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Coronary flow velocity reserve and inflammatory markers in living kidney donors. | LitMetric

Coronary flow velocity reserve and inflammatory markers in living kidney donors.

Int J Cardiol

Birmingham Cardio-Renal Group, Institute of Cardiovascular Sciences, University of Birmingham, Birmingham, United Kingdom; Department of Cardiology, Queen Elizabeth Hospital, Birmingham, United Kingdom.

Published: December 2020

AI Article Synopsis

Article 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7584109PMC
http://dx.doi.org/10.1016/j.ijcard.2020.08.013DOI Listing

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