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Updated: Dec 28, 2025
Normothermic Ex Vivo Kidney Perfusion for the Preservation of Kidney Grafts prior to Transplantation
Published on: July 15, 2015
Myocardial perfusion reserve of kidney transplant patients is well preserved
Johanna Päivärinta1,2, Kaj Metsärinne3, Eliisa Löyttyniemi4
1Department of Medicine, Division of Nephrology, Turku University Hospital, PL 52, Kiinamyllynkatu 4-8, 20521, Turku, Finland. johanna.paivarinta@fimnet.fi.
Insights
Kidney transplant patients with early-stage chronic kidney disease (CKD) show preserved stress myocardial perfusion (MP). Increased resting MP, likely due to sympathetic overactivation, explains reduced myocardial perfusion reserve (MPR) in these patients.
Area of Science:
- Cardiology
- Nephrology
- Nuclear Medicine
Background:
- Chronic kidney disease (CKD) is linked to endothelial dysfunction and heightened cardiovascular mortality.
- Endothelial dysfunction can be assessed by measuring myocardial perfusion reserve (MPR), a ratio of stress and rest myocardial perfusion (MP).
- MPR indicates the vascular bed's capacity for increased perfusion and microvascular responsiveness.
Purpose of the Study:
- To evaluate MPR in kidney transplant recipients with early-stage CKD (stages 2-3).
- To compare MPR between kidney transplant patients and healthy controls using quantitative positron emission tomography (PET).
Main Methods:
- Utilized quantitative [15O]H2O positron emission tomography (PET) to measure myocardial perfusion.
- Assessed myocardial perfusion reserve (MPR) by calculating the ratio of stress to rest myocardial perfusion (MP).
- Corrected basal MP for cardiac workload using the rate-pressure product (RPP).
Main Results:
- Kidney transplant patients exhibited significantly higher resting MP compared to healthy controls (p=0.0015).
- After correcting for cardiac workload, the difference in resting MP between groups disappeared (p=0.55).
- Stress MP and corrected MPR (MPRcorr) did not differ significantly between kidney transplant patients and controls (p=0.53 and p=0.8, respectively).
Conclusions:
- Myocardial perfusion during stress is maintained in kidney transplant patients with CKD stages 2-3.
- The observed reduction in MPR is attributed to elevated resting MP.
- Increased resting MP is likely associated with heightened cardiac workload stemming from sympathetic overactivation in kidney transplant recipients.
Background:
Chronic kidney disease (CKD) is associated with endothelial dysfunction and increased cardiovascular mortality. Endothelial dysfunction can be studied measuring myocardial perfusion reserve (MPR). MPR is the ratio of stress and rest myocardial perfusion (MP) and reflects the capacity of vascular bed to increase perfusion and microvascular responsiveness. In this pilot study, our aim was to assess MPR of 19 patients with kidney transplant (CKD stages 2-3) and of ten healthy controls with quantitative [15O]H2O positron emission tomography (PET) method.
Results:
Basal MP was statistically significantly higher at rest in the kidney transplant patients than in the healthy controls [1.3 (0.4) ml/min/g and 1.0 (0.2) ml/min/g, respectively, p = 0.0015]. After correction of basal MP by cardiac workload [MPcorr = basal MP/individual rate pressure product (RPP) × average RPP of the healthy controls], the difference between the groups disappeared [0.9 (0.2) ml/min/g and 1.0 (0.3) ml/min/g, respectively, p = 0.55)]. There was no difference in stress MP between the kidney transplant patients and the healthy subjects [3.8 (1.0) ml/min/g and 4.0 (0.9) ml/min/g, respectively, p = 0.53]. Although MPR was reduced, MPRcorr (stress MP/basal MPcorr) did not differ between the kidney transplant patients and the healthy controls [4.1 (1.1) and 4.3 (1.6), respectively, p = 0.8].
Conclusions:
MP during stress is preserved in kidney transplant patients with CKD stage 2-3. The reduced MPR appears to be explained by increased resting MP. This is likely linked with increased cardiac workload due to sympathetic overactivation in kidney transplant patients.
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