Saudi Journal of Kidney Diseases and Transplantation

: 2020  |  Volume : 31  |  Issue : 5  |  Page : 1006--1013

Changes in Left Ventricular Mass and Cardiovascular Risk Factors after Kidney Transplantation

Sandeep Sreedharan1, Anil Mathew1, Zachariah Paul1, Navin Mathew2, KR Sundaram3, George Kurian1, Rajesh Nair1,  
1 Department of Nephrology, Amrita Institute of Medical Sciences and Research Centre, Kochi, Kerala, India
2 Department of Cardiology, Amrita Institute of Medical Sciences and Research Centre, Kochi, Kerala, India
3 Department of Biostatistics, Amrita Institute of Medical Sciences and Research Centre, Kochi, Kerala, India

Correspondence Address:
Anil Mathew
Department of Nephrology, Amrita Institute of Medical Sciences and Research Centre, Kochi, Kerala


Left ventricular hypertrophy (LVH), the most common structural cardiac complication, is the single most important cause for sudden cardiac death. There are no published data from India looking at the changes in left ventricular mass and cardiac dysfunction after kidney transplantation. We aimed to determine the changes in the left ventricular mass and other cardiovascular risk factors in kidney transplant recipients. This was a prospective observational study. All patients who underwent kidney transplantation at Amrita Institute of Medical Sciences and Research Centre, Kochi, Kerala, during the study period were included in the study. Measurement of clinical and biochemical parameters and echocardiography were done before, six months, and one year after transplantation. There was significant reduction in LV mass index (124.8 ± 39 vs. 102.2 ± 24.4 g/m2, P <0.001) and improvement in ejection fraction (57.8 ± 7 vs. 60.1 ± 1.9, P = 0.015) at the end of six months. There were significant differences in the mean hemoglobin, systolic, and diastolic blood pressures (P <0.001) during the study. There was also a significant reduction in the number of antihypertensive drugs required for blood pressure control. There was a significant reduction in LVH in the study group. There was also improvement in systolic and diastolic functions of the heart. There was also a significant improvement in blood pressure control both in terms of mean blood pressure levels as well as in terms of the number of anti-hypertensive drugs needed for blood pressure control. Renal transplantation ameliorates cardiovascular risk in renal transplant recipients.

How to cite this article:
Sreedharan S, Mathew A, Paul Z, Mathew N, Sundaram K R, Kurian G, Nair R. Changes in Left Ventricular Mass and Cardiovascular Risk Factors after Kidney Transplantation.Saudi J Kidney Dis Transpl 2020;31:1006-1013

How to cite this URL:
Sreedharan S, Mathew A, Paul Z, Mathew N, Sundaram K R, Kurian G, Nair R. Changes in Left Ventricular Mass and Cardiovascular Risk Factors after Kidney Transplantation. Saudi J Kidney Dis Transpl [serial online] 2020 [cited 2021 Sep 18 ];31:1006-1013
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Full Text


India has a large population with chronic kidney disease (CKD), which is ever-growing.[1] A rise in CKD implies a rise in cardiovascular diseases (CVD). CVD is the leading cause of mortality in patients with CKD.[1] Although the increased CV risk in CKD was assumed to be related to underlying diabetes and hypertension (HTN), low glomerular filtration rate and albuminuria were also found to be independent factors associated with higher CV risk.[2] Structural heart disease is an inevitable consequence of CKD, which is an important predisposing factor for sudden cardiac death. Left ventricular hypertrophy (LVH), the most common structural complication is the single most important cause for sudden cardiac death.[3] Renal transplantation ameliorates cardiovascular risk by restoring renal function and clearing the uremic milieu. Although several western studies have shown that there is a significant reduction in the prevalence of LVH and improvement in CV risk factors after kidney transplantation, there are contradictory reports also.[4] Indians, an ethnic group which has a high risk for CV mortality also have a high risk of LVH.[5] However, there are no published studies from India examining the changes in LV mass and cardiac function after kidney transplantation. Hence, this study was undertaken to examine changes in LVH, systolic and diastolic functions of the heart and other CV risk factors such as obesity, HTN, anemia, dyslipidemia and diabetes mellitus in one year after renal transplantation.


This prospective longitudinal observational study was conducted between December 2012 and December 2014 in the Departments of Nephrology and Cardiology, Amrita Institute of Medical Sciences (AIMS) and Research Centre, Kochi, India. A total of 50 patients undergoing renal transplantation were included and followed up for a duration of one year after renal transplant. An informed consent was obtained from the patients and the study was approved by the scientific and ethical committee of AIMS, Kochi.

A detailed history and clinical examination were obtained before transplantation when the patient was admitted to the hospital for the surgery. The follow-up examinations were done at six months and one year after transplantation in the transplant outpatient clinic at the Department of Nephrology, Amrita Institute of Medical Sciences. Detailed drug history was obtained during all visits. Anthropometric measurements were taken, and blood samples were obtained for the laboratory investigations which were done using standard protocols.


Echocardiography was done using Phillips HD 15 with a 5 MHz transducer probe by a consultant cardiologist. Two-dimensional echocardiography and M-mode echocardiography were performed. The M-mode recording perpendicular to the long axis of and through the center of the left ventricle at the papillary muscle level was taken as standard measurements of the systolic and diastolic wall thickness and chamber dimensions. Measurement of the thickness of interventricular septum (IVSd), the thickness of the posterior wall in the end-diastole (PWd) and the internal diameter of the left ventricle at end diastole (LVIDd) were taken.

To estimate the LV mass (LVM), Echo cube formula recommended by American Society of Echocardiography[6] was used: LVM = 0.8 (1.04 × [(LVIDd + IVSd + PWd)3 - LVIDd3]) + 0.6g. The left ventricular mass index (LVMI) was calculated by dividing LVM by body surface area (BSA). BSA was calculated using formula of Dubois and Dubois: BSA = 0.007184 × W0.425 × H0.725 (where W is weight in kg and H is height in cm). The calculation was done using the online calculator (Cardio math) of the Canadian Society of Echocardiography. LVMI was calculated using the same calculator by indexing with BSA.

LVH was defined as LVMI ≥95 g/m2 in females and ≥115 g/m2 in males.[7] Systolic dysfunction was defined as left ventricular ejection fraction <50%. Diastolic dysfunction was defined according to the E/A wave ratio: Normal: The E/A ratio between 1 and 2. The shape of the E-wave is quite symmetrical and the normal deceleration time is between 150 ms and 200 ms. E/A reversal was termed grade

I diastolic dysfunction. Increased E wave velocity with normal E/A ratio; “pseudo-normalization” was termed Grade II diastolic dysfunction. The E/A ratio ≥2 was termed Grade III diastolic dysfunction.

 Statistical Analysis

Out of the 50 patients enrolled, only 45 patients were considered for final analysis. Two patients passed away due to noncardiac reasons (pneumonia and sepsis), two of them had graft failure requiring to be re-initiated on dialysis, and one patient was lost to follow-up as he had to move to another country due to job-related reason. Paired sample t-test was used to compare the mean values of the clinical, biochemical, and echocardiographic parameters before transplantation and after transplantation at six months and one year. Pearson correlation analysis was used to determine the correlation between LV mass and clinical and biochemical parameters. McNemar's test was used to compare the frequency of LVH before and after transplantation. A P <0.05 was considered significant in this study. The Statistical Package for the Social Sciences for Windows version 15.0 (SPSS Inc., Chicago, IL, USA) was used for data analysis.


General characteristics

The study group comprised 31 males (68.9%) and 14 females (31.1%). Mean age was 34 ± 10 years, with a range of 20–58 years. The mean duration of dialysis was 8.4 ± 6.7 months. Eighteen patients (40%) were presumed to have chronic glomerulonephritis as native kidney disease. Twelve (26.7%) had biopsy proven IgA nephropathy, four (8.9%) had diabetic nephropathy; three (6.7%) each had focal segmental glomerulosclerosis and renal calculus disease; two (4.4%) each had Alport's syndrome and lupus nephritis and one patient had reflux nephropathy (2.2%). Mothers constituted 35.6% of the donors, 20% were wives and 13.3% sisters. Fathers constituted 11.1% of the donors, brothers 4.4% and one donor (2.2%) was husband. Deceased donors constituted 13.3% of all donors. Thirty-two patients were on tacrolimus, mycophenolate mofetil (MMF) and prednisolone and 13 patients were on cyclosporine, MMF and prednisolone. Surgical complications were seen in 6.7% of the study subjects, which included perigraft hematoma and lymphocele, which were treated. Delayed graft function was seen in 9.1% of the patients.

Cardiovascular risk factors before transplantation

Forty patients (88.9%) had a past history of HTN, five patients (11.1%) were known diabetics, five patients (11.1%) had a history of dyslipidemia and two patients (4.4%) had angiography proven coronary artery disease. One patient had undergone coronary artery bypass grafting (CABG) and the other person had undergone coronary angioplasty. Mean body mass index (BMI) was 21.6 ± 3.4 kg/m2, mean systolic blood pressure was 154 ± 22 mm Hg; mean diastolic blood pressure was 92 ± 9 mm Hg. Mean hemoglobin level before transplantation was 10.1 ± 1.3 g/dL, fasting blood sugar was 91 ±42 mg/dL, serum creatinine was 9.1 ± 2.3 mg/dL, total cholesterol was 165 ± 45 mg/dL, and serum triglyceride was 133 ± 58 mg/dL. Baseline echocardiographic parameters were as follows: Mean left atrial size was 35 ± 4.6 mm, mean LVIDS was 28.1 ± 6.0 mm, mean LVIDD was 47.3 ± 5.7 mm, IVS was 11.6 ± 1.6 mm, LVPW was 11.1 ± 1.6 mm, mean LV mass was 196.3 ± 65 g, LV mass indexed to BSA (LVMI) was 124.8 ± 39 g/m2. Four patients had EF <50%, with three of them having an EF <35%.

Changes in cardiovascular risk factors after transplantation

One year after transplantation, there was a significant improvement in BMI, systolic blood pressure, diastolic blood pressure, hemoglobin, total leukocyte count, total platelet count, fasting blood sugar, and serum creatinine [Table 1]. At the end of one year, there were significant reductions in the left ventricular size parameters. There was also a significant improvement in the mean EF [Table 2]. At one year following transplantation, all patients had EF of 50% or more. There was a significant reduction in the frequency of LVH also. However, no significant changes were observed between 6 months and one year [Table 3]. The mean LVMI before transplantation was 124.8 ± 39 g/m2, 102.2 ± 24 g/m2 six months after transplantation and 98.6 ± 23 g/m2 one year transplantation. There was a statistically significant reduction in the LVMI six months after transplantation (paired sample t-test; P <0.001); but no further reduction was noted between six months and one year (P = 0.263) [Figure 1]. The frequency of diastolic dysfunction was 67% before transplantation, 46.7% at six months and 22.2% at one year after transplantation. The reduction in the frequency was statistically significant (McNemar's test P = 004 after six months and P <0.001 after one year) [Figure 2]. The percentage of patients requiring anti-hypertensive medications were as follows: before transplantation: 95.6%, six months after transplantation: 80%, one year after transplantation: 55.6%. The reduction in the usage of anti-hypertensive medications were statistically significant (P = 0.016 after six months and P <0.001 after one year). NODAT was seen in 11.1% of the study population and 8.9% developed posttransplant erythrocytosis. Posttransplant dyslipidemia was seen in 8.9% of the study population.{Figure 1}{Figure 2}{Table 1}{Table 2}{Table 3}


LVH is an almost inevitable complication of CKD. The prevalence of LVH before transplantation in the current study was 62.2%. Several studies have reported a prevalence of LVH between 60% and 90% amongst patients on dialysis.[8],[9] A study from Delhi showed a prevalence of 96% in patients with severe CKD.[10] Laddha et al from Pune showed a prevalence of 74.3%.[11] A recent study done in Kolkata reported a prevalence of 87% in patients with severe CKD.[12]

Earlier studies have demonstrated an improvement in the LVM and reduction in LVH following kidney transplantation. Most of the studies have followed up the patients after one year.[13],[14] However, some studies have reported that the regression of LVH happens as early as four months after transplantation.[15] It is also not clear whether the reduction of the LVH is a continuous process or the process halts after the improvement or disappearance of the uremic milieu. We found out that there is a significant reduction in the LVM in the first six months following transplantation; however, there was no significant reduction thereafter. It was also evident that those patients who had abnormally high LVM had a more pronounced reduction than those who had normal LVM or mild hypertrophy. This finding is in concordance with previous studies.[13]

The prevalence of LVH significantly reduced from 62.2% before transplantation to 28.9% six months after transplantation. Taking into account our observation that the prevalence of LVH at the end of one year was 26.7%, it is suggestive that regression of LVM takes place during the initial period of transplantation, after which there is a slowing of process. Comparable studies have shown a reduction of LVH from 67% to 37% at the end of one year[13] and that reduction in the LVM mass started as early as one month after transplantation and continued till six months.[16] None of our patients developed LVH de-novo after transplantation. The reasons for the reduction of LVH in the first six months after transplantation could be many; blood pressure control, improvement in hemoglobin, and reversal of the uremic milieu ought to be imperative, especially in our study population where the duration of dialysis, age, and dyslipidemia were found not to be significantly correlated with LVM before transplant. Changes in the LVM after renal transplantation are related to changes in blood pressure, similar to the findings of an earlier study.[17]

Studies have shown that there is a significant improvement in LV systolic function following kidney transplantation.[18] We also found a significant improvement in LV systolic function in terms of improvement in mean ejection fraction (EF) at six months after transplantation. However, there was no significant improvement in the latter six months. We had four patients who had EF <50% prior to transplantation, which showed improvement in the posttransplant follow-up. Of the four patients with EF <50% prior to transplantation, only one continued to have systolic dysfunction at six months and, by the end of one year all of them had normal EF. Three patients who had EF of 35% before transplantation had a significant improvement in systolic function and all of the attained normal EF at the end of one year. This is another vital finding in our study, that there occurs a significant improvement in the LV systolic function in renal transplant recipients, and the most contributory period is six months following transplantation.

Diastolic dysfunction is common in patients on dialysis. The prevalence of diastolic dysfunction in patients with CKD ranged from 34% to 77%.[19],[20] A recent study from India comprising 70 patients on HD showed a prevalence of 61.4%.[6] Souza et al had reported a 43% improvement in the diastolic function in six months after transplantation.[16] Other studies have also noted a slower recovery of diastolic function at the end of one year after transplantation.[20] Our study showed that there was a significant reduction in the prevalence of diastolic dysfunction from 67% to 46.7% at the end of six months, and the reduction persisting in the next six months, to become 22.2% at the end of one year. This may suggest that the improvement diastolic function is a slower process compared to improvement in systolic function.

We found that there was a significant reduction in the mean systolic and diastolic blood pressure at the end of six months as well as at the end of one year following transplantation. There was a significant reduction in the use of anti-hypertensives and in terms of the number of drugs required for blood pressure control. None of the patients developed de novo HTN after transplantation. However, an absolute blood pressure control could not be achieved (55.6% of the patients required at least one anti-hypertensive medication at the end of one year). Several factors, including the use of CNIs, use of glucocorticoids, transplant renal artery stenosis and increased body weight have been implicated in HTN after transplantation. There was no significant difference between the cyclosporine and tacrolimus groups in terms of mean blood pressure values or number of anti-hypertensives required. The fact that there was a significant reduction in the use of anti-hypertensives (95.6% to 55.6%) at the end of one year is a significant positive finding of this study.

It has been shown that about 15%–30% of the renal transplant recipients develop new-onset diabetes after transplantation (NODAT).[21],[22] Data from India showed a prevalence of 19.2%.[23] The frequency of NODAT in this study group was 11.1%. The risk factors for NODAT include age, male gender, pre-transplant hyperglycemia, family history of diabetes, deceased donor transplantation, type of immunosuppressive therapy, cytomegalovirus disease and hepatitis C virus infection. Our study population being younger group compared to the other studies probably has resulted in a relatively lower prevalence of NODAT. Although it is known that the use of tacrolimus is associated with a higher risk of NODAT, we did not find such an association in our study.

At the time of transplantation, almost all patients are mostly anemic. Usually, the hemoglobin level improves by the 3rd month after transplantation. It was seen that the frequency of anemia reduces to 50% at the end of six months, which then further reduces to 10%–40% at the end of one year.[24],[25] Multiple factors predispose to the development of anemia following transplantation. Acute rejection episodes, elderly donor, failing graft function, bone marrow suppression caused by anti-metabolites (azathioprine, MMF) and multiple transplants are some of the factors that were identified.[24] We noticed a significant improvement in the mean hemoglobin levels at six months after transplantation.

There was a significant improvement in mean hemoglobin levels in the study group at the end of six months. The prevalence of anemia at the end of six months was 44% and at the end of one year was 42%. There were no specific factors that were associated with anemia such as age, gender, rejection episodes etc. This study was probably underpowered to arrive at any significant conclusions on this aspect.

Posttransplant erythrocytosis is not uncommon. The prevalence varies from 8%–15%. We noted a prevalence of 9.1% in our study group at the end of one year after transplantation. All of them were males. There were no thromboembolic events in any of those patients. PTE was not associated with worse graft outcome in our study. All of them underwent one or more venesection.

The frequency of posttransplant dyslipidemia was 8.9%, acute rejection episodes were seen in 17.8% of the patients and 6.7% of the patients had surgical complications, which included lymphocele and peri-graft hematoma. None of these factors were associated with graft loss or graft dysfunction.

An important limitation of the study is that we have not looked at the changes in the inflammatory markers and the mineral bone disorder in relation to the changes in LVM. This being a time-bound study with limited resources; it was beyond the scope of the study to look at the entire spectrum of cardiovascular risk factors. Moreover, it is also important to determine the risk factors associated non-regression of LVM and also de-novo LVH after transplantation.

We hope to continue the present study and address these issues once it is sufficiently powered. Furthermore, it would also be interesting to note how HTN and anemia changes over a long period, say five years or 10 years in this population.

Conflict of interest: None declared.


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