|Year : 2017 | Volume
| Issue : 4 | Page : 194-197
Prevalence of hypertension in postrenal transplant recipients: A retrospective tertiary care study
Georgi Abraham1, Anand Yuvaraj2, A Priya Haridas2, Madhusudan Vijayan2, Muthu Raajendhira2, Rajeevalochana Parthasarathy2, Milly Mathew2
1 Department of Nephrology, Madras Medical Mission, Chennai, Tamil Nadu; Department of Medicine, Pondicherry Institute of Medical Sciences, Puducherry, India
2 Department of Nephrology, Madras Medical Mission, Chennai, Tamil Nadu, India
|Date of Web Publication||28-Dec-2017|
Department of Nephrology, Madras Medical Mission, 4-A, Dr. J J Nagar, Mogappair, Chennai - 600 037, Tamil Nadu
Source of Support: None, Conflict of Interest: None
Aim: Posttransplant hypertension (HTN) is a strong predictor of patient and graft survival. As there is a paucity of data in India, this retrospective analysis was done to look at the blood pressure (BP) in 506 renal transplant recipients, with 240 males, 266 females, mean age 42.90 ± 13.31 years, looking at their BP, at the initial and after 1 year later. Methods: This is a retrospective tertiary care study looking at serial BP measurements in 506 renal transplant recipients, correlating with their body mass index (BMI), graft function, proteinuria, antihypertensive used, erythropoietin usage, echocardiography native kidney disease, and new-onset diabetes mellitus till 1 year after transplantation. Results: According to the Joint National Committee 7 classification, initial BP was normal in 24 (4.74%), pre-HTN in 145 (28.65%), HTN Stage I in 227 (44.86%), and Stage II in 110 (21.73%) patients. One year later, BP was normal in 43 (8.55%), pre-HTN in 153 (30.26%), HTN Stage I in 236 (46.71%), and Stage II in 74 (14.47%) patients. Diabetics had a higher initial systolic BP (SBP) (P = 0.005). Patients with left ventricular hypertrophy had a higher SBP 1 year later (P = 0.001). Patients with BMI > 35 kg/m2, had higher initial SBP (P = 0.01), initial diastolic BP (DBP) (P = 0.01) and also higher 1 year posttransplant SBP (P = 0.02) and DBP (P = 0.01). Conclusion: There was a high incidence of HTN in renal transplant recipients, 66.59% patients with HTN and 28.65% with pre-HTN in the initial posttransplant period, and 61.18% with HTN and 30.26% with pre-HTN in the 1-year posttransplant period.
Keywords: Blood pressure, diabetes mellitus, hypertension, left ventricular hypertrophy
|How to cite this article:|
Abraham G, Yuvaraj A, Haridas A P, Vijayan M, Raajendhira M, Parthasarathy R, Mathew M. Prevalence of hypertension in postrenal transplant recipients: A retrospective tertiary care study. Indian J Transplant 2017;11:194-7
|How to cite this URL:|
Abraham G, Yuvaraj A, Haridas A P, Vijayan M, Raajendhira M, Parthasarathy R, Mathew M. Prevalence of hypertension in postrenal transplant recipients: A retrospective tertiary care study. Indian J Transplant [serial online] 2017 [cited 2020 Mar 28];11:194-7. Available from: http://www.ijtonline.in/text.asp?2017/11/4/194/221856
| Introduction|| |
Transplantation is well-accepted therapeutic option in patients with end-stage renal disease, yet high incidence of cardiovascular disease (CVD) plays a determining role in long-term prognosis in this population. Among the risk factors for CVD, hypertension (HTN) plays a critical role, and the correlation between high BP and long-term survival is extremely significant. Moreover, HTN can also lead to graft failure, necessitating the resumption of chronic dialysis. With reference to the awareness, treatment and control (<140/90) of HTN in selected countries, it has been shown that India has a least awareness and control of blood pressure (BP). Immunosuppressants used in renal transplantation such as cyclosporine and tacrolimus have induced or exacerbated HTN, but tacrolimus has less of an effect on BP than cyclosporine. Management of BP should be aimed with medications, with minimal side effects and a lower cost. As there is a paucity of data in India, this retrospective analysis was done to look at the BP in 506 renal transplant recipients at the initial and 1-year posttransplant and their determinants.
| Methods|| |
A retrospective analysis of 506 transplant recipients, with 240 males and 266 females; mean age 42.90 ± 13.31 years, looking at their BP, at the initial and 1 year later. BP was classified according to the Joint National Committee (JNC) on prevention, detection, evaluation, and treatment of high BP (JNC 7) classification. The initial demographic profile of patients such as height (cm), weight (kg), body mass index (BMI) (kg/m 2), diabetes mellitus, proteinuria, two-dimensional (2D) echocardiogram (ECHO) showing concentric left ventricular hypertrophy (LVH), antihypertensives used, serum creatinine (μmol/l) at discharge posttransplant with the estimated glomerular filtration rate (eGFR) in modification of diet in renal disease (MDRD) formula, native kidney disease, hemoglobin (g/L), and usage of erythropoietin were looked at. Patients were classified into five stages according to the eGFR, as shown in [Table 1].
|Table 1: Stages of chronic kidney disease according to glomerular filtration rate|
Click here to view
Proteinuria was classified into nil, trace, 1+, 2+, 3+, and 4+, according to the dipstick reading. Type of antihypertensives used such as calcium channel blockers, beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, diuretics, and the centrally acting agents were also looked at. Native kidney diseases were grouped into diabetic nephropathy, hypertensive nephropathy, glomerulonephritis, polycystic kidney diseases and unknown. Each of these parameters were correlated with the initial and 1- year posttransplant systolic BP (SBP) and diastolic BP (DBP) and data were analyzed. All of our patients were on triple immunosuppression which included oral prednisolone (starting with 0.5 mg/kg/day followed by slow tapering over 2 months to a maintenance dose of 2.5–5 mg/day), oral mycophenolate mofetil (1.5–2 g/day), and oral tacrolimus (starting with a dose of 0.1 mg/kg/day, dose adjusted to the trough level).
| Results|| |
Initial clinical and demographic details, with BP initially and 1 year later, are as shown in [Table 2].
According to the JNC 7 classification, initial BP was normal (BP <120/80 mmHg) in 24 (4.74%) patients, pre-HTN (BP 120–139/80–89 mmHg) in 145 (28.65%), HTN Stage I (BP 140–159/90–99 mmHg) in 227 (44.86%), and Stage II (BP ≥160/100 mmHg) in 110 (21.73%) patients. One year later, BP was normal in 43 (8.55%), pre-HTN in 153 (30.26%), HTN Stage I in 236 (46.71%) and Stage II in 74 (14.47%) patients. Among 506 patients who were classified as chronic kidney disease according to their eGFR, 62 (12.25%) patients were in Stage I, with 198 (39.13%) patients in Stage II, 211 (41.69%) patients in Stage III, 20 (3.95%) patients in Stage IV, and 15 (2.96%) patients in Stage V.
Two-dimensional ECHO showing concentric LVH was noted in 304 (60.07%) patients, with no LVH in202 (39.92%). Patients with concentric LVH, had a higher SBP 1 year later, with mean 135 ± 4 mmHg when compared to patients with no LVH, with a mean SBP of 128 ± 5.6 mmHg (P = 0.001) as shown in [Figure 1].
|Figure 1: Posttransplant hypertension and left ventricular hypertrophy: Presence of concentric left ventricular hypertrophy on two-dimensional echocardiogram was associated with higher systolic blood pressure one year later (P = 0.001)|
Click here to view
Diabetics had a higher initial SBP with mean of 138 ± 5.6 mmHg when compared to nondiabetics with a mean of 132 ± 6 mmHg (P = 0.005) as shown in [Figure 2].
|Figure 2: Posttransplant hypertension and diabetes mellitus: Initial systolic blood pressure was high in diabetics when compared to nondiabetics (P = 0.005)|
Click here to view
Among 506 patients, patients with BMI ≥35 kg/m 2, had higher initial SBP (181 ± 14 mmHg) (P = 0.01), initial DBP (111 ± 6 mmHg) (P = 0.01) and also higher 1-year posttransplant SBP (171 ± 9 mmHg) (P = 0.02) and DBP (110 ± 9 mmHg) (P = 0.01).
It is shown that the initial and 1-year posttransplant BP did not have a correlation with the level of proteinuria (P = 0.66), types of antihypertensives used (P = 0.44), usage of erythropoietin (P = 0.76), level of serum creatinine (μmol/L), eGFR, and the type of native kidney disease (P = 0.87).
| Discussion|| |
BP frequently rises after kidney transplantation as HTN develops in up to 60–80 or more percent of renal allograft recipients. Poorly controlled BP is common among kidney transplant recipients. In a single-center study, it has been shown that only 5% of kidney transplant patients were normotensive, as defined by BPs <130/80 mmHg, as measured by ambulatory BP monitoring. Our study also depicts a greater incidence of posttransplant HTN.
Posttransplant HTN is a major traditional risk factor for atherosclerotic CVD, which is the leading cause of premature death and a major factor in death-censored graft failure in transplant recipients. BP plays a pivotal role in the pathogenesis of LVH. LVH is an independent risk factor for death and CVD in the general population, dialysis patients, and after kidney transplant. In a retrospective study of 500 transplant patients, baseline LVH defined using electrocardiographic criteria was a risk factor for death (relative risk [RR], 1.9) and congestive heart failure (RR, 2.27) and was independent of other major prognostic variables. Our study showed a greater prevalence of concentric LVH in our transplant patients, associated with a higher SBP during the later period of transplant.
Diabetes is associated with a poorer long-term survival in renal transplant recipients. Diabetics and association of the glycemic control with HTN and micro and macrovascular complications could be a contributing factor to posttransplant HTN. Initial SBP was higher in our diabetic population.
Obesity is associated with a higher incidence of delayed graft function, impaired graft survival, longer hospital stay, higher costs, higher incidence of new onset of diabetes after transplantation, and increased mortality. Our study showed a higher initial and 1-year posttransplant BP in patients with higher BMI.
Most of the major classes of antihypertensive medications have been studied and are effective in controlling HTN in transplant recipients. Dihydropyridine calcium-channel blockers are recommended for initial therapy since these agents dilate the afferent arteriole, thereby ameliorating vasoconstriction of the afferent arteriole induced by calcineurin inhibitors, namely cyclosporine and tacrolimus. Although most of our patients were on dihydropyridine calcium-channel blockers, we did not find any signification correlation with the antihypertensives used and the BP. Transplant renal artery stenosis and HTN are six times more common in end-to-end anastomosis than end-to-side anastomosis. At our center, we perform end-to-side anastomosis for all patients minimizing the risk of HTN.
| Conclusion|| |
There is a high incidence of HTN in renal transplant recipients, 66.59% patients with HTN and 28.65% with pre-HTN in the initial posttransplant period and 61.18% with HTN and 30.26% with pre-HTN in the 1-year posttransplant period. Patients with BMI ≥35 kg/m 2 have higher initial and 1-year posttransplant BP. Diabetics have a higher initial SBP and should be closely monitored. LVH on 2D ECHO is a predictor of higher SBP later in the posttransplant period.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Kaul A, Sharma RK, Gupta A, Singh U. Spectrum of hypertension in post transplant. J Assoc Physicians India 2010;58:221-4.
Opelz G, Wujciak T, Ritz E. Association of chronic kidney graft failure with recipient blood pressure. Collaborative Transplant Study. Kidney Int 1998;53:217-22.
Rao VK. Management of hypertension following renal transplantation. Indian J Nephrol 2001;11:1-50. [Full text]
Sailesh M, Norm RC. Hypertension management. Hypertension 2009;53:450-1.
Margreiter R, European Tacrolimus vs. Ciclosporin Microemulsion Renal Transplantation Study Group. Efficacy and safety of tacrolimus compared with ciclosporin microemulsion in renal transplantation: A randomised multicentre study. Lancet 2002;359:741-6.
Kasiske BL, Anjum S, Shah R, Skogen J, Kandaswamy C, Danielson B, et al.
Hypertension after kidney transplantation. Am J Kidney Dis 2004;43:1071-81.
Paoletti E, Gherzi M, Amidone M, Massarino F, Cannella G. Association of arterial hypertension with renal target organ damage in kidney transplant recipients: The predictive role of ambulatory blood pressure monitoring. Transplantation 2009;87:1864-9.
Mangray M, Vella JP. Hypertension after kidney transplant. Am J Kidney Dis 2011;57:331-41.
Midtvedt K, Hartmann A. Hypertension after kidney transplantation: Are treatment guidelines emerging? Nephrol Dial Transplant 2002;17:1166-9.
Rigatto C, Foley R, Jeffery J, Negrijn C, Tribula C, Parfrey P, et al.
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.
Montori VM, Basu A, Erwin PJ, Velosa JA, Gabriel SE, Kudva YC, et al.
Posttransplantation diabetes: A systematic review of the literature. Diabetes Care 2002;25:583-92.
Aalten J, Christiaans MH, de Fijter H, Hené R, van der Heijde JH, Roodnat J, et al.
The influence of obesity on short- and long-term graft and patient survival after renal transplantation. Transpl Int 2006;19:901-7.
Olyaei AJ, de Mattos AM, Bennett WM. Nephrotoxicity of immunosuppressive drugs: New insight and preventive strategies. Curr Opin Crit Care 2001;7:384-9.
Li JC, Ji ZG, Cai S, Jiang YX, Dai Q, Zhang JX, et al.
Evaluation of severe transplant renal artery stenosis with Doppler sonography. J Clin Ultrasound 2005;33:261-9.
[Figure 1], [Figure 2]
[Table 1], [Table 2]