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Time-dependent changes in cardiac growth after kidney transplantation: the impact of pre-dialysis ventricular mass
Domingo Hernández1, Ana González, Margarita Rufino
1Department of Nephrology, Hospital Universitario de Canarias, E-38320, La Laguna, Tenerife, Spain. dhmarrero@hotmail.com
Insights
Left ventricular hypertrophy (LVH) often persists after kidney transplantation (KT). Pre-dialysis LVH and not using ACE inhibitors are key factors that may continue cardiac growth post-KT.
Area of Science:
- Cardiology
- Nephrology
- Transplantation Medicine
Background:
- Left ventricular hypertrophy (LVH) is prevalent in chronic kidney disease (CKD).
- Understanding LVH progression in kidney transplant recipients is crucial.
Purpose of the Study:
- To investigate longitudinal changes in left ventricular mass (LVM) in CKD patients.
- To identify factors influencing LVM changes from pre-dialysis to post-kidney transplantation (KT).
Main Methods:
- A cohort of 60 CKD stages 4-5 patients underwent serial echocardiograms (pre-dialysis, dialysis, post-KT).
- Multiple linear regression and Cox proportional analyses were used to model LVM changes and identify risk factors.
Main Results:
- Baseline LVH was associated with higher BMI.
- 52% of patients with normal baseline LVM developed de novo LVH or significant LVM increase.
- Pre-dialysis LVMI, age, creatinine, and ACE inhibitor use post-KT were associated with LVM changes.
Conclusions:
- Successful KT does not always normalize LVM.
- Pre-dialysis LVMI and non-use of ACE inhibitors may contribute to persistent cardiac growth post-KT.
Background:
Left ventricular hypertrophy (LVH) is common in chronic kidney disease (CKD), including kidney transplant recipients. However, time-related left ventricular mass changes (DeltaLVM) from pre-dialysis stage to beyond the first post-transplant year have not been clearly identified.
Methods:
We studied a cohort of 60 stages 4-5 CKD patients without overt cardiac disease, who underwent three echocardiograms during follow-up: at pre-dialysis stage, on dialysis and after kidney transplantation (KT). Multiple linear regression was used to model DeltaLVM from baseline study. Cox proportional analysis was used to determine risk factors associated with either de novo LVH or>20% DeltaLVMI over time.
Results:
Patients with baseline LVH (n=37; 61%) had a higher body mass index (BMI) than those without LVH (n=23; 39%) (P=0.013). BMI, haemoglobin levels (P=0.047) and non-use of angiotensin-converting enzyme inhibitors (ACEI) (P=0.057) were associated with baseline left ventricular mass index (LVMI). Twelve out of 23 patients (52%) with normal LVM at baseline, developed either de novo LVH or>20% DeltaLVMI at follow-up. On the other hand, 29 (78%) of those with initial LVH maintained this abnormality, and 8 (22%) normalized LVM post-transplantation. Factors associated with DeltaLVMI were age (P=0.01), pre-dialysis LVMI (P<0.0001), serum creatinine (P=0.012) and the use of ACEI post-transplantation (P=0.009). In Cox analysis, pre-dialysis LVMI was associated with de novo LVH or>20% DeltaLVMI over time (hazard ratio 1.009; 95% confidence interval 1.004 to 1.015; P=0.001).
Conclusions:
Successful KT may not completely normalize LVM post-transplantation. Pre-dialysis LVMI, traditional risk factors and no use of ACEI may perpetuate cardiac growth following KT.
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