Coronary flow velocity reserve and inflammatory markers in living kidney donors

Ashwin Radhakrishnan; Anna Price; Luke Pickup; Jonathan Law; Kirsty McGee; Larissa Fabritz; Roxy  Senior; Richard Steeds; Charles Ferro; Jon Townend

doi:10.1016/j.ijcard.2020.08.013

Coronary flow velocity reserve and inflammatory markers in living kidney donors

Ashwin Radhakrishnan, Anna Price, Luke Pickup, Jonathan Law, Kirsty McGee, Larissa Fabritz, Roxy Senior, Richard Steeds, Charles Ferro, Jon Townend

Research output: Contribution to journal › Article › peer-review

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Abstract

Background: Coronary microvascular dysfunction is prevalent in chronic kidney disease (CKD), and may contribute to the development of myocardial dysfunction in CKD. Coronary flow velocity reserve (CFVR) is a marker of coronary microvascular function and falls with increasing CKD stage. Living kidney donors have renal function consistent with early stage CKD and concern has been raised about their cardiovascular risk. No studies to date have investigated the presence of coronary microvascular dysfunction in living kidney donors.

Methods: 25 healthy controls and 23 living kidney donors were recruited and underwent assessment with transthoracic echocardiography, Doppler CFVR, myocardial contrast echocardiography and serum multiplex immunoassay panels.

Results: Doppler CFVR was significantly reduced in living kidney donors compared to controls (mean CFVR 3.4 ± 0.7 vs 3.8 ± 0.6, mean difference 0.4 95% confidence interval 0.03–0.8, p =.036). Quantitative myocardial contrast echocardiography showed a trend towards reduced coronary flow reserve in living kidney donors. Compared to controls, living kidney donors had higher serum high sensitivity C reactive peptide (hsCRP) and lower levels of uromodulin.

Conclusions: This is the first study of CFVR in living kidney donors. We have shown that the modest drop in estimated glomerular filtration rate in living kidney donors is associated with lower values of Doppler CFVR compared to controls, suggesting that isolated reductions in renal function may lead to altered microvascular function. The increase in hsCRP and reduction in uromodulin suggests that chronic subclinical inflammation may contribute to altered microvascular function in this population.

Original language	English
Pages (from-to)	141-147
Number of pages	7
Journal	International Journal of Cardiology
Volume	320
Early online date	14 Aug 2020
DOIs	https://doi.org/10.1016/j.ijcard.2020.08.013
Publication status	Published - 1 Dec 2020

Bibliographical note

Funding Information:
The CRIB-FLOW study was funded by research grants from University Hospitals Birmingham Charity and the Metchley Park Medical Society . AMP, LCP and JPL are holders of British Heart Foundation Clinical Research Training Fellowships ( FS/16/73/32314 , FS/18/29/33554 and FS/19/16/34169 respectively). LF has received support via the Institute of Cardiovascular Sciences, University of Birmingham: Fondation Leducq & British Heart Foundation Accelerator Award ( AA/18/2/34218 ).

Funding Information:
LF has received institutional research grants and non-financial support from European Union, British Heart Foundation, Medical Research Council (UK), DFG and Gilead. LF is listed as inventor on two patents held by University of Birmingham (Atrial Fibrillation Therapy WO 2015140571, Markers for Atrial Fibrillation WO 2016012783). No other authors have any conflict of interest to declare.

Funding Information:
The CRIB-FLOW study was funded by University Hospitals Birmingham Charity and the Metchley Park Medical Society and carried out at the Centre for Rare Diseases which is part of the National Institute for Health Research (NIHR)/Wellcome Trust Birmingham Clinical Research Facility. The views expressed are those of the authors and not necessarily those of the National Health Service, the NIHR or the Department of Health.

Publisher Copyright:
© 2020 The Authors

Keywords

Coronary flow velocity reserve
Coronary microvascular dysfunction
Inflammation
Living kidney donors

ASJC Scopus subject areas

Cardiology and Cardiovascular Medicine

Access to Document

10.1016/j.ijcard.2020.08.013Licence: Creative Commons: Attribution (CC BY)

RadhakrishnanA2020CoronaryFinal published version, 463 KBLicence: Creative Commons: Attribution (CC BY)

https://doi.org/10.1016/j.ijcard.2020.08.013Licence: Creative Commons: Attribution (CC BY)

Scarred by kidney disease: FGF23 as a key mediator of cardiac fibrosis in patients with chronic kidney disease
Weston, C., Pavlovic, D., McGettrick, H. & Gough, R.
British Heart Foundation
1/08/19 → 28/02/23
Project: Research
A Prospective Study of the Effects of Kidney Transplantation on Chronic Kidney Disease Associated Cardiomyopathy using Magnetic Resonance Imaging
Gough, R.
British Heart Foundation
1/09/18 → 30/11/23
Project: Research
Effects of a Reduction in Renal Function on Cardiovascular Structure and Function: A 5 Year Study of Kidney Donors
Gough, R.
British Heart Foundation
1/08/17 → 31/07/20
Project: Research

Cite this

@article{563670d883714412a24a629065af856d,

title = "Coronary flow velocity reserve and inflammatory markers in living kidney donors",

abstract = "Background: Coronary microvascular dysfunction is prevalent in chronic kidney disease (CKD), and may contribute to the development of myocardial dysfunction in CKD. Coronary flow velocity reserve (CFVR) is a marker of coronary microvascular function and falls with increasing CKD stage. Living kidney donors have renal function consistent with early stage CKD and concern has been raised about their cardiovascular risk. No studies to date have investigated the presence of coronary microvascular dysfunction in living kidney donors. Methods: 25 healthy controls and 23 living kidney donors were recruited and underwent assessment with transthoracic echocardiography, Doppler CFVR, myocardial contrast echocardiography and serum multiplex immunoassay panels. Results: Doppler CFVR was significantly reduced in living kidney donors compared to controls (mean CFVR 3.4 ± 0.7 vs 3.8 ± 0.6, mean difference 0.4 95% confidence interval 0.03–0.8, p =.036). Quantitative myocardial contrast echocardiography showed a trend towards reduced coronary flow reserve in living kidney donors. Compared to controls, living kidney donors had higher serum high sensitivity C reactive peptide (hsCRP) and lower levels of uromodulin. Conclusions: This is the first study of CFVR in living kidney donors. We have shown that the modest drop in estimated glomerular filtration rate in living kidney donors is associated with lower values of Doppler CFVR compared to controls, suggesting that isolated reductions in renal function may lead to altered microvascular function. The increase in hsCRP and reduction in uromodulin suggests that chronic subclinical inflammation may contribute to altered microvascular function in this population.",

keywords = "Coronary flow velocity reserve, Coronary microvascular dysfunction, Inflammation, Living kidney donors",

author = "Ashwin Radhakrishnan and Anna Price and Luke Pickup and Jonathan Law and Kirsty McGee and Larissa Fabritz and Roxy Senior and Richard Steeds and Charles Ferro and Jon Townend",

note = "Funding Information: The CRIB-FLOW study was funded by research grants from University Hospitals Birmingham Charity and the Metchley Park Medical Society . AMP, LCP and JPL are holders of British Heart Foundation Clinical Research Training Fellowships ( FS/16/73/32314 , FS/18/29/33554 and FS/19/16/34169 respectively). LF has received support via the Institute of Cardiovascular Sciences, University of Birmingham: Fondation Leducq & British Heart Foundation Accelerator Award ( AA/18/2/34218 ). Funding Information: LF has received institutional research grants and non-financial support from European Union, British Heart Foundation, Medical Research Council (UK), DFG and Gilead. LF is listed as inventor on two patents held by University of Birmingham (Atrial Fibrillation Therapy WO 2015140571, Markers for Atrial Fibrillation WO 2016012783). No other authors have any conflict of interest to declare. Funding Information: The CRIB-FLOW study was funded by University Hospitals Birmingham Charity and the Metchley Park Medical Society and carried out at the Centre for Rare Diseases which is part of the National Institute for Health Research (NIHR)/Wellcome Trust Birmingham Clinical Research Facility. The views expressed are those of the authors and not necessarily those of the National Health Service, the NIHR or the Department of Health. Publisher Copyright: {\textcopyright} 2020 The Authors",

year = "2020",

month = dec,

day = "1",

doi = "10.1016/j.ijcard.2020.08.013",

language = "English",

volume = "320",

pages = "141--147",

journal = "International Journal of Cardiology",

issn = "0167-5273",

publisher = "Elsevier",

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TY - JOUR

T1 - Coronary flow velocity reserve and inflammatory markers in living kidney donors

AU - Radhakrishnan, Ashwin

AU - Price, Anna

AU - Pickup, Luke

AU - Law, Jonathan

AU - McGee, Kirsty

AU - Fabritz, Larissa

AU - Senior, Roxy

AU - Steeds, Richard

AU - Ferro, Charles

AU - Townend, Jon

N1 - Funding Information: The CRIB-FLOW study was funded by research grants from University Hospitals Birmingham Charity and the Metchley Park Medical Society . AMP, LCP and JPL are holders of British Heart Foundation Clinical Research Training Fellowships ( FS/16/73/32314 , FS/18/29/33554 and FS/19/16/34169 respectively). LF has received support via the Institute of Cardiovascular Sciences, University of Birmingham: Fondation Leducq & British Heart Foundation Accelerator Award ( AA/18/2/34218 ). Funding Information: LF has received institutional research grants and non-financial support from European Union, British Heart Foundation, Medical Research Council (UK), DFG and Gilead. LF is listed as inventor on two patents held by University of Birmingham (Atrial Fibrillation Therapy WO 2015140571, Markers for Atrial Fibrillation WO 2016012783). No other authors have any conflict of interest to declare. Funding Information: The CRIB-FLOW study was funded by University Hospitals Birmingham Charity and the Metchley Park Medical Society and carried out at the Centre for Rare Diseases which is part of the National Institute for Health Research (NIHR)/Wellcome Trust Birmingham Clinical Research Facility. The views expressed are those of the authors and not necessarily those of the National Health Service, the NIHR or the Department of Health. Publisher Copyright: © 2020 The Authors

PY - 2020/12/1

Y1 - 2020/12/1

N2 - Background: Coronary microvascular dysfunction is prevalent in chronic kidney disease (CKD), and may contribute to the development of myocardial dysfunction in CKD. Coronary flow velocity reserve (CFVR) is a marker of coronary microvascular function and falls with increasing CKD stage. Living kidney donors have renal function consistent with early stage CKD and concern has been raised about their cardiovascular risk. No studies to date have investigated the presence of coronary microvascular dysfunction in living kidney donors. Methods: 25 healthy controls and 23 living kidney donors were recruited and underwent assessment with transthoracic echocardiography, Doppler CFVR, myocardial contrast echocardiography and serum multiplex immunoassay panels. Results: Doppler CFVR was significantly reduced in living kidney donors compared to controls (mean CFVR 3.4 ± 0.7 vs 3.8 ± 0.6, mean difference 0.4 95% confidence interval 0.03–0.8, p =.036). Quantitative myocardial contrast echocardiography showed a trend towards reduced coronary flow reserve in living kidney donors. Compared to controls, living kidney donors had higher serum high sensitivity C reactive peptide (hsCRP) and lower levels of uromodulin. Conclusions: This is the first study of CFVR in living kidney donors. We have shown that the modest drop in estimated glomerular filtration rate in living kidney donors is associated with lower values of Doppler CFVR compared to controls, suggesting that isolated reductions in renal function may lead to altered microvascular function. The increase in hsCRP and reduction in uromodulin suggests that chronic subclinical inflammation may contribute to altered microvascular function in this population.

AB - Background: Coronary microvascular dysfunction is prevalent in chronic kidney disease (CKD), and may contribute to the development of myocardial dysfunction in CKD. Coronary flow velocity reserve (CFVR) is a marker of coronary microvascular function and falls with increasing CKD stage. Living kidney donors have renal function consistent with early stage CKD and concern has been raised about their cardiovascular risk. No studies to date have investigated the presence of coronary microvascular dysfunction in living kidney donors. Methods: 25 healthy controls and 23 living kidney donors were recruited and underwent assessment with transthoracic echocardiography, Doppler CFVR, myocardial contrast echocardiography and serum multiplex immunoassay panels. Results: Doppler CFVR was significantly reduced in living kidney donors compared to controls (mean CFVR 3.4 ± 0.7 vs 3.8 ± 0.6, mean difference 0.4 95% confidence interval 0.03–0.8, p =.036). Quantitative myocardial contrast echocardiography showed a trend towards reduced coronary flow reserve in living kidney donors. Compared to controls, living kidney donors had higher serum high sensitivity C reactive peptide (hsCRP) and lower levels of uromodulin. Conclusions: This is the first study of CFVR in living kidney donors. We have shown that the modest drop in estimated glomerular filtration rate in living kidney donors is associated with lower values of Doppler CFVR compared to controls, suggesting that isolated reductions in renal function may lead to altered microvascular function. The increase in hsCRP and reduction in uromodulin suggests that chronic subclinical inflammation may contribute to altered microvascular function in this population.

KW - Coronary flow velocity reserve

KW - Coronary microvascular dysfunction

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JO - International Journal of Cardiology

JF - International Journal of Cardiology

ER -

Coronary flow velocity reserve and inflammatory markers in living kidney donors

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

Access to Document

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Projects

Scarred by kidney disease: FGF23 as a key mediator of cardiac fibrosis in patients with chronic kidney disease

A Prospective Study of the Effects of Kidney Transplantation on Chronic Kidney Disease Associated Cardiomyopathy using Magnetic Resonance Imaging

Effects of a Reduction in Renal Function on Cardiovascular Structure and Function: A 5 Year Study of Kidney Donors

Cite this