|Year : 2015 | Volume
| Issue : 2 | Page : 70-73
Left Ventricular Hypertrophy in Kidney Transplant Recipients in Sub-Saharan Africa
Aminu S Muhammad1, Naidoo Sagren2, Pravin Manga3, Muhammad S Nazir3, Saraladevi Naicker2
1 Department of Medicine, Division of Nephrology, Faculty of Health Sciences, University of Witwatersrand, Johannesburg, South Africa; Department of Medicine, Yariman Bakura Specialist Hospital, Gusau, Zamfara State, Nigeria
2 Department of Medicine, Division of Nephrology, Faculty of Health Sciences, University of Witwatersrand, Johannesburg, South Africa
3 Department of Medicine, Division of Cardiology, Faculty of Health Sciences, University of Witwatersrand, Johannesburg, South Africa
|Date of Submission||16-Nov-2014|
|Date of Acceptance||18-Feb-2015|
|Date of Web Publication||20-May-2015|
Dr. Aminu S Muhammad
Department of Medicine, Yariman Bakura Specialist Hospital, Gusau, PMB 1010, Gusau, Zamfara State, Nigeria
Background: Left ventricular hypertrophy (LVH) is present in 67-70% of patients on chronic dialysis and in up to 40-60% of kidney transplant recipients (KTRs) and is associated with graft dysfunction. We determined the prevalence of LVH and its association with graft function among KTRs in a South African transplant center. Materials and Methods: Adult recipients of kidney transplant at the Charlotte Maxeke Johannesburg Academic Hospital between January 2005 and December 2009 were recruited. Patients' records were assessed for information on their posttransplant follow-up. All patients had transthoracic echocardiography and carotid Doppler done for assessment of cardiac status and carotid intima-media thickness (CIMT) respectively. Graft dysfunction was defined as estimated glomerular filtration rate of <60 ml/min/1.73 m 2 based on the modification of diet in renal disease formula. Inferential and modeling statistics were applied as appropriate using SPSS, and P ≤ 0.05 considered significant. Results: One hundred KTRs underwent echocardiography. There were 63% males, and the mean age of the study population was 42.2 ± 12.42 with a range of 19-70 years. The mean duration posttransplant was 59.28 ± 18.59 months with a range of 36-84 months. LVH was present in 76% of the study population; 51% had concentric LVH, and 25% had eccentric LVH. Graft dysfunction was found in 52%. Risk factors for LVH were longer duration on dialysis P = 0.017, cigarette smoking P = 0.032, increased CIMT P = 0.05, higher cumulative steroid dose P < 0.0001 and increased waist circumference P = 0.03. LVH was associated with graft dysfunction, χ2 = 9.22, P = 0.008. Conclusion: LVH is prevalent in our KTRs and is associated with graft dysfunction.
Keywords: Graft dysfunction, kidney transplant recipients, left ventricular hypertrophy, South Africa
|How to cite this article:|
Muhammad AS, Sagren N, Manga P, Nazir MS, Naicker S. Left Ventricular Hypertrophy in Kidney Transplant Recipients in Sub-Saharan Africa. Sub-Saharan Afr J Med 2015;2:70-3
|How to cite this URL:|
Muhammad AS, Sagren N, Manga P, Nazir MS, Naicker S. Left Ventricular Hypertrophy in Kidney Transplant Recipients in Sub-Saharan Africa. Sub-Saharan Afr J Med [serial online] 2015 [cited 2021 Jan 26];2:70-3. Available from: https://www.ssajm.org/text.asp?2015/2/2/70/157423
| Introduction|| |
Left ventricular hypertrophy (LVH) is present in 67-70% of patients on chronic dialysis and in up to 40-60% of kidney transplant recipients (KTRs); it is associated with reduced patient survival and is inversely correlated with graft function.  Improved kidney function following transplantation ameliorates LVH; however, a degree of LVH persists and may be exacerbated as graft function declines.  Graft dysfunction may increase LVH through hypertension, volume expansion, hyperparathyroidism, and/or altered calcium-phosphate homeostasis. , Volume and pressure overload, renin-angiotensin aldosterone system, immunosuppressive therapy, anemia, and genetic factors contribute to the pathogenesis of LVH. Cardiac growth limits compliance of the left ventricle increases coronary vascular resistance and decreases capillary length density leading to a reduction in the ratio of capillary perfusion to myocardial supply. Consequently, the hypertrophic myocardium becomes more sensitive to ischemia and more vulnerable to arrhythmias, congestive heart failure, and sudden death.  Steroid-induced sodium and water retention contributes to cardiac hypertrophy regardless of hypertension.  Rapamycin, a mammalian target for rapamycin inhibitor has been shown to cause regression of LVH in KTRs. 
In this study, we determined the prevalence of LVH and its association with graft function among KTRs at Charlotte Maxeke Johannesburg Academic Hospital (CMJAH), South Africa.
| Materials and Methods|| |
Adult recipients of kidney transplant at the CMJAH between January 2005 and December 2009 were recruited. A questionnaire that captured various cardiovascular risk factors was administered. Patients' records were assessed for information on their posttransplant follow-up. Body mass index (BMI), body surface area (BSA), and waist circumference of all patients were determined. All patients had transthoracic echocardiography (using Philips iE33 machine equipped with S5-1 1-5 MHz transducer allowing for M-mode, two-dimensional and color Doppler measurements [Philips Corporation USA]) and carotid Doppler done for assessment of cardiac status and carotid intima-media thickness (CIMT), respectively. Left ventricular mass was divided by BSA to calculate the left ventricular mass index (LVMI). , The cutoff points for LVMI were >134 g/m 2 for males and >110 g/m 2 for females.  Systolic dysfunction was defined as ejection fraction <50%, while diastolic dysfunction was defined as abnormal left ventricular relaxation pattern.  Graft dysfunction was defined as estimated glomerular filtration rate (GFR) of <60 ml/min/1.73 m 2 based on the modification of diet in renal disease formula. Inferential and modeling statistics applied as appropriate using SPSS version 17 (SPSS Inc., Chicago, IL, USA), and P ≤ 0.05 considered significant.
| Results|| |
One hundred KTRs underwent echocardiography. There were 63% males and 37% females. The mean age of the study population was 42.2 ± 12.4 years with a range of 19-70 years. The mean age of male recipients was 43.59 ± 11.3 years and for females was 39.84 ± 13.93 years. There were 77% blacks, 7% whites, 5% Asians, and 11% mixed race KTRs. Mean duration of follow-up after transplantation was 59.28 ± 18.59 months. Mean duration on dialysis before the transplant was 48.60 ± 28.67. Thirty percent were on maintenance immunosuppression with tacrolimus, mycophenolate mofetil and prednisolone, 28% on cyclosporine, mycophenolate mofetil and prednisolone, 14% on tacrolimus, azathioprine and prednisolone, 5% on cyclosporine, azathioprine and prednisolone; 19% had rapamune as part of their regimen. Only proteinuria and smoking status were significantly different among the recipients with LVH and those without as depicted in the baseline characteristics of the study population in [Table 1].
Left ventricular hypertrophy was present in 76% of the study population; 51% had concentric LVH, and 25% had eccentric LVH. The mean ± standard division (SD) LVMI of the study population was 129.01 ± 45.28 g/m 2 , mean ± SD LVMI in males was 139.91 ± 45.55 g/m 2 and 110.46 ± 38.77 g/m 2 in females, respectively (P = 0.001). The mean left ventricular ejection fraction of the study population was 70.04 ± 9.71 ml/min with a range of 41-91 ml/min. Systolic dysfunction was present in 12% of the KTRs and diastolic dysfunction in 64%. Correlation of LVMI with clinical variables is shown in [Table 2]. Association of LVH with categorical variables is shown in [Table 3]. Graft dysfunction was seen in 52% of the study subjects. Association of LVH with different stages of chronic kidney disease is shown in [Table 4].
Though many factors were associated with increased LVH on bivariate analysis, on multivariate analysis using regression model only longer duration on dialysis, cigarette smoking, higher cumulative steroid dose, increased CIMT, and increased waist circumference were found to be risk factors for LVH. Logistic regression analysis showing risk factors for LVH is depicted in [Table 5].
| Discussion|| |
Left ventricular hypertrophy is present in 40-60% of KTRs, and its persistence in the 1 st year after renal transplantation is associated with reduced patient survival. It has also been shown to be the strongest predictor of all-cause mortality, together with diabetes in KTRs. ,, In this study, we found the prevalence of LVH in our KTRs to be high, similar to the report by Middleton et al.  but lower than that reported by Parfrey et al.  The high prevalence of LVH in our study could be due to the fact that the majority of our patients were black, a racial group with increased preponderance of hypertensive heart disease.  Luyckx et al. and Amira et al. both reported an LVH prevalence of 68% and 69%, respectively, among predominantly black South African dialysis populations in Johannesburg. , Concentric LVH was the most common type seen in this study and it was associated with diastolic dysfunction. The same observation has been reported in several studies. ,, Dzemidzic et al.  reported LVH prevalence of 37% at the end of first transplant year in their Bosnian KTRs cohort, which was present in 70% at the time of transplantation with 40% having diastolic dysfunction. Diastolic dysfunction was present in 64% of our cohort, which is similar to the reported prevalence by Dzemidzic et al. LVH showed a negative correlation with hemoglobin, GFR and parathyroid hormone levels.  Duration on dialysis, BMI and hypertension had significant correlation with LVH, similar to the report by De Lima et al.,  where they found regression of LVH and normalization of carotid artery properties followed successful kidney transplantation. There was no association between angiotensin converting enzyme inhibitor/angiotensin receptor blocker and rapamycin use with LVH in this study; this could be as a result of a small sample size, and the fact that there were small numbers of our KTRs on rapamycin and they tend to be switched back to calcineurin inhibitors once they become proteinuric.
Risk factors for LVH in this study were longer duration on dialysis, cigarette smoking, higher cumulative steroid dose, increased CIMT, and waist circumference. As patients dialyze for longer periods, hemodynamic alterations make development of LVH more likely to occur. , Recipients of a graft from a deceased donor had more LVH, this could be as a result of a long wait for an organ while the wait list keeps getting longer, and dialysis duration is prolonged. , Cigarette smoking has been reported to be associated with graft dysfunction and increased risk for adverse cardiovascular disease outcome in KTRs; , it was an independent risk factor for LVH and was associated with graft dysfunction in this study. Rigatto et al. found anemia and high blood pressure to be risk factors for LVH in their cohort of KTRs.  Steroids have been found to be associated with LVH regardless of hypertension; this mechanism is thought to be as a result of salt and water retention. 
An important limitation of this study was that the pretransplant cardiac assessment of these patients was not available; it would have shed more light as to what extent cardiac remodeling is affected by a successful transplantation in our sub-Saharan KTRs. In spite of its limitations, this study has provided a useful insight into prevalence and predictors of LVH in the predominantly black South African KTRs and would form the basis for a well-planned multi center prospective study with the aim of determining the extent to which kidney transplantation ameliorates the cardiovascular complications of uremic cardiomyopathy in the African population.
| Acknowledgment|| |
We wish to acknowledge the contributions of Prof Russel Britz and Dr Ben Wambugu of the Divisions of Vascular Surgery and Nephrology respectively, University of Witwatersrand, Johannesburg, South Africa.
| References|| |
Paoletti E, Amidone M, Cassottana P, Gherzi M, Marsano L, Cannella G. Effect of sirolimus on left ventricular hypertrophy in kidney transplant recipients: A 1-year nonrandomized controlled trial. Am J Kidney Dis 2008;52:324-30.
Middleton RJ, Parfrey PS, Foley RN. Left ventricular hypertrophy in the renal patient. J Am Soc Nephrol 2001;12:1079-84.
Suwelack B, Witta J, Hausberg M, Müller S, Rahn KH, Barenbrock M. Studies on structural changes of the carotid arteries and the heart in asymptomatic renal transplant recipients. Nephrol Dial Transplant 1999;14:160-5.
Hernández D. Left ventricular hypertrophy after renal transplantation: New approach to a deadly disorder. Nephrol Dial Transplant 2004;19:1682-6.
Takeda Y, Yoneda T, Demura M, Miyamori I, Mabuchi H. Sodium-induced cardiac aldosterone synthesis causes cardiac hypertrophy. Endocrinology 2000;141:1901-4.
Kaddoura S. Echo Made Easy. International Edition. London: Churchill Livingstone; 2002.
Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass in man. Anatomic validation of the method. Circulation 1977;55:613-8.
Paoletti E, Cannella G. Reducing the risk of left ventricular hypertrophy in kidney transplant recipients: The potential role of mammalian target of rapamycin. Transplant Proc 2009;41 6 Suppl:S3-5.
Parfrey PS, Harnett JD, Foley RN, Kent GM, Murray DC, Barre PE, et al.
Impact of renal transplantation on uremic cardiomyopathy. Transplantation 1995;60:908-14.
Chapman JN, Mayet J, Chang CL, Foale RA, Thom SA, Poulter NR. Ethnic differences in the identification of left ventricular hypertrophy in the hypertensive patient. Am J Hypertens 1999;12:437-42.
Luyckx VA, Yip A, Sofianou L, Jhangri GS, Mueller TF, Naicker S. Cardiac function in an African dialysis population with a low prevalence of pre-existing cardiovascular disease. Ren Fail 2009;31:211-20.
Amira OC, Naicker S, Manga P, Sliwa K, Mia A, Raal F, et al.
Adiponectin and atherosclerosis risk factors in African hemodialysis patients: A population at low risk for atherosclerotic cardiovascular disease. Hemodial Int 2012;16:59-68.
Dzemidzic J, Rasic S, Saracevic A, Rebic D, Uncanin S, Srna A, et al.
Predictors of left ventricular remodelling in kidney transplant recipents in the first posttransplant year. Bosn J Basic Med Sci 2010;10 Suppl 1:S51-5.
De Lima JJ, Vieira ML, Viviani LF, Medeiros CJ, Ianhez LE, Kopel L, et al.
Long-term impact of renal transplantation on carotid artery properties and on ventricular hypertrophy in end-stage renal failure patients. Nephrol Dial Transplant 2002;17:645-51.
Fellström B, Jardine AG, Soveri I, Cole E, Neumayer HH, Maes B, et al.
Renal dysfunction is a strong and independent risk factor for mortality and cardiovascular complications in renal transplantation. Am J Transplant 2005;5:1986-91.
Rigatto C, Parfrey P, Foley R, Negrijn C, Tribula C, Jeffery J. Congestive heart failure in renal transplant recipients: Risk factors, outcomes, and relationship with ischemic heart disease. J Am Soc Nephrol 2002;13:1084-90.
Kasiske BL, Klinger D. Cigarette smoking in renal transplant recipients. J Am Soc Nephrol 2000;11:753-9.
Cosio FG, Falkenhain ME, Pesavento TE, Yim S, Alamir A, Henry ML, et al.
Patient survival after renal transplantation: II. The impact of smoking. Clin Transplant 1999;13:336-41.
Rigatto C, Foley R, Jeffery J, Negrijn C, Tribula C, Parfrey P. Electrocardiographic left ventricular hypertrophy in renal transplant recipients: Prognostic value and impact of blood pressure and anemia. J Am Soc Nephrol 2003;14:462-8.
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]