Chronic kidney disease is associated with an increased left ventricular (LV) mass. Few data are available regarding the effect of renal transplantation on LV mass regression or the clinical factors associated with LV mass regression. Patients with ≥1 year of chronic kidney disease followed by successful renal transplantation were identified. All patients underwent echocardiography ≥6 months before transplantation with repeat echocardiography ≥1 year after transplantation. An experienced echocardiographer, who was unaware of the clinical data, performed all linear measurements in the parasternal long-axis projection, including systolic and diastolic LV chamber dimensions and LV wall thickness. The LV mass was calculated as follows: 0.8 × {1.04 [(LV internal dimension at end diastole + posterior wall thickness at end diastole + LV wall thickness at the cardiac base for the anteroseptum) 3 − (LV internal dimension at end diastole) 3 ]} + 0.6 g. Candidate clinical variables for an association with LV mass regression were assembled, including age, gender, race, donor type, renal disease etiology, medications (insulin, oral hypoglycemics, antihypertensives, statins, and antirejection medications), and co-morbidities. Patients were separated into 2 groups according to presence and absence of LV mass regression. A total of 105 patients (mean age 54 years; 58 men) were included in the study with a mean follow-up of 1.7 years. Of the 105 patients, 57 had significant LV mass regression (mean difference −37.2 ± 31.3 g/m 2 ) and 48 had no significant regression (mean difference 15.7 ± 17.1 g/m 2 ). The extent of the LV mass before transplantation was the only predictor of mass regression after transplantation (odds ratio 1.50, 95% confidence interval 1.26 to 1.80). In conclusion, significant LV mass regression is present in most patients after renal transplantation. The extent of the LV mass before transplantation was the only clinical predictor of regression.
Patients with chronic kidney disease frequently have concomitant left ventricular (LV) hypertrophy and increased overall LV mass. LV hypertrophy in these patients is often due to longstanding systemic hypertension and diabetes mellitus and is associated with a worsened clinical outcome. Although hemodialysis relieves symptoms of uremia and improves the quality of life of patients with end-stage renal disease, it also promotes LV hypertrophy, possibly from acute and repetitive hemodynamic perturbations. There is conflicting and inadequate data on whether significant regression of LV hypertrophy occurs after renal transplantation. We aimed to determine the extent of LV mass regression on long-term follow-up in a large group of patients with chronic kidney disease after renal transplantation and to identify the clinical factors associated with LV mass regression.
Methods
The present study was a retrospective study that used the Saint Luke’s Hospital (Kansas City, Missouri) renal transplant registry. The Saint Luke’s Hospital institutional review board approved the study. Patients with ≥1 year of documented chronic kidney disease who subsequently underwent renal transplantation and who had also undergone echocardiography ≥6 months before transplant (baseline echocardiography) and echocardiography ≥1 year after transplant (follow-up echocardiography) were included in the present study. The patients were excluded if they also underwent heart transplantation or experienced organ rejection <1 year after transplant. In patients with multiple renal transplants before a successful renal transplant, the total duration of dialysis was considered. All echocardiograms were digitally acquired and archived at the study performance. Echocardiographic images were reviewed by an experienced observer (T.R.C.), who was unaware of the clinical data and the results of the corresponding pre- or post-transplant echocardiogram for the individual patient. Measurements of the LV internal dimension in diastole and LV wall thickness at the cardiac base for the anteroseptum and inferolateral walls were performed in the parasternal long-axis projection using electronic calipers on an internally calibrated and commercially available workstation (ProSolv Cardiovascular, Indianapolis, Indiana). All images were acquired using commercially available echocardiographic platforms with harmonic imaging to optimize endocardial border delineation. The LV mass was calculated using the 2-dimensional linear formula recommended by the American Society of Echocardiography as follows: LV mass = 0.8 × {1.04[(LV internal dimension at end diastole + LV wall thickness at the inferolateral walls + LV wall thickness at the cardiac base for the anteroseptum) 3 − (LV internal dimension at end diastole) 3 ]} + 0.6 g. The reported height and weight at each echocardiogram was used to calculate the body surface area in meters squared, and the LV mass was indexed to grams/m 2 . Approximately 10% of studies were interpreted by a separate observer (M.L.M.) for the determination of the LV mass interobserver variability. Candidate clinical variables for an association with LV mass regression were assembled after detailed chart review, including age, gender, race, donor type, renal disease etiology, medications (insulin, oral hypoglycemics, antihypertensives, statins, and antirejection medications), and co-morbidities (diabetes mellitus, systemic hypertension, cerebral vascular disease, coronary artery disease, heart failure, and dyslipidemia).
Demographic data are reported between the LV mass regression and no regression groups as the mean ± standard deviation for continuous variables and number (%) for categorical variables. To ascertain the predictors of the LV mass change, all variables of clinical interest and with a univariate p value of <0.1 were entered into a logistic regression model. The variables included gender, dialysis, statin use, angiotensin-converting enzyme inhibitor use after echocardiography, baseline LV mass index, and interval between baseline and follow-up echocardiography. A Forest plot was constructed to display the odds ratio and 95% confidence intervals of each variable of interest. Statistical significance was defined as p ≤0.05. All statistical analyses were performed by the Saint Luke’s Mid America Heart Institute’s Department of Biostatistics using SAS, version 9.2 (SAS Institute, Cary, North Carolina).
Results
From January 2000 to January 2010, 128 patients underwent renal transplantation at Saint Luke’s Hospital. Of these patients, 23 were excluded because of a lack of an echocardiogram, the presence of chronic kidney disease for <1 year, graft rejection <1 year after transplant, or concomitant heart transplantation. The remaining 105 patients (mean age 54 years; 58 men) constituted the study group. The interobserver variability for LV mass assessment was 7 g/m 2 . Demographic data are listed in Table 1 . Of the 105 patients, 87 underwent dialysis before transplantation and had chronic kidney disease stage V for ≥1 year before transplantation. The remaining patients had chronic kidney disease stage III and IV. The mean interval for dialysis was 2.2 years, the mean interval from the baseline echocardiogram to transplantation was 1.1 years, and the mean interval from transplantation to the follow-up echocardiogram was 2.2 years. The extent of the LV mass before transplant was the only clinical predictor of LV mass regression after transplant (odds ratio 1.50, 95% confidence interval 1.26 to 1.80; Figure 1 and 2 ).
| Variable | Total (n = 105) | Change in LV Mass (n = 57) | No Change in LV Mass (n = 48) | p Value |
|---|---|---|---|---|
| Age (years) | 53.8 ± 12.3 | 54.8 ± 12.1 | 52.7 ± 12.5 | 0.366 |
| Men | 58 (55%) | 38 (54%) | 20 (57%) | 0.781 |
| Dialysis | 87 (83%) | 55 (79%) | 32 (91%) | 0.099 |
| Diabetes mellitus | 56 (53%) | 36 (51%) | 20 (57%) | 0.580 |
| Systemic hypertension | 98 (93%) | 65 (93%) | 33 (94%) | 0.782 |
| Stroke | 9 (9%) | 7 (10%) | 2 (5.7%) | 0.460 |
| Coronary artery disease | 45 (43%) | 30 (43%) | 15 (43%) | 1 |
| Heart failure | 13 (12%) | 11 (16%) | 2 (6%) | 0.142 |
| Dyslipidemia | 52 (50%) | 36 (51%) | 16 (46%) | 0.581 |
| Before transplantation | ||||
| Angiotensin-converting enzyme inhibitor | 28 (27%) | 20 (29%) | 8 (23%) | 0.533 |
| Angiotensin receptor blocker | 23 (22%) | 13 (19%) | 10 (29%) | 0.243 |
| β blocker | 76 (72%) | 50 (71%) | 26 (74%) | 0.758 |
| After transplantation | ||||
| Angiotensin-converting enzyme inhibitor | 25 (24%) | 21 (30%) | 4 (11%) | 0.035 |
| Angiotensin receptor blocker | 27 (26%) | 18 (26%) | 9 (26%) | 1 |
| β Blocker | 79 (75%) | 51 (73%) | 28 (80%) | 0.424 |
| Dialysis initiation to transplant (years) | 3.0 ± 3.0 | 3.2 ± 3.4 | 2.7 ± 2.6 | 0.472 |
| Echocardiogram to transplant (years) | 1.1 ± 1.2 | 1.1 ± 1.3 | 1.0 ± 0.9 | 0.471 |
| Transplant to echocardiogram (years) | 2.2 ± 2.1 | 2.2 ± 1.9 | 2.2 ± 2.3 | 0.992 |
| Duration from pretransplant echocardiogram to post-transplant echocardiogram (years) | 3.2 ± 2.2 | 3.3 ± 2.0 | 3.0 ± 2.4 | 0.548 |
| Left ventricular mass index (g/m 2 ) | ||||
| Before transplant | 120.5 ± 41.3 | 138.9 ± 43.0 | 98.8 ± 26.1 | <0.001 |
| After transplant | 106.4 ± 29.6 | 103.2 ± 29.0 | 110.2 ± 30.2 | 0.231 |
| Left ventricular mass index difference (g/m 2 ) | −13.0 ± 36.9 | −37.2 ± 31.3 | 15.7 ± 17.1 | NA |
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