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Saudi Journal of Kidney Diseases and Transplantation
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ORIGINAL ARTICLE Table of Contents   
Year : 1999  |  Volume : 10  |  Issue : 4  |  Page : 470-480
Hypertension in Renal Transplantation: Saudi Arabian Experience


1 Saudi Center for Organ Transplantation, Saudi Arabia
2 Jeddah Kidney Center, Saudi Arabia
3 Riyadh Armed Forced Hospital, Saudi Arabia

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   Abstract 

To evaluate the prevalence, etiologic factors and therapy of hypertension in actively followed up transplant population in Saudi Arabia; we retrospectively reviewed the records of the active renal transplant patients at two large transplant centers in Riyadh and Jeddah in Saudi Arabia. These subjects were transplanted between January 1979 and November 1998. The patients were grouped according to the measurement of blood pressure; group 1 (considered normo-tensive): blood pressure below 140/90 mmHg, group2: blood pressure between 140­159/90-99, group 3: blood pressure 160-179/100-109 group 4: equal to or above 180/110. There were 1115 patients' records included in the study. The mean duration of transplantation was 66.9 ± 50.1 months. According to the level of measured blood pressure, there were 641 (57.5%) patients in the normotensive group (group 1), 404 (36.3%) patients in the mildly hypertensive group (group 2) 64 (5.7%) patients in the moderately severe hypertension group (group 3) and only six (0.5%) patients in the severe hypertension group (group 4). The estimated prevalence of hypertension in this study was almost 85%. We found no significant difference in the prevalence of hypertension in terms of gender, year of transplantation, duration of transplantation, type of donor, number of previous transplants, diagnosis of renal artery stenosis, etiology of kidney disease, diagnosis of diabetes after transplantation, diagnosis of cerebrovascular accidents, or mean dose of prednisolone and cyclosporine. There was a statistically significant association between increased level of blood pressure and old age (above 50 years), original disease associated with hypertension, history of hypertension on dialysis, acute rejection (once or more), presence of protienuria (more than 0.3 mg/day), abnormality of ECG, or serum creatinine above 300 µmol/L. We conclude that hypertension is highly prevalent in the renal transplant population in Saudi Arabia. Risk factors for the development of hypertension or its complication should be more aggressively approached in order to protect the patients and their grafts alike.

Keywords: Renal Transplantation, Hypertension, cyclosporine, Therapy, Cardiovascular.

How to cite this article:
Souqiyyeh MZ, Shaheen FA, Sheikh IA, Al-Khader AA, Fedhail H, Al-Sulaiman M, Mousa D, Al-Hawas F. Hypertension in Renal Transplantation: Saudi Arabian Experience. Saudi J Kidney Dis Transpl 1999;10:470-80

How to cite this URL:
Souqiyyeh MZ, Shaheen FA, Sheikh IA, Al-Khader AA, Fedhail H, Al-Sulaiman M, Mousa D, Al-Hawas F. Hypertension in Renal Transplantation: Saudi Arabian Experience. Saudi J Kidney Dis Transpl [serial online] 1999 [cited 2019 Sep 19];10:470-80. Available from: http://www.sjkdt.org/text.asp?1999/10/4/470/37204

   Introduction Top


Renal transplantation is an established method of renal replacement therapy in patients with end stage renal failure. [1] Despite the improvement, after transplantation, in the overall survival of patients and renal grafts, cardiovascular disease is still the prime cause of death accounting for almost 50% of mortality in this population. [2],[3]

Hypertension is an important risk factor for the progression of chronic renal disease [4] and decrement of renal graft survival when it develops or persists after transplantation.[5],[6]

The effect on progressing of cardiovascular disease is less clear. [7] This may be due to the multiple factors involved in this progression, such as underlying diseases, diabetes, hyperlipidemia, age, male gender and smoking. If added to these factors, hypertension is important risk factors for cardiovascular disease.[8]

The etiology of post-transplant hyper­tension is multifactor. Dysfunction of the renal allograft [9] and immunosuppressive therapy [10] are usually added to the common risk factors such as family history, obesity, original kidney disease, and pre-transplant hypertension.[11],[12]

In this study, we attempt to evaluate the prevalence, etiologic factors and therapy of hypertension in actively followed up transplant population in Saudi Arabia.


   Patients and Methods Top


We retrospectively reviewed the records of the active renal transplant patients at two large transplant centers in Riyadh and Jeddah in Saudi Arabia, transplanted between January 1979 and November 1998.

The review of history included type of donor type of original kidney disease, history of hypertension (on dialysis and after transplantation), diagnosis of graft artery disease, number of acute rejection episodes in the first year and history of cerebrovascular accidents.

The review of the physical examination included the last three consecutive measu­rements of blood pressure and body weight.

The review of the laboratory date included electrocardiogram (ECG), last three consecutive measurements of serum creatinine level, plasma cholesterol level and 24-hour urine protein level. The review of current therapy included the type and dosing of immunosuppressive and antihypertensive.

The patients were grouped according to the measurement of blood pressure. Group 1: blood pressure below 140/90 mmHg (mean arterial pressure (MAP) <106), group 2: blood pressure between 140­159/90-99 mmHg (MAP 106-119), group 3: blood pressure 160-179/100-109 mmHg (MA) 120-132) and group 4: equal to or above 180/110 mmHg (MAP>132). The patients were also regrouped according to the number of antihypertensive medications they were taking at the time of the study; group I: no medications, group II: one medication, group III: two medications, group IV: three or more medications.

Statistical Methods

We used the analysis of variance (ANOVA) to compare the equality of means for any three or more groups of quantitative variables such as age, weight, plasma creatinine etc. the two sample independent t-test was used to compare the equality of means for any two groups. Chi­square test was used to compare categorical variables such as sex, type of transplant etc. The P value was set as significant if below 0.05.


   Results Top


There were 1115 patients records included in the study. There were 741 (66.5%) males and 374 (33.5%) females with mean age of 38.2 ± 12.3 years (range 4-76 years). The mean weight of the patients was 66.9 ± 16.4 kg. [Table - 1] shows the dates of transplantation of the study patients.

The mean duration of transplantation was 66.9 ± 50.1 months. The renal grafts were from cadaver donors in 26.1%, living related donors in 39.9%, and living non related in 34.0% of the recipients. There were 1074 (96.3%) study patients who had renal transplantation for the first time, while41 (3.7%) recipients had more than one renal transplant. History of the pre­transplantation status of blood pressure (on dialysis) was available in 1004 (90.04%) of patients. Of these 735 (65.9%) had history of documented hypertension. In the remaining 269 patients, who were normotensive at transplantation, the starting date of hypertension after transplantation was specified in 104 (9.3%) patients; and 56 (54%) of these developed hypertension in the first three months post-transplantation.

The original renal disease was unknown (bilateral small kidneys by ultrasound) in 601 (53.9%) recipients. Hypertension as a cause of renal failure of the original kidneys was diagnosed in 276 925.01%) patients without diabetes mellitus and in 116 (10.4%) with diabetes. Congenital and other primary kidney diseases were diagnosed in 122 (10.94%) patients. Diagnosis of diabetes after transplantation was in 247 (22.15%) study patients with an increment of 53% in comparison to those patients with original kidney disease associated with diabetes.

Of all the study patients acute rejection occurred once in 313 (28.07%) and twice or more in 19 (1.71%). There were only five patients with a history of cerebrovascular accident and seven patients with history of diagnosis of renal artery stenosis in the renal allograft.

According to the level of measured blood pressure, there were 641 (57.5%) patients in the normotensive group (group 1), 404 (36.3%) patients in the mildly hypertensive group (group 2), 64 (5.7%) patients in the moderately serve hypertension group (groups 3) and only six (0.5%) patients in the severe hypertensive group (group 4). For purpose of analysis, we combined groups 3 and 4.

ECG was available on 1069 patients. The tracings were reported as normal in 990 (92.6%) patients and compatible with left venrtricular hypertrophy, ischemia and/or strain in 79 (7.4%) patients.

The mean serum creatinine was 231.8 ± 207 µmol/L, the mean serum cholesterol level was 5.7 ± 1.4 mmol/L and the mean 24-hour urine protein was 0.54 ± 0.96 g/L. All the study patients were on cyclosporine except 46 (4.1%). The mean dose of cyclosporine was 3.3 ± 1.7 mg/Kg/day. There were 646 (57.9%) patients receiving azathioprine and 22 (1.97%) receiving mycophenolate mofetil.

There were only 185 (16.6%) study patients not on any antihypertensive treatment (group I), 411 (36.9%) on one drug (group II), 434 (38.9%) on two drugs (group III), 85 (7.6%) on three drugs (group IV). [Table - 2] shows the types of antihypertensive used in the study patients. Calcium channel blockers were the most frequently used antihypertensive followed by beta-blockers, whatever the combination utilized.

The comparison of the groups of patients depending on the blood pressure measurement showed no significant difference in terms of gender, transplant date, duration of transplantation, type of donor, number of transplants, diagnosis of graft-renal artery stenosis, diagnosis of diabetes after transplantation, diagnosis of cerebrovascular accidents, number of patients treated by azathioprine, mean dose foprednisolone or treatment with mycophenolate mofetil.

However, there was a positive correlation between the development of hypertension and old age, the presence of history of hypertension on dialysis, number of episodes of rejection, lower mean cyclosporine dose, mean serum creatinine, mean serum cholesterol, mean 24-hour urine protein and abnormality of ECG, [Table - 3].

The comparison of the study patients according to the number of antihypertensive medications used (including severity of hypertension) showed no significant differences in gender, year of transplant date, duration of transplantation, type of donor, number of transplants, diagnosis of renal artery stenosis, diagnosis of diskettes after transplantation, diagnosis of cerebrovascular accidents, number of patients treated by azathioprine, mean serum creatinine and mean serum cholesterol.

However, the severity of hypertension correlated positively with old age, heavier body weight, type of original kidney disease, history of hypertension on dialysis, number of episodes of rejection, lower mean cyclosporine dose, lower mean dose of prednisolone, treatment with mycophenolate mofetil, mean 24-hour urine protein and abnormality of ECG, [Table - 4].

There were 173 (15.5%) of the study patients with normal blood pressure and not on any treatment. Accordingly, the estimated prevalence of hypertension in this study was almost 85%. Of the study patients, 468 (41.9%) were on antihypertensive medications and attained good control of their blood pressure, 462 (41.5%) were on meditations but the blood pressure not adequately controlled and 12 (1.1%) were noted to have hypertensive levels (mostly mild to moderately severe hypertension) but were never put on any antihypertensive medications.

In order to evaluate the contribution of the possible risk factors to the pathogenesis of hypertension, the study patients were regrouped according to each of the following factors. Age, gender, body weight, renal function, type for original kidney disease, diagnosis of diabetes after transplantation, diagnosis of renal artery stenosis, episodes of rejections, cyclosporine usage and dosage, prednisolone dose, year of transplant, duration of transplant, type of donor and number of previous transplants

Furthermore, the study patients were regrouped according to probable vascular complications related to hypertension. Indicator parameters were the occurrence of cerebrovascular accidents, high serum cholesterol levels, presence of protienuria and ECG abnormalities.

The evaluation of the risk factors involved comparison of patients according to the level of blood pressure and number of antihypertensives used in treatment.

There was a statistically significant tendency for only increased level of blood pressure usage of more antihypertensives in patients of older age (above 50 years), original renal disease associated with hypertension, history of hypertension on dialysis, acute rejection (once or more), presence of protienuria (>0.3 mg/day) or abnormality of ECG. There was a statistically significant tendency for only increased level of blood pressure without a tendency for use of more antihypertensives in those patients having duration of transplantation more than 12 months or serum creatinine above 300 µmol/L.

There was a statistically significant tendency for only increased use of more antihypertensives without a tendency for increased level of blood pressure in those patients having treatment with cyclosporine regardless of the dose.

There was no statistically significant tendency for increased level of blood pressure and/or use of more antihypertensives with gender, body weight, diagnosis of diabetes after transplantation, history of cerebrovascular accident, diagnosis of renal artery stenosis in the transplanted graft, year of transplantation, type of donor, number of transplantation, use of steroids or serum cholesterol level.

There was no correlation of rate of acute rejection with the dose of prednisolone therapy. However, there was a positive correlation of acute rejection with the use of a combination of azaioprine, prednisolone and cyclosporine. No such correlation was observed with the use of prednisolone and cyclosporine for immunosuppression.

Further comparison between the 173 patients who had normal blood pressure (and not on antihypertensive therapy) and the rest of the study patients showed no statistically significant differences between them except for higher mean cyclosporine daily dose (3.66 vs. 3.23 mg/Kg/day respectively, P<0.003) and higher mean prednisolone daily dose (0.17 vs. 0.15 mg/Kg/day respectively, P< 0.01). However, these results are not clinically significant. The evaluation of the risk factors showed similar results to those obtained from comparison of the blood pressure groups stratified according to severity of hypertension and status of treatment.


   Discussion Top


The definition of hypertension in our study depended on the criteria set by the 6th Joint USA National Committee (JNC-VI) established in 1997. [13] The stratification of patients in our study helped to evaluate the effect of severity of hypertension and status of therapy ore than mere stratification according to normal and abnormal blood pressure regardless of therapy. Prevalence of hypertension in post renal transplant patients varies between 40-80%.[11],[14] In our study, prevalence was 85%, which agrees with the higher figures of previous reports.

The pathogenesis of hypertension post renal transplantation involves general risk factors and specific factors such as the dysfunction of the renal graft and the side effects of the immunosuppressive therapy.

The general risk factors of hypertension post renal transplantation include older age, [15] original kidney disease, [16],[17] family history, [11],[18] male gender, [19] body weight [20], [21] or body mass index, [22] and history of hypertension on dialysis.[4]

In our study, we found that old patients had higher prevalence of hypertension than the young patients. Moreover, those patients with history of original kidney disease associated with hypertension, and/or history of hypertension on dialysis had higher prevalence of hypertension after transplantation. The reported diagnosis of graft-renal artery stenosis was very low in our study, which may be due to its retrospective design. The patients with increased weight had no increase tendency for higher prevalence of hypertension. Furthermore, we did not find a significant effect of gender on the prevalence of hypertension in this study.

Dysfunction of the renal allograft results usually from immunologic and non immunologic factors. [9] Acute and chronic rejections are the major immunologic factors. [23],[24] furthermore, Acute rejection is a major risk factor for chronic rejection, and develops mainly during primary dysfunction of the renal graft after prolonged cold ischemia or from inadequate immunosuppression especially high-risk patients. [25],[26] Hypertension is an important non-immunologic factor to cause or aggravate the dysfunction of the renal graft, and is also caused or aggravated by the dysfunction of the renal graft. [26],[27]

In our study, we found a similar significant correlation between the occurrence of acute rejection and prevalence of hypertension. Furthermore, we found a tendency for hypertension with time after transplantation; nevertheless, we found no correlation between the year of transplantation, number of previous transplants or donor type and the prevalence of hypertension. Like others, [26],[27]

We found a significant correlation between level of renal allograft dysfunction and prevalence of hypertension. Moreover, our study showed that increased protienuria and renal graft dysfunction were more prevalent in the uncontrolled hypertensive patients than the controlled ones.

Previous reports showed an escalating effect of administration of cyclosporine on prevalence of hypertension. [28],[29] We found increased prevalence of treatment of hypertension with the usage of cyclosporine in comparison to those not on cyclosporine. However, there was a statistically significant increase correlation with mean dose of cyclosporine, though the difference may not be clinically significant. The mechanism of effect of cyclosporine on the pathogenesis of hypertension is still not clear, however, direct vasculopathy has been proposed. [30] Steroids are known as a risk factor to develop or aggravate hypertension. [31],[32],[33] However, we found no correlation between doses of prednisolone and prevalence of hypertension in our study. This may be related to the small doses used in conjunction with cyclosporine. We did not find a correlation of rejection and imunosuppession except in those who were on azatioprine, cyclosporine and prednisolone, which may result from the lower doses of cyclosporine in this three-drug immunosuppressive regimen in comparison to the cyclosporine two drug regimen.

In addition to its effects on renal function, hypertension is a known risk factor for development of cardiac [34],[35],[36],[37],[38] and cerebrovascular complications. [39],[40],[41] In our study, there was an increased prevalence of signs of ischemia and left ventricular dysfunction of ECG of the patients with uncontrolled hypertension. Despite the low rate of cerebrovascular accidents in our study, there were inadequate data about the mortality related to it. There was a significant number of patients in our study with elevated serum cholesterol as was reported by others. [42],[43] However, there was no significant difference of cholesterol serum level between those patients with controlled and uncontrolled blood pressure. Overall, the findings in our study dictate the need for more aggressive management of hypertension and other risk factors such as weight and cholesterol reduction, besides optimization of renal function by aggressive control of acute and chronic rejection.

Antihypertensive therapy type and efficacy have been addressed by our study. There was a tendency to use calcium channel blockers and adrenergic beta blockers in our transplant population more than angiotensin converting enzyme inhibitors. Others have advocated this strategy. [44],[45],[46],[47],[48],[49],[50],[51],[52],[53] However, there was a significant number of patients with uncontrolled blood pressure reaching 54%. There were 297 (26%) patients in our study whose blood pressure was 130-139/80-84 mmHg (MAP>100). Such level of blood pressure has been considered recently as high normal range. Accordingly, these patients can be added to the group of uncontrolled blood pressure, since they have renal transplant. [13] This makes the percentage of patients of not well controlled blood pressure rises to almost 80%. Even if non-compliance is a major contributing factor, the treating physicians should minimize it in the transplant patients. Direct patient-education may be helpful. More aggressive therapy is also recommended.

We conclude that like other population sin other countries, hypertension is highly prevalent in the renal transplant population in Saudi Arabia. Risk factors for the development of hypertension or its complications should be more aggressively approached in order to protect patients and their grafts alike.

 
   References Top

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2.Geerlings W, tufveson G, Ehrich JH, et al. Report on management of renal failure in Europe. XXIII. Nephrol Dial Transplant 1994;9(Suppl 1):S6-25.  Back to cited text no. 2    
3.Unted State Renal Data System 1998 annual Data Report. Causes of death. Am J Kidney Dis 1998;32(Suppl 1):S81-88.  Back to cited text no. 3    
4.Perneger TV, whelton PK, Klag MJ. History of hypertension in patients treated for end-stage renal disease. J Hypertens 1997;15(4):451-6.  Back to cited text no. 4    
5.Opelz G, Wujciak T, Ritz E. Association of chronic kidney graft failure with recipient blood pressure. Collaborative Transplant Study. Kidney Int 1998;53(1):217-22.  Back to cited text no. 5    
6.Bock HA. Chronic rejection and hypertension: a chicken-and-egg problem. Nephrol Dial Transplant 1995;10(7):1126-8.  Back to cited text no. 6    
7.Kasiske BL, Guijaro C, Massy ZA, Wiederkehr KR, Ma JZ. Cardiovascular disease after renal transplantation. J am Soc Nephrol 1996;7(1):158-65.  Back to cited text no. 7    
8.De Lemos JA, Hillis LD. Diagnosis and management of coronary artery disease in patients with end-stage renal disease on hemodialysis. J Am Soc Nephrol 1996;7(10):2044-54.  Back to cited text no. 8    
9.Perez FM, Rodriguez CA, Garcia FT, Fernandez RC; Valdes F. Early immunologic and nonimmunologic predictors of arterial hypertension after renal transplantation. Am J Kidney Dis 1999;33(1):21-8.  Back to cited text no. 9    
10.Jarowenko MV, Flechner SM, Vana Buren CT, Lorber MI, Kahan BD. Influence of cyclosporine on post­transplant blood pressure respone. Am J Kidney Dis 1987;10(2):98-103.  Back to cited text no. 10    
11.Budde K, Waiser J, Fritche L, et al. Hypertension in patients after renal transplantation. Transplantation Proc 1997;29(1-2):209-11.  Back to cited text no. 11    
12.Warholm C, Wilczek H, Petterson E. Hypertension two years after renal transplantation: causes and consequences. Transpl Int 1995;8(4):286-92.  Back to cited text no. 12    
13.Joint National committee on Prevention, Detention, Evaluation, and Treatment of High Blood Pressure. The sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med 1997; 157:2413.  Back to cited text no. 13    
14.Mailloux LU, Haley WE. Hypertension in the ESRD patient: pathophysiology, therapy, outcomes and future directions. Am J Kidney Dis 1998;32(5):705-19.  Back to cited text no. 14    
15.Anderson GH Jr, Blakeman N, Streten DHP. The effect of age on prevalence of secondary forms of hypertension in 4429 consecutively referred patients. J hypertension1994;12:609-15.  Back to cited text no. 15    
16.Mathew TH. Recurrent disease after renal transplantation. Transplant Rev 1991;5:31-45.  Back to cited text no. 16    
17.Rengel M, gomes DSG, Inchaustegui L, et al. Renal artery stenosis after renal transplantation; diagnosis and therapeutic approach. KI 1998;(Supple 68):S99-106.  Back to cited text no. 17    
18.Guidi E, Cozzi MG, Minetti E, Bianchi G. Donor and recipient family histories of hypertension influence renal impairment and blood pressure during acute rejections. J Am Soc Nephrol 1998;9(11):2102-7.  Back to cited text no. 18    
19.Kasiske BL. Risk factor for cardiovascular disease after renal transplantation. Miner electrolyte Metab. 1993;19(3):186-95.  Back to cited text no. 19    
20.Ribstein J, de Cailar G, Mimran A. Combined renal effects of overweight and hypertension. Hypertension 1995;26:610-15.  Back to cited text no. 20    
21.Kanner WB, Ahang T, Garrison RJ. Is obesity-related hypertension less of a cardiovascular risk: the Framingham study. Am Heart J 1990;120:1195-1201.  Back to cited text no. 21    
22.Selmer R, Tverdal A. Body mass index and cardiovascular mortality at different levels of blood pressure: a prospective study of Norwegian men and women. J Epidemiol community Health 1995;49:265-70.  Back to cited text no. 22  [PUBMED]  
23.First MR, Neylan JF, Rocher LL, Tejani A. Hypertension after renal transplant­tation. J Am Soc nephrol 199;4(8 Suppl):S30-6.  Back to cited text no. 23    
24.Ponticelli C, Montagnino G, Aroldi A, Angelini C, Braga M, Tarantino. Hypertension. Hypertension after renal transplantation. Am J Kidney Dis 1993;21(5 Suppl 2):73-8.  Back to cited text no. 24    
25.Perez FM, Rodriguez CA, Bouza P, Valdes F. The prognostic significance of acute renal failure after renal transplantation in patients treated with cyclosporine. Q J M 1998;91(1):27-40.  Back to cited text no. 25    
26.Paul LC, Benediktsson H. Post­transplant hypertension and chronic renal allograft failure. Kidney Int 1995;(Suppl 52):S34-7.  Back to cited text no. 26    
27.Perz FM, Rodriquez CA, Bouza P, Garcia FT, Moncalian J, oliver J, Valdes F. Outcome of grafts with long-lasting delayed function after renal transplantation. Transplantation. 1996;62(1):42-7.  Back to cited text no. 27    
28.Sandrini S, Gaggia P, Bracehi M, Gaggiotti M, brunori G, Maiorca R. Arterial hypertension in renal transplantation. Contrib Nephrol 1996;119:16-25.  Back to cited text no. 28    
29.Sutherland F, Burgess E, Klassen J, Buckle S, Paul LC. Post-transplant conversion from cyclosporine to azathioprine: effect on cardiovascular risk profile. Transpl Int 1993;6(3):129-32.  Back to cited text no. 29    
30.Radermacher J, Meiners M, Bramlage C, et al. Pronounced renal vascoconstriction and systemic hypertension in renal transplant patients treated with cyclosporine A versus FK 506. Transpl Int 1998;111):3-10.  Back to cited text no. 30    
31.Fryer JP, Granger DK, Leventhal JR, Gillingham K, Najarian JS, Matas AJ. Steroid-related complications in the cyclosporine era. Clin Transplant 1994;8(3):224-9.  Back to cited text no. 31    
32.Pirsch JD, Armbrust KJ, Knechtle SJ, et al. Effect of steroid withdrawal on hypertension and cholesterol levels in living related recipients. Transplant Proc 1991;23(1):1363-4.  Back to cited text no. 32    
33.Hariharan S, Schroeder TJ, Weiskittel P, Alexsander JW, First MR. Prednisone withdrawal in HLA identical and one haplotype-matched live-related donor and cadaver renal transplant recipients. Kidney Int 1993;44(Suppl 43):S30-5.  Back to cited text no. 33    
34.Brown JH, Hunt LP, Vites NP, Short CD, Gokal R, Mallick NP. Comparative mortality from cardiovascular disease in patients with chronic renal failure. Nephrol Dial Transplant 1994;9(8):1136-42.  Back to cited text no. 34    
35.Brunner FP, Selwood NH. Profile of patients on RRT in Europe and death rates due to major causes of death groups. The EDTA Registration Committee. Kidney Int 1992;42(Suppl 38):S4-15.  Back to cited text no. 35    
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37.Arned SM, Mallat KJ, Westendorp RJ, van der Woude FJ, van Es LA. Patient survival after renal transplantation; more than 25 years follow-up. Nephrol dial Transplant 1997;12(8):1672-9.  Back to cited text no. 37    
38.Koch M, Gradaus F, Schoebel FC, Leschke M, Grabensee B. Relevance of conventional cardiovascular risk factors for the prediction of coronary artery disease in diabetic patients on renal replacement therapy. Nephrol Dial Transplant. 1997;12(6):1187-91.  Back to cited text no. 38    
39.Mathias CJ. Role of the central nervous system in human secondary hypertension. J Cardiovasc Pharmacol 1987;10(Suppl 12):S93-9.  Back to cited text no. 39  [PUBMED]  
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41.Eluf NJ, Lotufo PA, de-Lolio CA. Treatment of hypertension and the decline of mortality caused by cerebrovascular accidents. Rev Saude Publica 1990;24(4):332-6.  Back to cited text no. 41    
42.Aakhus S, Dahl K, Wideroe TE. Hyperlipidaemia in renal transplant patients. J intern Med 1996;239(5):407-15.  Back to cited text no. 42    
43.Sharma AK, Myers TA, Hunninghake DB, Matas AJ, Kashtan CE. Hyperlipidemia in long-term survivors of pediatric renal transplant transplantation. Clin Transplant 1994;8)3 Pt1):252-7.  Back to cited text no. 43    
44.Traindl O, Falger S, Reading S, et al. The effects of lisinopril on renal function in proteinuric renal transplant recipients. Transplantation 1993;5596):1309-13.  Back to cited text no. 44    
45.Martinez CA, Hueso M, Sanz V, Rejas J, Alsina J, Grinyo JM. Treatment of hypertension after renal transplantation: long-term efficacy of verapamil, enalapril, and doxazosin. Kidney Int Suppl 1998;68:S130-4.  Back to cited text no. 45    
46.Venkat RG, Feehally J, Elliott HL, et al. Renal and hemodynamic effects of amlodipine and nifedipine in hypertensive renal transplant recipient. Nephrol Dial Transplat 1998;13(10):2612-6.  Back to cited text no. 46    
47.Grekas D, dioudis C, Kaleverosoglou I, et al. Management of moderate to severe hypertension and proteinuria by nifedipine retard and perindopril after renal transplantation. Clin Nephrol 1995;44(5):299-302.  Back to cited text no. 47    
48.Raine AE. Does antihypertensive therapy modify chronic allograft failure? Kidney Int Suppl 1995;52:S107-11.  Back to cited text no. 48  [PUBMED]  
49.Vander SM. Hene RJ, Floor M, Blankestijn PJ, Koomans HA. Hypertension after renal transplantation. Calcium channel or converting enzyme blockade? Hypertension 1995;25(1):77-81.  Back to cited text no. 49    
50.Abu-Romeh SH, El Khatib D, Rashid A, et al. Comparative effects of enarlapril and nifedipine on renal hemodynamics in hypertensive renal allograft recipients. Clin Nephrol 1992;37(4):183-8.  Back to cited text no. 50    
51.Ferguson CJ, Williams JD, Hillis AN, Parry-Jones D, Salaman JR. Effects of the calcium channel blocker diltiazem on cyclosporine nephrotoxicity in renal transplant recipients. Clin Transplant 1992;6:391-8.  Back to cited text no. 51    
52.Mourad G, Ribstein J, Mimran A. Converting-enzyme inhibitor versus calcium antagonist in cyclosporine­treated renal transplants. Kidney Int 1993;43(2):419-25.  Back to cited text no. 52    
53.Ahmad T, Coulthard MG, Eastham EJ. Reversible renal failure due to the use of captopril in a renal allograft recipient treated with cyclosporine. Nephrol Dial Transplant 1989;4(4):311-2.  Back to cited text no. 53    

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Correspondence Address:
Muhammad Ziad Souqiyyeh
Saudi Center for Organ Transplantation, P.O. Box 27049, Riyadh 11417
Saudi Arabia
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