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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2005  |  Volume : 16  |  Issue : 4  |  Page : 443-452
Post-Transplantation Hypertension

Associate Prof. of Medicine, Renal Transplant Unit, Nephrology Department, Hospital 12 de Octubre, Madrid, Spain

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How to cite this article:
Morales JM. Post-Transplantation Hypertension. Saudi J Kidney Dis Transpl 2005;16:443-52

How to cite this URL:
Morales JM. Post-Transplantation Hypertension. Saudi J Kidney Dis Transpl [serial online] 2005 [cited 2022 Aug 7];16:443-52. Available from: https://www.sjkdt.org/text.asp?2005/16/4/443/32839

   Introduction Top

It is well known that renal transplantation is the treatment of choice for most patients with end-stage renal disease. Despite marked improvements in short-term renal allograft function and survival with administration of newer immunosuppressive drugs, [1],[2] renal graft losses continue to be a constant over the time.

Chronic allograft nephropathy and death with graft function are the most important causes of late graft loss. [3],[4] Immunological and non­immunological factors have been identified as important risk factors to develop chronic allograft nephropathy. [5] Notably, cardiovascular disease is the leading cause of death in renal transplant patients with a functioning graft. [3],[5]

Arterial hypertension (AH) is a frequent and important complication after renal transplant­ ation. [3],[6],[7],[8],[9],[10] In fact, AH has been reported to be an independent non-immunological risk factor for graft failure [6],[7],[8],[9] and has also been associated with increased post-transplant cardiovascular morbidity and mortality. [11],[12] Hypertension contributes to both problems and therefore requires early and correct management after renal transplantation.

   Definition Top

Although there is no an universal consensus in renal transplant patients, AH has been defined as systolic blood pressure ≥140 mm Hg and/ or diastolic blood pressure ≥ 90 mm Hg and/or need for treatment with antihypertensive drugs; [13] some studies have not considered the administration of diuretics as therapy.

Accurate diagnosis of post-transplant hyper­tension is essential and ambulatory blood pressure monitoring (ABPM) could be useful. ABPM seems to be a more sensitive method for diagnosis of hypertension than the sole reliance on office blood pressure, particularly in renal transplant recipients. [14]

   Prevalence and Clinical Characteristics Top

Hypertension is a common complication after renal transplantation, presenting in 60-85% of patients treated with anti-calcineurin drugs. In fact, > 50% of patients with well-functioning grafts exhibit arterial hypertension. [6],[7],[8],[9],[10] A study from Spain during the last decade showed a progressive and significant increase in the prevalence of hypertension during follow-up after renal transplantation in the three studied periods: 1990, 1994 and 1998. Patients trans­planted in 1990 exhibited arterial hypertension in 81% at five years versus 85% among those transplanted in 1994. [15]

Cyclosporin A (CsA) - induced AH has been described in autoimmune diseases and in renal, liver, heart and bone marrow transplantation. [1],[16] While the prevalence of hypertension varies between 20 and 25% in patients with auto­immune diseases, AH in renal transplant patients, with concomitant usage of corticosteroids, ranges between 50 and 85% as commented before. In the most relevant U.S. and European pivotal studies comparing patients receiving tacrolimus vs CsA, there was no difference in the incidence of AH. [2],[17] However, after five years follow-up, in the American study, the use of anti-hypertensive drugs was significantly lower in patients receiving tacrolimus; 81% vs 91.3% [18] The most recent European multi­center study comparing tacrolimus vs CsA microemulsion showed that the incidence of new-onset or worsening AH was less common in the tacrolimus group (16% vs 23%), [19] In the Spanish study commented before, the prevalence and severity was lower in patients treated with tacrolimus vs CsA. [15]

Post-transplant AH is clinically characterized by an absence of the nocturnal decrease of blood pressure, especially in CsA treated patients. [4] In general, it can co-exist with some degree of renal dysfunction and with other cardiovascular risk factors such as hyper­cholesterolemia, hyperglycemia, obesity and smoking. Occasionally, accelerated hypertension with microangiopathic hemolytic anemia, encephalopathy and convulsions can occur. [20]

   Clinical Impact of Arterial Hypertension after Renal Transplantation Top

Frei et al reported that AH was independently associated with the development of progressive allograft dysfunction as other typical risk factors such as HLA mismatching and acute rejection episodes. [6] Cosio et al demonstrated a relation­ship between mean arterial blood pressure at six months post-transplant and allograft survival in African American recipients. [7] Opelz studied 29,751 renal transplant recipients from Europe who received kidneys from cadaveric donors and demonstrated that there was a statistically significant association bet­ween elevated systolic blood pressure at one year and allograft failure. [8] The principal limitation of the study was that these authors did not adjust for one-year renal function, raising the suggestion that graft failure could be the cause and not the consequence of AH. Mange et al demonstrated that systolic, diastolic and mean arterial blood pressure at one-year post-transplant strongly predict graft survival adjusted for baseline renal function suggesting that a more aggressive control of blood pressure may prolong allograft survival. [9] Although, in the recent epidemiological Spanish study, AH was not associated with graft survival, [15] previous data strongly suggest that AH negatively influences allograft survival.

In the general population, control of AH can decrease cardiovascular morbidity and mortality. Although, there is scarce information on the role of post-transplant hypertension as a cardio­vascular risk factor, the importance of AH on cardiovascular disease in transplant patients is evident particularly because these patients have a higher risk of cardiovascular mortality than normal population. In fact, relative risk of death by a cardiovascular event in a renal transplant patient between 25-34 years is ten times higher than a similar individual without renal disease. [12]

   Pathogenesis Top

The etiology of AH frequently is multi­factorial; immunosuppressive drugs, chronic allograft nephropathy, recurrent and the native kidney disease, renal artery stenosis and presence of the diseased native kidneys can be the most important factors responsible for post-trans­plant hypertension. [13],[20] [Table - 1]

   Immunosuppressive Drugs Top


It is clear that corticosteroids contribute to AH since their discontinuation in stable patients reduced blood pressure in most cases. [21] Several factors related to steroid therapy such as sodium retention as well as increase in cardiac output and renal vascular resistance may induce AH. [13] It has been demonstrated that the daily dose as well as cumulative dose of prednisone are related to blood pressure. Fortunately, in the current immunosuppressive era, corticosteroid usage is not a major risk for AH due to rapid reduction in dosage. [13],[15] In fact, one group estimated that the incidence of AH induced by corticosteroids was only 15% in their patient population. [22]

Calcineurin Inhibitors

Currently, CsA and tacrolimus continue to be the choice for basic immunosuppressive regimens in renal transplantation. [23] It is well known that the immunosuppressive and nephrotoxic effects of CsA and tacrolimus depend of calcineurin inhibition. [1],[2],[20] Calcineurin is a protein phosphatase with important regulatory effects blocking the expression of T-cell activation genes. Calcineurin is present in several tissues including the kidney, vascular smooth muscle and nervous system, all of which are targets for hypertension. It has been suggested that calcineurin inhibition in these tissues causes an increase in sodium and water retention, vasoconstriction and sympathetic activity. [20]

CsA and tacrolimus cause acute and chronic nephrotoxicity and AH. [20],[21],[22],[23],[24],[25],[26],[27],[28],[29] Mechanisms of these renal and vascular effects are multi­factorial, including vasoconstriction of the afferent pre-glomerular arterioles, increase in systemic vascular resistance, increase in sympathetic nervous tone and activation of the renin-angiotensin system. [30] These may reflect an imbalance between vasoconstrictive factors, such as endothelin and thromboxane, and vasodilator factors such as nitric oxide and prostacyclin in CsA/tacrolimus treated patients. [30] The experimental administration of an endothelin-receptor antagonist controlled CsA-induced hypertension, strongly suggesting that endothelin may play an important role in the development of AH. [20]

Tacrolimus has been considered to be as nephrotoxic as CsA. Nevertheless, tacrolimus has been associated with less systemic vaso­constriction and less AH than CsA after liver transplantation. [25] Notably, AH after renal transplantation is less frequent and severe in patients on tacrolimus as against those on CsA. [18] Also, the presence of AH at one year was more strongly associated with CsA but not with tacrolimus. [15] Some authors also reported a decrease of mean arterial blood pressure after conversion from CsA to tacro­limus. [28] Recent studies on healthy subjects have shown that tacrolimus resulted in mean arterial pressure lower and renal vascular resi­stance, together with higher effective renal plasma flow, renal blood flow and glomerular filtration rate than CsA. [29]

Other Immunosuppressive Drugs

Renal and blood pressure data from all the available literature support that mycophenolate mofetil is not nephrotoxic and does not have any hypertensive effect. [31] Sirolimus too is not a [32] nephrotoxic drug and it does not induce AH.

However, in the phase III studies using sirolimus in combination with CsA, mild renal functional impairment and a higher frequency of AH were observed in the study patients when compared with control groups. Also, it has been demonstrated that sirolimus potentiates the nephrotoxic effects of CsA, which could explain the increase of blood pressure. [23]

   Renal Dysfunction Top

Renal dysfunction with a variable degree of renal insufficiency is frequent after renal transplantation and it represents an important cause of high blood pressure. [13],[30] Several mechanisms such as salt and water retention, inappropriate activation of renin-angiotensin system and an increase of sympathetic activity are probably involved in the pathogenesis of AH in transplanted patients with renal dysfunction. [30] Acute rejection, chronic allograft nephropathy, chronic CsA or tacrolimus nephro­toxicity, obstructive uropathy, de novo or recurrent glomerulonephritis can induce renal insufficiency after renal transplantation, which in turn can induce AH.

In one study, the degree of renal function was associated with the number of antihypertensive drugs: in patients with normal renal function (serum creatinine < 1.3 mg/dl) the number was two while in patients with serum creatinine between 1.3-2 mg/dl the number of antihyper­ tensives was four. [13]

Pre-Transplant Hypertension

The presence of pre-transplant AH is currently considered as a risk factor for developing post­transplant hypertension. Two studies demon­strated that in transplanted patients treated with CsA, the presence of pre-transplant hypertension was an independent risk factor for AH at three months and one year post-transplant. [33],[34]

Donor Hypertension

There is data concerning the role of the trans­planted kidney in the presence or absence of post-transplant hypertension. It has been reported that AH and increased antihypertensive drug requirements post-transplant occurred more frequently in recipients from "normotensive" families who received a kidney from a donor with a "hypertensive family". [35] Also, a greater hypertensive response during acute rejection has been published after transplantation of a kidney from a hypertensive family into a recipient from a normotensive family. [36] Why genetic factors predispose to the development of post-transplant hypertension is unknown.

Transplant Renal Artery Stenosis

The reported incidence of transplant renal artery stenosis (TRAS) varies between 1.5 and 7%. This varied incidence is probably due to problems of retrospective surveys, differences in policies for angiography and differences in definition of stenosis. Some studies showing the results of angiography in all functioning grafts have shown TRAS in 23% of patients, confirming that radiological stenosis often do not represent a functional stenosis. TRAS results from damage to the renal artery during retrieval or cannulation during perfusion, kinking of a long artery, a poor anastomosis technique, mainly in end-to-end anastomosis, or chronic rejection of the renal artery. [37]

The usual time of presentation of TRAS is three months to two years after transplantation, with a peak incidence at six months. The key to the diagnosis of TRAS is to consider this possibility in all patients with deteriorating renal function and/or sudden onset of hypertension or uncontrolled AH. An elevation of serum creatinine after the administration of an angio­tensin converting enzyme inhibitor (ACEI) or an angiotensin receptor blocker (ARB) is suggestive but not diagnostic of renovascular disease of the graft. Another presentation of TRAS is the development of sudden left ventricular failure without obvious reasons. In some patients, polycythemia is associated with TRAS. [38]

Clinical examination may reveal the presence of a bruit in the graft area but TRAS can be present with no audible bruit. Although doppler ultrasonography is the preferred screening modality, angiography or, more accurately, digital substraction angiography is the gold standard for diagnosis of TRAS. [39] Magnetic resonance angiography with gadolinium is the most recent and promising test for the diagnosis of TRAS.

Concerning treatment, percutaenous trans­luminal angioplasty can be technically useful in up to 80% of cases, although 20% will develop recurrent stenosis. [38] Stent placement used in combination with angioplasty may be useful, particularly in those with recurrent stenosis of the renal artery. [40] Surgery for correction of TRAS is indicated in patients with severe and resistant hypertension or with proximal recipient arteriosclerotic disease. [38]

The Presence of Native Kidneys

Another cause of post-transplant hypertension is the presence of native kidneys with hyper­ secretion of renin and an increase in sympathetic activity. [41] In the past, in patients with severe hypertension, bilateral nephrectomy was performed in order to improve the control of blood pressure. [13] Results of this procedure were questionable; it seems to be logical due to the multiple mechanisms involved in the pathogenesis of post-transplant hypertension. [42] Currently, with the modern and potent anti­hypertensive drugs, bilateral nephrectomy is not recommended.

Other Pathogenic Factors

Other factors that have been associated with post-transplant hypertension include obesity, alcohol, a familial history of hypertension, transplantation of the right kidney, delayed graft function, prolonged ischemia times, older donor and female recipients. [13],[33]

   Treatment Top

The management of post-transplant hyper­tension is extremely important since cardio­vascular disease is the major cause of morbidity and mortality in renal transplant patients and hypertension has also been implicated as a risk factor for graft failure. Therefore, blood pressure lowering is an integral part of post­transplant care. [43],[44]

Although there is no general consensus about the optimal blood pressure after renal trans­plantation, The National Kidney Foundation Task Force on cardiovascular disease [43] and The European Best Practice Guidelines for Renal Transplantation [45] have recommended that blood pressure should be < 130/85 mm Hg for renal transplant recipients without proteinuria and < 125/75 mm Hg for patients with proteinuria.

To control post-transplant AH, several lines of therapy should be started: general measures, use of antihypertensive drugs, and treatment of modifiable pathogenic factors as well as concomitant cardiovascular risk factors. [43,[44]

General non-pharmacological measures should be given priority. They include avoidance of an increase of body weight, sodium restriction in the diet, low caloric diet, regular exercise and avoidance of smoking. [46],[47] All these must be clearly recommended during post-transplant follow-up.

   Antihypertensive Therapy Top

In spite of these measures, pharmacological therapy is necessary in most cases [Table - 2]. Although all antihypertensive drugs are useful in renal transplant patients, the most commonly used drugs are calcium channel blockers (CCB) and angiotensin converting enzyme inhibitors (ACEI). [43],[45] Many physicians prefer a CCB because in addition to antihypertensive efficacy, it minimizes cyclosporine-induced renal vaso­ constriction. [47],[48] Also, it has not been demon­strated that CCB have a clear benefit over ACEI on renal function and long-term graft survival. [48],[49],[50],[51] ACEI have been shown to be effective in controlling hypertension and decreasing proteinuria in renal transplant patients. [45] Therefore, the choice of the drug should depend on the presence or not of pro­teinuria. In patients without proteinuria, a CCB could be used but in proteinuric patients an ACEI should be indicated. [43],[44],[45] Recently, angio­tension II receptor antagonists (ARA) have been used to control post-transplant hyper­tension. In addition to their antihypertensive effect, these drugs can decrease proteinuria, serum TGF-B1 and endothelin in patients with chronic allograft nephropathy. [52],[53] Before ACEI/ARA therapy, TRAS should be excluded by duplex Doppler study. [45]

Beta-blockers have been considered as the first line of therapy in renal transplant patients with hypertension and a history of coronary artery disease because of their capacity to decrease morbidity and mortality after acute myocardial infarction. Nevertheless, beta­blocker therapy can worsen other post-transplant cardiovascular risk factors as hyperlipidemia and in diabetic patients may decrease or mask the symptoms of hypoglycemia. [47] a-Blockers are the other family of antihyper­tensive drugs that can be used in renal trans­plant patients mainly if they have associated prostatic hypertrophy. [47] Diuretics are excellent in transplant patients with excess fluid and sodium overload. [47]

In patients with uncontrolled hypertension with one agent alone, the combination of CCB and ACEI/ARB can be a good option. In case a third drug is needed, beta-blockers or a­blockers can be useful with CCB and ACEI/ ARB. The fourth step of therapy can be diuretics. Sometimes, in patients with permanent proteinuria, it is possible to use ACEI plus ARB with good clinical tolerance although renal function and serum potassium should be monitored. [4],[47]

Finally, in patients with severe uncontrolled hypertension and/or deterioration of renal function in spite of these measures, other causes of hypertension should be excluded, especially TRAS. [45]

   Treatment of Modifiable Pathogenic Risk Factors Top

As commented before, calcineurin inhibitors play an important pathogenic role in the development of post-transplant hypertension. Fortunately, MMF and sirolimus do not have any hypertensive effect. New combinations including MMF in a triple therapy regimen can reduce blood pressure by reducing/eliminating CsA. [23],[54] Non-nephrotoxic protocols, using sirolimus as the primary immunosuppressive agent, could possibly reduce the incidence of post-transplant hypertension. 23 Also, in patients receiving sirolimus-CsA-steroids, a lower blood pressure is achieved after the elimination of CsA. [55] With these new regimens, it is also possible to minimize/stop steroids and decrease blood pressure. [23] Therefore, new regimens with MMF and sirolimus permitting several combinations offer good efficacy and safe alternatives to the classic immunosuppre­ssive protocols to improve the incidence and clinical impact of post-transplant hypertension.

Sometimes, a switch to tacrolimus from CsA has been documented to be useful in reducing high blood pressure. [23]

If TRAS is evident, correct therapy should be started, as commented before. If hypertension is due to the presence of arteriovenous fistulae, embolization is mandatory. [4]

Finally, it is also very important to control other concomitant cardiovascular risk factors present in renal transplant patients such as diabetes, hyperlipidemia, obesity, smoking, hyperhomocysteinemia and hyperuricemia. [4] Notably, it has recently been documented that statins not only decrease cholesterol levels but also decrease blood pressure. [56] If this finding is confirmed, it will enable us to control better the cardiovascular risk factors after renal transplantation

In summary, post-transplant arterial hyper­tension is highly prevalent after renal trans­plantation and may contribute to cardiovascular disease and late graft failure. Accurate diagnosis of hypertension is essential and ABPM could be useful for it. Immunosuppressive drugs (steroids, CsA and tacrolimus) may be important factors contributing to high blood pressure. Management of post-transplant hypertension is extremely important and several lines of therapy should be started: general measures, especially avoiding post-transplant obesity, use of antihypertensive drugs, treatment of modifiable risk factors and control of con­comitant cardiovascular risk factors such as diabetes, hyperlipidemia, etc. A rational use of antihypertensive drugs is mandatory, depending on the presence or absence of proteinuria. In proteinuric patients ACEI/ARB are recom­mended. Also, new immunosuppressive combi­nations with MMF and sirolimus offer new alternatives to improve the incidence and clinical impact of post-transplant hypertension.

However, many issues remain yet unresolved, especially the type of drugs or combinations to be used and the clinical importance of the degree of blood pressure control. [57]

   References Top

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53.Campistol JM, Iiiigo P, Jimenez W, et al. Losartan decreases plasma levels of TGF beta 1 in transplant patients with chronic allograft nephropathy. Kidney Int 1999;56: 714-9.  Back to cited text no. 53    
54.Smak-Gregoor PJ, Sevaux RG, Ligtenberger G, et al. Withdrawal of cyclo­sporine or prednisone six months after kidney transplantation in patients on triple drug therapy. A randomized, propsective, multi-center study. J Am Soc Nephrol 2002; 13:1365-73.  Back to cited text no. 54    
55.Johnson RW, Kreis H, Oberbauer R, et al. Sirolimus allows early cyclosporine withdrawal in renal transplantation resulting in improved renal function and lover blood pressure. Transplantation 2001;72:777-86.  Back to cited text no. 55  [PUBMED]  [FULLTEXT]
56.Prasad GV, Ahmed A, Nash MM, Zaltzman JS. Blood pressure reduction wit HMG­CoA reductase inhibitors in renal transplant recipients. Kidney Int 2003;63(1):360-4.  Back to cited text no. 56    
57.Tylicki I, Habicht A, Watschinger B, Horl WH. Treatment of hypertension in renal transplant recipients. Curr Opin Urol 2003; 13:91-8.  Back to cited text no. 57    

Correspondence Address:
Jose M Morales
Renal Transplant Unit, Nephrology Department, Hospital 12 de Octubre Caretera de Andalucia Km 5.400 28041-Madrid
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Source of Support: None, Conflict of Interest: None

PMID: 18202502

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