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Split renal function in patients with unilateral atherosclerotic renal artery stenosis—effect of renal angioplasty

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Author(s): Aso Saeed ^* ^, , Elzbieta Nowakowska- Fortuna ^* , Gert Jensen ^*

Publication date (Electronic): 03 July 2017

Journal: Clinical Kidney Journal

Publisher: Oxford University Press

Keywords: colour duplex sonography, renal angiography, renal artery stenosis, renovascular hypertension, split renal function

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Abstract

Objective

To evaluate the effect of percutaneous transluminal renal angioplasty (PTRA) on split renal function (SRF) in patients with unilateral atherosclerotic renal artery stenosis (ARAS).

Methods

We performed a retrospective analysis of all consecutively examined patients at our centre with significant ARAS undergoing PTRA during 2002–07. A significant ARAS was defined as a lesion with a trans-stenotic mean arterial pressure gradient of at least 10 mmHg or a diameter stenosis >50% on angiography. Ambulatory (24 h) systolic and diastolic blood pressure (ASBP and ADBP, respectively) and calculated SRF using ^99mTc-DTPA renal scintigraphy were evaluated before (baseline) and 4 weeks after PTRA.

Results

ASBP and ADBP were significantly lower 4 weeks after PTRA compared with baseline levels. Although total estimated glomerular filtration rate (eGFR; four-variable Modification of Diet in Renal Disease equation) had not changed by PTRA, analysis of SRF showed significantly increased eGFR in stenotic kidneys and a comparable reduction in eGFR in non-stenotic kidneys 4 weeks after PTRA.

Conclusions

In patients with unilateral ARAS, PTRA significantly improved eGFR in stenotic kidneys and decreased filtration in contralateral, non-stenotic kidneys. These potentially beneficial effects may not be apparent when total renal function remains stable. The clinical significance of these findings needs to be evaluated further.

Related collections

Most cited references 21

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Revascularization versus medical therapy for renal-artery stenosis.

Keith Wheatley, Natalie Ives, Richard Gray … (2009)

Percutaneous revascularization of the renal arteries improves patency in atherosclerotic renovascular disease, yet evidence of a clinical benefit is limited. In a randomized, unblinded trial, we assigned 806 patients with atherosclerotic renovascular disease either to undergo revascularization in addition to receiving medical therapy or to receive medical therapy alone. The primary outcome was renal function, as measured by the reciprocal of the serum creatinine level (a measure that has a linear relationship with creatinine clearance). Secondary outcomes were blood pressure, the time to renal and major cardiovascular events, and mortality. The median follow-up was 34 months. During a 5-year period, the rate of progression of renal impairment (as shown by the slope of the reciprocal of the serum creatinine level) was -0.07x10(-3) liters per micromole per year in the revascularization group, as compared with -0.13x10(-3) liters per micromole per year in the medical-therapy group, a difference favoring revascularization of 0.06x10(-3) liters per micromole per year (95% confidence interval [CI], -0.002 to 0.13; P=0.06). Over the same time, the mean serum creatinine level was 1.6 micromol per liter (95% CI, -8.4 to 5.2 [0.02 mg per deciliter; 95% CI, -0.10 to 0.06]) lower in the revascularization group than in the medical-therapy group. There was no significant between-group difference in systolic blood pressure; the decrease in diastolic blood pressure was smaller in the revascularization group than in the medical-therapy group. The two study groups had similar rates of renal events (hazard ratio in the revascularization group, 0.97; 95% CI, 0.67 to 1.40; P=0.88), major cardiovascular events (hazard ratio, 0.94; 95% CI, 0.75 to 1.19; P=0.61), and death (hazard ratio, 0.90; 95% CI, 0.69 to 1.18; P=0.46). Serious complications associated with revascularization occurred in 23 patients, including 2 deaths and 3 amputations of toes or limbs. We found substantial risks but no evidence of a worthwhile clinical benefit from revascularization in patients with atherosclerotic renovascular disease. (Current Controlled Trials number, ISRCTN59586944.) 2009 Massachusetts Medical Society

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Stenting and medical therapy for atherosclerotic renal-artery stenosis.

Christopher J. Cooper, Timothy P Murphy, Donald E Cutlip … (2014)

Atherosclerotic renal-artery stenosis is a common problem in the elderly. Despite two randomized trials that did not show a benefit of renal-artery stenting with respect to kidney function, the usefulness of stenting for the prevention of major adverse renal and cardiovascular events is uncertain. We randomly assigned 947 participants who had atherosclerotic renal-artery stenosis and either systolic hypertension while taking two or more antihypertensive drugs or chronic kidney disease to medical therapy plus renal-artery stenting or medical therapy alone. Participants were followed for the occurrence of adverse cardiovascular and renal events (a composite end point of death from cardiovascular or renal causes, myocardial infarction, stroke, hospitalization for congestive heart failure, progressive renal insufficiency, or the need for renal-replacement therapy). Over a median follow-up period of 43 months (interquartile range, 31 to 55), the rate of the primary composite end point did not differ significantly between participants who underwent stenting in addition to receiving medical therapy and those who received medical therapy alone (35.1% and 35.8%, respectively; hazard ratio with stenting, 0.94; 95% confidence interval [CI], 0.76 to 1.17; P=0.58). There were also no significant differences between the treatment groups in the rates of the individual components of the primary end point or in all-cause mortality. During follow-up, there was a consistent modest difference in systolic blood pressure favoring the stent group (-2.3 mm Hg; 95% CI, -4.4 to -0.2; P=0.03). Renal-artery stenting did not confer a significant benefit with respect to the prevention of clinical events when added to comprehensive, multifactorial medical therapy in people with atherosclerotic renal-artery stenosis and hypertension or chronic kidney disease. (Funded by the National Heart, Lung and Blood Institute and others; ClinicalTrials.gov number, NCT00081731.).

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Central pulse pressure and aortic stiffness determine renal hemodynamics: pathophysiological implication for microalbuminuria in hypertension.

Sadayoshi Ito, Junichiro Hashimoto (2011)

A significant link has been reported between aortic stiffening and renal microvascular damage, but the underlying mechanism remains poorly understood. We hypothesized that alterations in central and renal hemodynamics are responsible for this link. In 133 patients with hypertension, pressure waveforms were recorded on the radial, carotid, femoral, and dorsalis pedis arteries with applanation tonometry to estimate the aortic pressures and aortic (carotid-femoral) and peripheral (carotid-radial and femoral-dorsalis pedis) pulse wave velocities. Flow-velocity waveforms were recorded on the renal segmental arteries with duplex ultrasound to calculate the resistive index (RI) as [1 - (end-diastolic velocity/peak systolic velocity)] and on the femoral arteries to calculate the reverse/forward flow index and diastolic/systolic forward-flow ratio. Albuminuria was defined as urinary albumin/creatinine ratio ≥30 mg/g of creatinine. The renal RI (mean: 0.65±0.07) was strongly correlated (P<0.001) with the aortic pulse pressure (r=0.62), incident pressure wave (r=0.55), augmented pressure (r=0.49), and aortic pulse wave velocity (r=0.51), although not with the mean arterial pressure or peripheral pulse wave velocities. The correlations remained highly significant after consideration of confounders including age, cholesterol, hemoglobin A(1c), and glomerular filtration rate. The renal RI was inversely correlated with the femoral reverse and diastolic forward flow indices. Both aortic pulse pressure and renal RI correlated with the urinary albumin/creatinine ratio independent of confounders. Each 0.1 increase in renal RI was associated with a 5.4-fold increase in the adjusted relative risk of albuminuria. In conclusion, increased aortic pulse pressure causes renal microvascular damage through altered renal hemodynamics resulting from increased peripheral resistance and/or increased flow pulsation.

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Author and article information

Journal

Journal ID (nlm-ta): Clin Kidney J

Journal ID (iso-abbrev): Clin Kidney J

Journal ID (publisher-id): ckj

Title: Clinical Kidney Journal

Publisher: Oxford University Press

ISSN (Print): 2048-8505

ISSN (Electronic): 2048-8513

Publication date (Print): August 2017

Publication date (Electronic): 03 July 2017

Publication date PMC-release: 03 July 2017

Volume: 10

Issue: 4

Pages: 496-502

Affiliations

[* ]Institute of Medicine, Department of Molecular and Clinical Medicine/Nephrology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden

Author notes

[* ]Correspondence and offprint requests to: Aso Saeed; E-mail: aso.saeed@ 123456vgregion.se

Article

Publisher ID: sfx052

DOI: 10.1093/ckj/sfx052

PMC ID: 5569696

SO-VID: 42afca72-400a-4ed1-9cd4-7400ed479db5

Copyright © © The Author 2017. Published by Oxford University Press on behalf of ERA-EDTA.

License:

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

Date received : 05 March 2017

Date accepted : 05 May 2017

Page count

Pages: 7

Categories

Subject: Vascular Disease

ScienceOpen disciplines: Nephrology

Keywords: colour duplex sonography,renal angiography,renal artery stenosis,renovascular hypertension,split renal function

Data availability:

ScienceOpen disciplines: Nephrology

Keywords: colour duplex sonography, renal angiography, renal artery stenosis, renovascular hypertension, split renal function

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