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      Transplant renal artery stenosis: clinical manifestations, diagnosis and therapy

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          Abstract

          Transplant renal artery stenosis (TRAS) is a well-recognized vascular complication after kidney transplant. It occurs most frequently in the first 6 months after kidney transplant, and is one of the major causes of graft loss and premature death in transplant recipients. Renal hypoperfusion occurring in TRAS results in activation of the renin–angiotensin–aldosterone system; patients usually present with worsening or refractory hypertension, fluid retention and often allograft dysfunction. Flash pulmonary edema can develop in patients with critical bilateral renal artery stenosis or renal artery stenosis in a solitary kidney, and this unique clinical entity has been named Pickering Syndrome. Prompt diagnosis and treatment of TRAS can prevent allograft damage and systemic sequelae. Duplex sonography is the most commonly used screening tool, whereas angiography provides the definitive diagnosis. Percutaneous transluminal angioplasty with stent placement can be performed during angiography if a lesion is identified, and it is generally the first-line therapy for TRAS. However, there is no randomized controlled trial examining the efficacy and safety of percutaneous transluminal angioplasty compared with medical therapy alone or surgical intervention.

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          Most cited references68

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          STUDIES ON EXPERIMENTAL HYPERTENSION

          These experiments indicate that, in dogs at least, ischemia localized to the kidneys is a sufficient condition for the production of persistently elevated systolic blood pressure. When the constriction of both main renal arteries is made only moderately severe in the beginning, the elevation of systolic blood pressure is unaccompanied by signs of materially decreased renal function. In this respect the hypertension in these animals resembles the hypertension which is associated with so called benign nephrosclerosis in man. Subsequent increase of the constriction of the main renal arteries does not materially damage renal function, probably because of adequate development of accessory circulation. More delicate methods for detecting a change may yet prove that some damage does occur. Almost complete constriction of both main renal arteries, from the beginning, results in great elevation of systolic blood pressure which is accompanied by severe disturbance of renal function and uremia. This resembles the type of hypertension which is associated with so called malignant nephrosclerosis, in the sense of Fahr (17). In several of the animals with persistent elevation of systolic blood pressure, anatomical changes were observed in the glomeruli, vessels and parenchyma of the kidneys which are most probably directly referable to the ischemia. It is hoped that these investigations will afford a means of studying the pathogenesis of hypertension that is associated with renal vascular disease.
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            Metaanalysis of the relative nephrotoxicity of high- and low-osmolality iodinated contrast media.

            To determine whether low-osmolality contrast media (LOCM) are less nephrotoxic than high-osmolality contrast media (HOCM), the authors searched MEDLINE and EMBASE databases and other sources to find randomized trials with data collected on changes in glomerular filtration rate or serum creatinine (SCr) level with LOCM and HOCM. Forty-five trials were found. Data were unavailable from 14 trials. When the P values from the other 31 trials were pooled, an overall P value of .02 was found. Among 24 trials with available data, the mean change in SCr was 0.2-6.2 mumol/L less with LOCM than HOCM. Among 25 trials with available data, the pooled odds of a rise in SCr level of more than 44 mumol/L with LOCM was 0.61 (95% confidence interval [CI], 0.48-0.77) times that after HOCM. For patients with existing renal failure, this odds ratio was 0.5 (CI, 0.36-0.68), while it was 0.75 (CI, 0.52-1.1) in patients without prior renal failure. Greater changes in SCr level occurred only in those with existing renal failure and were less common with LOCM (odds ratio, 0.44; CI, 0.26-0.73). Use of LOCM may be beneficial in patients with existing renal failure.
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              Hypertension after kidney transplantation.

              Few studies have examined the possible role of blood pressure (BP), independent of acute rejection and graft function, on outcomes after kidney transplantation. We investigated the prevalence, treatment, control, and clinical correlates of hypertension and its association with outcomes, using multivariate analyses with time-dependent covariates, in a retrospective cohort of 1,666 kidney transplant recipients. Hypertension was common, and its control was poor. For example, at 1 year, only 55.5% had a BP less than 140 mm Hg. Control improved only slightly in 1993-2002 compared to 1976-2002, even as patients administered 2 or more antihypertensive medications at 1 year increased from 43.5% to 54.6%. Independent correlates of higher BP included male sex, age, donor age, diabetes, body mass index, the presence of native kidneys, and delayed graft function. Previous acute rejection was associated with higher BP at virtually all times after transplantation, and these associations were independent of estimated creatinine clearance (C(Cr)). Conversely, an association between BP and subsequent acute rejection was not statistically significant when differences in C(Cr) were taken into account. After adjusting for the effects of acute rejection, C(Cr), and other variables, each 10 mm Hg of systolic BP was associated with an increased relative risk for graft failure (1.12; 95% confidence interval, 1.08 to 1.15; P < 0.0001), death-censored graft failure (1.17; 1.12 to 1.22; P < 0.0001), and death (1.18; 1.12 to 1.23; P < 0.0001). High BP is closely tied to graft function, but nevertheless is an independent risk factor for graft failure and mortality. Better strategies are needed to control BP after kidney transplantation.
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                Author and article information

                Journal
                Clin Kidney J
                Clin Kidney J
                ckj
                ndtplus
                Clinical Kidney Journal
                Oxford University Press
                2048-8505
                2048-8513
                February 2015
                09 December 2014
                09 December 2014
                : 8
                : 1
                : 71-78
                Affiliations
                [1 ]Department of Medicine, University of Rochester School of Medicine and Dentistry , Rochester, NY, USA
                [2 ]Department of Medicine, Albert Einstein College of Medicine , Bronx, NY, USA
                [3 ]Department of Surgery, Albert Einstein College of Medicine , Bronx, NY, USA
                [4 ]Department of Medicine, Maimonides Medical Center , Brooklyn, NY, USA
                [5 ]Department of Radiology, Albert Einstein College of Medicine , Bronx, NY, USA
                Author notes
                Correspondence to: Wei Chen; E-mail: wei_chen@ 123456urmc.rochester.edu
                [*]

                W.C. started this work when she was at the Albert Einstein College of Medicine and completed it after she started working at the University of Rochester School of Medicine and Dentistry.

                Article
                sfu132
                10.1093/ckj/sfu132
                4310434
                25713713
                fbbb43cb-4105-4082-aed7-b482065fb22c
                © The Author 2014. Published by Oxford University Press on behalf of ERA-EDTA.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

                History
                : 14 August 2014
                : 13 November 2014
                Categories
                Hypertension in Transplantation

                Nephrology
                flash pulmonary edema,hypertensive crisis,pickering syndrome,renal artery pseudoaneurysm,transplant renal artery stenosis

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