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Year : 2018  |  Volume : 12  |  Issue : 3  |  Page : 199-204

Prevalence, clinical profiles, and outcome of hypertension in renal transplant recipients

Institute of Nephrology, Madras Medical College, Chennai, Tamil Nadu, India

Date of Web Publication28-Sep-2018

Correspondence Address:
Dr. S Ganesh Aravind
A110, TNHB Colony, KTC Nagar, Tirunelveli - 627 011, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijot.ijot_37_18

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Background: Hypertension is more prevalent risk factor for cardiovascular morbidity and mortality among renal transplant recipients. Materials and Methods: It is a retrospective study conducted to assess the prevalence, clinical profiles, and outcome of hypertension in renal transplant recipients. Posttransplant hypertension was defined as systolic blood pressure (BP) ≥140 mmHg, diastolic BP ≥80 mmHg, or the need of antihypertensive medication. Donor and recipient demographical details were obtained from medical records. Patients who underwent second renal transplant or graft nephrectomy were excluded from the study. Results: Among 375 patients, 88% were male. The mean age of our study population was 35.82 ± 9.37 years. Almost 82.67% of patients had posttransplant hypertension, of which 80.97% had pretransplant hypertension. Nearly 19.03% patients developed hypertension posttransplant. Following transplantation, hypertension resolved in 12.85%. The prevalence of well controlled, poorly controlled, and resistant posttransplant hypertension was 49.68%, 50.32%, and 7.42%, respectively. Majority of them (90.97%) received calcium channel blockers. In univariate analyses, recipient sex, pretransplant hypertension, etiology of kidney disease, female donors, female donors of male recipient's subgroup, use of cyclosporine, left ventricular mass, weight gain, and presence of metabolic syndrome were statistically significant. In multiple logistic regression analyses, recipient sex, presence of metabolic syndrome, and use of cyclosporine were associated with posttransplant hypertension. Kaplan–Meier analyses showed low graft survival in posttransplant hypertensive patients when compared to normotensives. Conclusion: The prevalence of hypertension in our renal transplant recipients was 82.67%. Early identification of risk factors, treatment, and adequate BP control will improve the long-term patient, graft survival.

Keywords: Hypertension, kidney transplantation, posttransplant hypertension

How to cite this article:
Maasila A T, Chandrabose C S, Balasubramaniyan T, Gopalakrishnanan N, Dhanapriya J, Dineshkumar T, Sakthirajan R, Aravind S G. Prevalence, clinical profiles, and outcome of hypertension in renal transplant recipients. Indian J Transplant 2018;12:199-204

How to cite this URL:
Maasila A T, Chandrabose C S, Balasubramaniyan T, Gopalakrishnanan N, Dhanapriya J, Dineshkumar T, Sakthirajan R, Aravind S G. Prevalence, clinical profiles, and outcome of hypertension in renal transplant recipients. Indian J Transplant [serial online] 2018 [cited 2023 Feb 5];12:199-204. Available from: https://www.ijtonline.in/text.asp?2018/12/3/199/242437

  Introduction Top

Hypertension is a most commonly present in end-stage renal disease (ESRD) patients and its prevalence of 80%–85% among kidney transplant recipients. Various studies have shown the prevalence of 80% in immediate posttransplant and 50% in late posttransplant period. About 10%–20% of them have severe/accelerated hypertension.[1] Hypertension is a major risk factor for atherosclerosis, increased cardiovascular morbidity, mortality, and allograft dysfunction in transplant patients. There is significant correlation between hypertension and long-term graft and patient survival.[2] Various risk factors including use of calcineurin inhibitors (CNIs), obesity, delayed graft function (DGF), and graft dysfunction contributing to hypertension were analyzed in this study.

  Materials and Methods Top

It is a retrospective study conducted at Rajiv Gandhi Government General Hospital, Madras Medical College, Chennai, involving renal transplant recipients who are on follow-up at nephrology outpatient department. Posttransplant hypertension was defined as systolic blood pressure (BP) ≥140 mmHg, diastolic BP ≥80 mmHg (JNC 7), or the need of antihypertensive medication. Controlled hypertension was defined as control of target BP with treatment, whereas uncontrolled hypertension was defined as systolic BP ≥140 mmHg or diastolic BP ≥90 mmHg with treatment. Resistant hypertension was defined as uncontrolled hypertension requiring three antihypertensive drugs of different classes. Second transplant, graft nephrectomy patients were excluded from the study. Ethical committee clearance was obtained. BP was measured twice sitting posture after a rest period of 15 min (office BP monitoring). Donor and recipients demographical details from medical records were studied. In addition to above body mass index (BMI), weight gain, waist circumference, fasting blood sugar, lipid profile, retinopathy changes, two-dimensional (2D) echo assessment and calculation of the left ventricular (LV) mass by area-length method, LV hypertrophy (LVH), pretransplant hypertension, pretransplant diabetes, donor age, DGF, immunosuppressive medication, control of BP, antihypertensive medication, rejection episodes, anti-rejection therapy given, transplant renal artery stenosis (TRAS), coronary artery disease, and graft function were recorded. Statistical analysis was done using SPSS version 20, Armonk, New York, USA. Statistical significance was considered when P < 0.05. Multiple logistic regressions were used to determine the risk factors related to posttransplant hypertension. Kaplan–Meier analyses were used to predict graft survival in posttransplant patients.

  Results Top

Among the total number of 375 patients, 88% (301) patients were male [Figure 1].
Figure 1: The prevalence of posttransplant hypertension over 5 years

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The mean age of the study population was 35.86 ± 9.32 years. Out of 375 patients, 82.67% (310) had patients posttransplant hypertension, of which 80.97% (251) patients found to have persistent hypertension even after transplantation, that is, 251 patients had hypertension pretransplant and continued to have hypertension posttransplant. Among posttransplant hypertensive group (310), 19.03% (59) patients developed new onset of hypertension posttransplant. After renal transplantation, hypertension resolved in 12.85% (37) patients, that is, 37 pretransplant hypertension patients had no hypertension posttransplant. Among 310 patients, 49.68% (154) had well-controlled hypertension and 50.32% (156) had poorly controlled hypertension. The prevalence of resistant hypertension among 156 poorly controlled hypertensive patients was 7.42% (23 patients) [Figure 2].
Figure 2: The prevalence of hypertension at 1 year of posttransplant period

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Majority of them 90.97% (282) have received calcium channel blockers (CCBs) as one of the antihypertensive medications. Of hypertensive patients, 45.49% (141) were on single antihypertensive drug, while 35.81% (111) patients required at least two antihypertensive medications and 16.13% (50) hypertensive patients required three or more antihypertensive drugs. About 54.19% (168) patients were required more number of antihypertensive drugs compared to baseline pretransplant number of antihypertensive medications. However, 34.19% (106) had levels controlled with their same number of baseline pretransplant drugs, and 10.97% (34) of the study population were needed less antihypertensive drugs for control of hypertension. About 61.61% (191) had chronic glomerulonephritis as a cause for ESRD and 4.8% (18) were diabetics in hypertensive group. About 22.26% (69) had a positive family history of hypertension.

There was no statistically significant difference observed for donor age, donor side of the kidney, cold ischemic time, type of transplant, and DGF between two groups. The factors found to have statistically significant difference are recipient sex, pretransplant hypertension, etiology of kidney disease, female donors, female donors of male recipients, weight gain, use of cyclosporine, LV mass, presence of metabolic syndrome, and posttransplant hypertension [Table 1].
Table 1: Clinical profiles of renal transplant recipients*

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The incidence of acute rejection, use of antirejection therapy, and graft dysfunction were noted high in hypertensive cohort but not statistically significant. Among the hypertension group, eight patients had TRAS whereas only one patient had TRAS in nonhypertensive group. All patients were subjected to vascular intervention (stenting/angioplasty) and had followed by good BP control. Twenty-six patients had posttransplant erythrocytosis. With regard to CNI therapy, 55.16% (171) patients received tacrolimus and 44.51% (138) patients received cyclosporine-based immunosuppression. Around 11.29% (35) patients had evidence of CNI toxicity in renal allograft biopsy. Regarding metabolic profile, there was no statistical difference regarding dyslipidemia, BMI, smoking, LVH, retinopathy changes, and CAD between two groups.

In univariate analysis, male recipients (P = 0.02), pretransplant hypertension (P = 0.0001), etiology of kidney disease (P < 0.01), female donor (P < 0.04), female donor to male recipients (P < 0.003), weight gain (P = 0.0001), LV mass (P < 0.001), use of cyclosporine (P = 0.04), and presence of metabolic syndrome (P < 0.001) were significantly associated with posttransplant hypertension. In multiple logistic regression analyses, only recipient sex, presence of metabolic syndrome, and use of cyclosporine were associated with posttransplant hypertension.

  Discussion Top

Posttransplant hypertension occurs in up to 80% of renal transplant recipients.[3],[4] The prevalence of hypertension at 1-year posttransplant in our study is 82.67%. Hypertension is an important traditional risk factor for cardiovascular disease, which is the leading cause of death and death-censored graft failure in renal transplant recipients. The 2012 kidney disease: improving global outcomes guidelines recommend a target BP ≤130/80 mmHg for kidney transplant recipients. In spite of regular follow-up, BP control is suboptimal in renal transplant recipients. Włodarczyk et al. reported 25% BP control (<140/90) in transplant patients.[5] Around 49.67% (154) of patients had controlled BP in our hypertensive cohort at 1 year. The higher incidence of hypertension may be due to increased follow-up, screening for hypertension, or due to white coat hypertension. Kasiske et al. showed 51% of uncontrolled hypertension at 1 year, when compared to our study, 50.32% (156) of patients had uncontrolled hypertension.[3] BP values obtained at home usually lower than the office values and similar to values obtained by ambulatory BP monitoring (ABPM). ABPM is the most sensitive method in detecting uncontrolled hypertension followed by home BP monitoring and office BP monitoring.[6] The presence of masked hypertension and nocturnal hypertension can be recognized through ABPM. ABPM provides a better correlation with target organ damage such as LVH.[7] Pérez Fontán et al. showed that pretransplant hypertension associated with posttransplant hypertension.[8] In our study, pretransplant hypertension had significant association with posttransplant hypertension. Regarding native kidney disease, 61.61% (191) patients had chronic glomerulonephritis as a cause of ESRD in hypertensive group. It was significantly associated with posttransplant hypertension.

Factors predisposing to posttransplant hypertension is complex and multifactorial [Table 2].
Table 2: Causes of posttransplant hypertension

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Among treatable causes of posttransplant hypertension, eight patients had TRAS whom BP was well-controlled after vascular intervention (stenting/angioplasty).[9] Totally 26 patients had posttransplant erythrocytosis and were initiated on angiotensin-converting enzyme (ACE) inhibitors. Immunosuppression medication such as CNI predisposes to hypertension. Corticosteroids considered being an important cause of hypertension in renal transplant patients. Various studies had shown that either lower dose steroid or withdrawal of steroids reduced the risk of posttransplant hypertension but associated with increased risk of acute rejection which predisposes to hypertension.[10] All our patients were on low-dose steroids on maintenance. About 44.66% (131) patients were on cyclosporine, and 55.34% (154) patients were on tacrolimus. The pathophysiology of cyclosporine-induced hypertension due to direct renal vasoconstriction decreasing the glomerular filtration rate (GFR) which causes renal sodium retention. Tacrolimus activates the renal sodium chloride cotransporter which causes sodium retention.[11],[12] In our study, the use of cyclosporine was significantly associated with posttransplant hypertension.

Various studies showed that CCBs, when compared to placebo or no treatment, had reduced graft loss and improved GFR. Compared with CCBs, the use of ACE inhibitors was associated with a significant reduction in GFR, proteinuria, and hemoglobin but associated with increased incidence of hyperkalemia. Dihydropyridine CCBs reduce afferent arteriole vasoconstriction induced by CNI. Hence, CCBs preferred as the first line of drug in renal transplant recipients. No data regarding graft loss, patients' survival was reported when comparing ACE inhibitors to either placebo or CCBs.[13] In our study, around 90.97% (282) patients were on CCBs and [Figure 3] 27.42% (85) patients were on ACE inhibitor [Table 3].
Figure 3: Antihypertensive drugs in posttransplant patients

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Table 3: Antihypertensive drugs profile in posttransplant patients

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Posttransplantation weight gain is associated with the occurrence of new onset of diabetes after transplantation, hypertension, dyslipidemia, insulin resistance, and chronic allograft nephropathy and graft loss. Average weight gain 1-year posttransplant was 10.3 kg in a study by Clunk et al. whereas it was 12 kg in our study.[14] Weight gain was significantly associated with posttransplant hypertension.

Metabolic syndrome is more prevalent and risk factor for chronic graft dysfunction, graft loss, cardiovascular disease, new onset of diabetes, and patients survival after renal transplantation which may contribute to posttransplant hypertension. The prevalence of metabolic syndrome in our study was 25.81% versus 37.7% reported by Porrini et al.[15] There was a significant association between metabolic syndrome and posttransplant hypertension in our study.

Hypertensive retinopathy changes were observed in 16.13% (50) patients, whereas the study by Raczyńska et al. reported an incidence of 28% with follow-up of 10 years.[16] The reason for less number of hypertensive retinopathy changes in our study population may be due to less number of follow-up years. LVH is a predictor of higher systolic BP later in the posttransplant period. LVH and LV mass is a major and independent risk factor for cardiovascular morbidity.[17],[18] The measurement of LV mass by 2D ECHO using area length method was used to assess cardiac end-organ damage by arterial hypertension. LV mass has been regarded as the best measure of LVH. Among hypertensive group, 15.48% (48) patients had LVH on 2D ECHO, 32.58% (101) had LV mass >116 gm. There was statistically significant association observed between LV mass and posttransplant hypertension in our study. Microvascular involvement is less due adequate of BP control and improvement of LV mass with restoration of renal function.

Donor factors such as family history of HTN, elderly age, gender, donor HTN, and quality of the graft are the risk for posttransplant hypertension.[5],[19],[20] Our study demonstrated a significant relation between female donors with male recipients and hypertension. Graft survival was poor with female donors when compared to male donors due to small kidney size and lower transplanted kidney weight/volume.[21],[22] Hypertension is a strong predictor for graft loss. There is dual relationship between BP and graft dysfunction. Impaired graft function is associated with elevated BP and increased risk of future posttransplant hypertension.[2],[23]

There was no statistical difference regarding donor age, donor side of kidney, cold ischemic time, type of transplant, and DGF between two groups. In our study, graft survival in posthypertension patients was poor when compared to nonhypertensive patients. Analysis by Kaplan–Meier analyses showed posttransplant hypertension and occurrence of graft dysfunction was statistically significant [Figure 4].
Figure 4: Kaplan–Meier analyses of graft survival

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In multiple logistic regression analysis, male gender (P < 0.01), presence of metabolic syndrome (P < 0.001), and use of cyclosporine (P = 0.06) were associated with posttransplant hypertension [Table 4] and [Figure 5].
Table 4: Multiple logistic regression analyses

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Figure 5: Multiple logistic regression analyses – Adjusted odds ratio for posttransplant hypertension

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  Conclusion Top

The prevalence of posttransplant hypertension is 82.6% in our study. It is an important risk factor for cardiovascular morbidity and mortality. Early identification of risk factors and its intervention, adequate BP control can improve the long-term survival of the graft and patient. Male recipients, pretransplant hypertension, weight gain, increased LV mass, female donors, use of cyclosporine, and presence of metabolic syndrome had statistically significant association with posttransplant hypertension in our study.

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  References Top

Luke RG. Hypertension in renal transplant recipients. Kidney Int 1987;31:1024-37.  Back to cited text no. 1
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.  Back to cited text no. 2
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.  Back to cited text no. 3
Kasiske BL, Chakkera HA, Roel J. Explained and unexplained ischemic heart disease risk after renal transplantation. J Am Soc Nephrol 2000;11:1735-43.  Back to cited text no. 4
Włodarczyk Z, Glyda M, Kościanska L, Kołodziejczyk J, Sulikowska B, Manitius J, et al. Prevalence of arterial hypertension following kidney transplantation – A multifactorial analysis. Ann Transplant 2003;8:43-6.  Back to cited text no. 5
Stenehjem AE, Gudmundsdottir H, Os I. Office blood pressure measurements overestimate blood pressure control in renal transplant patients. Blood Press Monit 2006;11:125-33.  Back to cited text no. 6
Tomson CR. Ambulatory blood pressure measurement in kidney transplantation: An overview. Transplantation 2003;76:1643-4.  Back to cited text no. 7
Pérez Fontán M, Rodríguez-Carmona A, García Falcón T, Fernández Rivera C, Valdés F. Early immunologic and nonimmunologic predictors of arterial hypertension after renal transplantation. Am J Kidney Dis 1999;33:21-8.  Back to cited text no. 8
Beecroft JR, Rajan DK, Clark TW, Robinette M, Stavropoulos SW. Transplant renal artery stenosis: Outcome after percutaneous intervention. J Vasc Interv Radiol 2004;15:1407-13.  Back to cited text no. 9
Knight SR, Morris PJ. Steroid avoidance or withdrawal after renal transplantation increases the risk of acute rejection but decreases cardiovascular risk. A meta-analysis. Transplantation 2010;89:1-4.  Back to cited text no. 10
Roullet JB, Xue H, McCarron DA, Holcomb S, Bennett WM. Vascular mechanisms of cyclosporin-induced hypertension in the rat. J Clin Invest 1994;93:2244-50.  Back to cited text no. 11
Hoorn EJ, Walsh SB, McCormick JA, Fürstenberg A, Yang CL, Roeschel T, et al. The calcineurin inhibitor tacrolimus activates the renal sodium chloride cotransporter to cause hypertension. Nat Med 2011;17:1304-9.  Back to cited text no. 12
Cross NB, Webster AC, Masson P, O'connell PJ, Craig JC. Antihypertensives for kidney transplant recipients: Systematic review and meta-analysis of randomized controlled trials. Transplantation 2009;88:7-18.  Back to cited text no. 13
Clunk JM, Lin CY, Curtis JJ. Variables affecting weight gain in renal transplant recipients. Am J Kidney Dis 2001;38:349-53.  Back to cited text no. 14
Porrini E, Delgado P, Bigo C, Alvarez A, Cobo M, Checa MD, et al. Impact of metabolic syndrome on graft function and survival after cadaveric renal transplantation. Am J Kidney Dis 2006;48:134-42.  Back to cited text no. 15
Raczyńska D, Ślizień M, Bzoma B, Dębska-Ślizień A, Glasner L, Raczyńska K, et al. A10-year monitoring of the eyesight in patients after kidney transplantation. Medicine (Baltimore) 2018;97:e9822.  Back to cited text no. 16
Abraham G, Yuvaraj A, Haridas AP, Vijayan M, Raajendhira M, Parthasarathy R, et al. Prevalence of hypertension in post renal transplant recipients: A retrospective tertiary care study. Indian J Transplant 2017;11:194-7.  Back to cited text no. 17
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Hewing B, Dehn AM, Staeck O, Knebel F, Spethmann S, Stangl K, et al. Improved left ventricular structure and function after successful kidney transplantation. Kidney Blood Press Res 2016;41:701-9.  Back to cited text no. 18
Guidi E, Menghetti D, Milani S, Montagnino G, Palazzi P, Bianchi G, et al. Hypertension may be transplanted with the kidney in humans: A long-term historical prospective follow-up of recipients grafted with kidneys coming from donors with or without hypertension in their families. J Am Soc Nephrol 1996;7:1131-8.  Back to cited text no. 19
Feduska NJ Jr. Donor factors in cadaveric renal transplantation. Clin Transpl 1993;21 351-7.  Back to cited text no. 20
Kim YS, Moon JI, Kim DK, Kim SI, Park K. Ratio of donor kidney weight to recipient bodyweight as an index of graft function. Lancet 2001;357:1180-1.  Back to cited text no. 21
Vacher-Coponat H, McDonald S, Clayton P, Loundou A, Allen RD, Chadban SJ, et al. Inferior early posttransplant outcomes for recipients of right versus left deceased donor kidneys: An ANZDATA registry analysis. Am J Transplant 2013;13:399-405.  Back to cited text no. 22
Cheigh JS, Haschemeyer RH, Wang JC, Riggio RR, Tapia L, Stenzel KH, et al. Hypertension in kidney transplant recipients. Effect on long-term renal allograft survival. Am J Hypertens 1989;2:341-8.  Back to cited text no. 23


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]

  [Table 1], [Table 2], [Table 3], [Table 4]


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