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Volume: 20 Issue: 11 November 2022


Significant Improvement of Cardiac Dysfunction After Kidney Transplant: A Case Report

Kidney transplant is known to reverse cardiac dysfunction in patients with end-stage renal disease, and low ejection fraction in kidney transplant candidates is considered to be a contraindication for transplant. We present a significant improvement in cardiac dysfunction after successful kidney transplant in a 21-year-old male recipient. Kidney transplant may be beneficial for cardiac function in transplant recipients who have impaired cardiac function prior to the procedure and caused by uremic toxins.

Key words : Cardiac improvement, Ejection fraction, Kidney transplantation


Patients with end-stage renal disease who are receiving ongoing hemodialysis treatment are prone to experience impaired cardiac function from uremic cardiomyopathy. Etiology is not clearly understood, but a decrease in uremic toxins after intensive hemodialysis sessions and after successful kidney transplantation significantly improves cardiac function.1 On the other hand, low ejection fraction (EF) is considered to be a contraindication for kidney transplant preoperatively.2 In this case report, we present a successfully performed kidney transplant in a patient with heart failure with reduced EF prior to the operation, and we describe the dramatic recovery in cardiac function just after kidney transplant and in long-term follow-up.

Case Report

A 21-year-old male patient with end-stage renal disease had been referred for preoperative evaluation prior to kidney transplant. He had been receiving hemodialysis for more than 16 months. He had experienced repeated episodes of congestive heart failure, and his symptoms gradually exacerbated. Echocardiography showed a left ventricular diastolic diameter of 57 mm, a left ventricular systolic diameter 47 mm, and a reduced EF of 38% with accompanying global hypokinesia, mild mitral regurgitation, and mild pericardial effusion. Left ventricular end diastolic volume was 127 mL, and left ventricular end systolic volume was 79 mL. Dipyridamole myocardial perfusion scintigraphy also showed an EF of 27% with akinesia in septal and apical segments, as well as hypokinesia in other segments of the myocardium. He was considered a high-risk kidney transplant recipient and was offered selective coronary angiography for risk stratification. His coronary angiography results showed no coronary artery disease, andafter 3 consecutive sessions of intensive hemodialysis he received a successful kidney transplant from a 68-year-old living donor (his grandmother).

On the third day after transplant, we repeated transthoracic echocardiography of the recipient, and, despite ongoing global hypokinesia, the EF had dramatically improved to 44%. In the third month after transplant, EF had increased to 60%, with a decrease in left ventricular end diastolic volume to 115 mL and a decrease in left ventricular end systolic volume to 46 mL. He exhibited no signs or symptoms of heart failure in follow-up evaluations. After removal of uremic toxins with successful kidney transplant, significant improvement of cardiac function and EF was observed in this kidney transplant recipient.


A kidney transplant recipient candidate with significantly decreased systolic function who is diagnosed during cardiology consultation prior to kidney transplant represents a common scenario.3 Although patients with a long history of dialysis who show little or no improvement in cardiac function associated with irreversible cardiac damage after kidney transplant have been reported in some studies, patients with no coronary artery disease may gain a benefit after decrease of uremic levels. Uremia has been associated with sympathetic overactivity and autonomic neuropathy. Additionally, impaired cardiac sympathetic activity due to uremia, as confirmed by myocardial iodine-131-radiolabeled meta-iodobenzylguanidine uptake scintigraphy, has been shown to be reversible after successful kidney transplant.2,4

In our patient, the cardiac dysfunction may be associated with uremic toxins that negatively affected systolic function. Normal coronary angiography and rapid improvement of EF after kidney transplant implies that high uremic levels in patients on hemodialysis may be responsible for cardiac systolic dysfunction when these patients are subsequently considered as potential transplant candidates.5,6 Our case shows that cardiac dysfunction in kidney transplant candidates without coronary artery disease may not be an absolute contraindication for kidney transplant.


Cardiac dysfunction in patients on hemodialysis may significantly improve after successful kidney transplant, especially in patients who have normal coronary arteries. Clearance of uremic toxins and improvement in sympathetic overactivity may be the primary reasons for this cardiac improvement. Impaired cardiac function should not be accepted as an absolute contraindication in kidney transplant recipient candidates.


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  2. Mimura I, Kawarazaki H, Momose T, Shibagaki Y, Fujita T. Improvement of cardiac function after kidney transplantation with dilated cardiomyopathy and long dialysis vintage. NDT Plus. 2009;2(6):479-481. doi:10.1093/ndtplus/sfp110
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  3. Chinnappa S, El Nahas M, Mooney A. Reversal of asymptomatic cardiac dysfunction following renal transplantation. Clin Kidney J. 2021;14(2):720-722. doi:10.1093/ckj/sfaa010
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  4. Lim K, Ting SMS, Hamborg T, et al. Cardiovascular functional reserve before and after kidney transplant. JAMA Cardiol. 2020;5(4):420-429. doi:10.1001/jamacardio.2019.5738
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  5. Yilmaz KC, Akgun AN, Keskin S, et al. The effect of renal transplantation on cardiac functions. Saudi J Kidney Dis Transpl. 2020;31(5):1051-1056. doi:10.4103/1319-2442.301170
    CrossRef - PubMed
  6. Karacaglar E, Akgun AN, Muderrisoglu IH, Haberal M. Incidence of cardiovascular events after renal transplantation. Exp Clin Transplant. 2020;18(Suppl 1):70-72. doi:10.6002/ect.TOND-TDTD2019.P18
    CrossRef - PubMed

Volume : 20
Issue : 11
Pages : 1046 - 1047
DOI : 10.6002/ect.2022.0337


From the 1Department of Cardiology, Memorial Hospital, Ankara; and the 2Department of Cardiology, Baskent University, Ankara, Turkey
Acknowledgements: The authors have not received any funding or grants in support of the presented research or for the preparation of this work and have no declarations of potential conflicts of interest.
Corresponding author: Begum Yetis Sayin, Department of Cardiology, Memorial Ankara Hospital, Mevlana Bulvarı 1422, Sokak no:4, Balgat, Ankara, Turkey
Phone: +90 506 2763246