriovenous fistula (Figure 2B; Movie S3). Immediately after the procedure, her blood pressure dropped to 120/75 mm Hg.Download figureDownload PowerPointFigure 2. Invasive angiography images using carbon dioxide injection. A, At angiography it is possible to recognize the right renal artery (black arrow) and the arteriovenous fistula (white arrows). B, After delivery of the vascular plug Amplatzer device (14 mm; white arrow), it is possible to notice the closure of the arteriovenous fistula (black arrow).At discharge, her blood pressure was 125/75 mm Hg on the same therapy she had at admission: atenolol, hydrochlorothiazide, amiloride, lercanidipine, and valsartan. At one-month follow-up, she was still normotensive with lercanidipine and valsartan only. Three months later, the occlusion of the arteriovenous fistula was confirmed at contrast-enhanced Doppler ultrasound. The patient's last follow-up visit was in January 2018 and she was still normotensive on the same medical therapy.Dr Jennings: This lady was initially diagnosed with left renal artery stenosis with a Doppler ultrasound. I cannot imagine that a fistula like this could be missed. At that time, did she not have cardiac dilation, which you would expect to see in someone with a high stroke volume like this? Perhaps the fistula was missed, and it has gradually progressed. The other possibility is that something has happened in the meantime to create the lesion. I do not think we know the answer.Dr Maiolino: It is difficult to say exactly what happened retrospectively. Presumably, the fistula progressed with time; it increased in flow, and this affected the cardiovascular system, even though we did not see overt left ventricular dilatation.Dr Sharabi: The only explanation I have to your question is perhaps that the local hemodynamics changed after the closure. Perhaps, what was considered nonsignificant renal artery stenosis was in retrospect significant artery stenosis because of the flow that went to the remaining kidney. Otherwise, it is a miracle why, after this procedure, her blood pressure was well controlled. Instead of 7 medications, she needed only 2 medications. So maybe local hemodynamic changes cured her.Prof Rossi: In fact, if you look carefully at the very first image that you saw of the fistula (Figure 1), the aorta downstream of the fistula was curved and funneling, which is consistent with the idea that she developed a steal of blood flow through the arteriovenous fistula and rendered the left kidney and the distal aorta relatively hypoperfused because of a Venturi effect. The other explanation that we had was that the 50% renal artery stenosis hemodynamically was totally irrelevant and that she developed nephroangiosclerosis in the left kidney shown by the high resistivity index.Dr van Twist: Could it be that the patient started taking her pills after she had this intervention in accord with Professor Burnier's earlier question?Dr Maiolino: Of course, this is a possibility, but the probability is low as blood pressure fell rapidly after the procedure and remained low.Dr van Twist: I do not understand why closure of the fistula leads to a decrease in blood pressure, as this is, in fact, exactly the opposite to implantation of a ROX Coupler, which results in a blood pressure decrease?Dr Maiolino: We will review the ROX Coupler trial later.Prof de Leeuw: A lot of data from the surgical literature show that when you clamp an arteriovenous fistula, there is an immediate rise in blood pressure. Did you see any changes during the operation that could provide an extra argument that the fistula was indeed the problem?Dr Maiolino: Actually, the blood pressure dropped quickly after the arteriovenous fistula closure.Prof de Leeuw: But what happened when the arteriovenous fistula was clamped?Dr Maiolino: As I said, there was a decrease of the invasively assessed blood pressure that was continuously recorded from the closure of the arteriovenous fistula until the removal of the arterial sheath, that is, approximately ten minutes. To the best of my knowledge, the blood pressure decrease secondary to an arteriovenous fistula creation has been disputed in the acute phase (minutes),3 while it is controversial in the subacute phase (days-weeks) with studies demonstrating an increase,3 no effect,4 or a decrease of blood pressure.5 On the other hand, closest to our case is the closure of arteriovenous fistulas that has been carried out in studies on patients, unfortunately without a sham-controlled group. The acute arteriovenous fistula closure has been reported to have either an increasing6,7 or no effect8,9 on blood pressure, whereas the subacute arteriovenous fistula closure determines an increase10,11 or no effect on blood pressure.12,13Dr Barigou: You did not do hormonal examination, and I do not understand why. If a patient has significant hypertension, we try to do it. One really important point: is there a renin-secreting remnant that could be related to the vessels that remained in the organ? There could have been part of the kidney related to this fistula that has been secreting renin for a long time. It could be a renin-dependent hypertension. That would also explain why after excluding the lesion, the blood pressure dropped radically. This is a hypothesis, but unfortunately, we do not have hormones.Dr Maiolino: Our long-standing experience is that if we did the hormones on multiple drugs, they would be not interpretable. Moreover, as I already mentioned, with such high systolic blood pressure, it was felt to be unsafe to try a washout or a switch approach, particularly in a patient with a rupture-prone arteriovenous fistula.Dr Petramala: What happened to her urinary albumin excretion after treatment of the fistula?Dr Maiolino: We did check her albumin excretion in January 2018, and it had normalized.Prof de Leeuw: Another point puzzles me. We know from patients with arteriovenous fistulas, like patients with beriberi or Paget disease, that they become volume overloaded. You stated that this patient had no signs of volume overload. How do you explain this?Dr Maiolino: It depends what do you mean with volume overload. The patient did not have a clinically detectable volume overload, as she did not have left ventricle dilatation, no signs of peripheral edema, or hepatojugular reflux. Of course, we are not capable of excluding a subclinical volume overload.Prof de Leeuw: But, if you have experience in patients with beriberi for instance, or other types of Paget disease, you always find some peripheral edema.Prof Rossi: I think it depends, Peter, very much on the stage when you see the patients. Actually, this lady has normal left ventricular systolic function, as Dr Maiolino pointed out. It depends, also, very much on the size of the fistula. Obviously, she had a hyperdynamic circulation, and I agree with you that, eventually, she would have gone into heart failure. In our experience in a patient with chronic renal failure prepared for dialysis, we have had to close the arteriovenous fistula because of nocturnal paroxysmal dyspnea and worsening exertional dyspnea, portending to overt decompensated heart failure. This was another reason of concern.With regard to adherence to treatment, I think she was adherent, and, in fact, we have a clue to that. The electrocardiogram did not show tachycardia, which is expected with this type of hemodynamics, because she was taking the prescribed atenolol.Dr Jennings: She certainly had a huge pulse pressure consistent with a significant arteriovenous anastomosis.Dr Courand: Another hypothesis is that there was steal of the fistula on the left kidney. When we see the left kidney on the computed tomography we observe a very small renal artery and with probably ischemic renal left kidney. When the fistula was closed, there was good perfusion on the left kidney.Dr Maiolino: This is a good possibility and is supported by an article published by Kang et al14 in the American Journal of Renal Physiology in 2011 on a rodent model of arteriovenous fistula. The authors demonstrated that the creation of an arteriovenous fistula causes the expected increase in the arteriovenous fistula blood flow and in cardiac output secondary to a decrease in peripheral vascular resistance. On the contrary, this model is associated with a decrease of the renal blood flow and an increase of the renal vascular resistance.Take-Home MessagesContrast guidelines do not always warrant safety, and the use of carbon dioxide instead of iodine contrast dye is feasible in allergic patients.Secondary forms of hypertension should always be considered and ruled out before accepting a diagnosis of resistant hypertension.An arteriovenous fistula can be overlooked for years and result in target organ damage.Resistant hypertension, particularly with a markedly elevated systolic pressure, might be due to an arteriovenous fistula, and its closure might resolve resistant hypertension. As was pointed out earlier, this is not consistent with the data from the literature, more specifically with the results of the ROX Coupler hypertension trial2 that reported on the effects of the ROX Coupler device, which creates a fistula between the iliac artery and iliac vein. The conclusion of the authors is that the arteriovenous fistula is associated at six and twelve months with a significantly reduced office and 24-hour ambulatory monitoring blood pressure compared to controls.However, there are some words of caution in relation to the ROX Coupler hypertension-controlled trial: (1) there was no systematic screening for secondary hypertension or therapeutic adherence; (2) it was an open-label study with no blinding and no sham control group. These are key points, as we learned from the SIMPLICITY HTN-3 trial how important it is to have proper selection of the patients and adequate controls in interventional trials. (3) Finally, the rate of complications was not very low, and follow-up was short term.All the issues raised by the audience on the presented case and its discrepancies compared to the ROX Coupler hypertension trial are appropriate. However, we need to consider that the ROX Coupler trial follow-up period was one year, and there is the possibility that the conflicting results are secondary to the fact that our clinical case involves an arteriovenous fistula persistent for decades. Moreover, it may well depend on the size of the fistula and the associated amount of flow through it. In this case, there is little doubt that the fistula allowed very high flow with high venous return to the heart, increased stroke volume and accounting for the high systolic pressure.SummaryIn summary, long-term exposure to a large, iatrogenic high-flow fistula caused very severe systolic hypertension to develop, which was resistant to standard treatment. Closure of the fistula with percutaneous embolization resulted into a marked improvement of the hypertension, which became responsive to drug treatment.AcknowledgmentsWe are grateful to the following session audience members for contributing to the discussion: Alexandre Persu, Abraham A. Kroon, Ehud Grossman, Michael Bursztyn, Wilko Spiering, Sharad Ratanjee, Michel Burnier, Yehonatan Sharabi, Mohammed Barigou, Luigi Petramala, and Pierre-Yves Courand.DisclosuresNone.Sources of FundingNone.FootnotesThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.Presented at the European Meeting on Hypertension and Cardiovascular Protection, Barcelona, Spain, June 10, 2018, as part of the Clinical-Pathological Conference chaired by Anna F. Dominiczak and Garry L.R. Jennings. Giuseppe Maiolino presented the case.The online-only Data Supplement is available with this article at https://www.ahajournals.org/doi/suppl/10.1161/HYPERTENSIONAHA.118.12068.Correspondence to Giuseppe Maiolino, University of Padua, via Giustiniani 2, Padova 35128, Italy. Email giuseppe.[email protected]comReferences1. Carey RM, Calhoun DA, Bakris GL, et al. Resistant Hypertension: Detection, Evaluation, and Management: A Scientific Statement From the American Heart Association.Hypertension. 2018; 72:e53–e90. doi: 10.1161/HYP.0000000000000084LinkGoogle Scholar2. Lobo MD, Sobotka PA, Stanton A, et al; ROX CONTROL HTN Investigators. Central arteriovenous anastomosis for the treatment of patients with uncontrolled hypertension (the ROX CONTROL HTN study): a randomised controlled trial.Lancet. 2015; 385:1634–1641. doi: 10.1016/S0140-6736(14)62053-5CrossrefMedlineGoogle Scholar3. Savage MT, Ferro CJ, Sassano A, Tomson CR. 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Arteriovenous fistula closure after renal transplantation: a prospective study with 24-hour ambulatory blood pressure monitoring.Transplantation. 2008; 85:482–485. doi: 10.1097/TP.0b013e318160f163CrossrefMedlineGoogle Scholar12. Movilli E, Viola BF, Brunori G, Gaggia P, Camerini C, Zubani R, Berlinghieri N, Cancarini G. Long-term effects of arteriovenous fistula closure on echocardiographic functional and structural findings in hemodialysis patients: a prospective study.Am J Kidney Dis. 2010; 55:682–689. doi: 10.1053/j.ajkd.2009.11.008CrossrefMedlineGoogle Scholar13. van Duijnhoven EC, Cheriex EC, Tordoir JH, Kooman JP, van Hooff JP. Effect of closure of the arteriovenous fistula on left ventricular dimensions in renal transplant patients.Nephrol Dial Transplant. 2001; 16:368–372.CrossrefMedlineGoogle Scholar14. Kang L, Yamada S, Hernandez MC, Croatt AJ, Grande JP, Juncos JP, Vercellotti GM, Hebbel RP, Katusic ZS, Terzic A, Nath KA. Regional and systemic hemodynamic responses following the creation of a murine arteriovenous fistula.Am J Physiol Renal Physiol. 2011; 301:F845–F851. doi: 10.1152/ajprenal.00311.2011CrossrefGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited ByDominiczak A and Meyer T (2019) Hypertension, Hypertension, 75:1, (3-4), Online publication date: 1-Jan-2020. May 2019Vol 73, Issue 5 Advertisement Article InformationMetrics © 2019 American Heart Association, Inc.https://doi.org/10.1161/HYPERTENSIONAHA.118.12068PMID: 30905196 Originally publishedMarch 25, 2019 PDF download Advertisement SubjectsHypertension
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