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Saudi Journal of Kidney Diseases and Transplantation
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Year : 1999  |  Volume : 10  |  Issue : 3  |  Page : 333-348
Hypertension in Renal Allograft Recipients

Department of Internal Medicine-Nephrology, University Hospital Charite, Campus Charite-Mitte, Humboldt-University, Berlin, Germany

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Hypertension is a frequent complication after renal transplantation. It contributes to the considerable cardiovascular morbidity and mortality in renal allograft recipients. Additionally, it has a major impact on long-term allograft survival. The pathogenesis of post transplant hypertension is multifactorial. Besides common risk factors, renal allograft recipients accumulate specific risk factors related to the original renal disease, renal transplantation per se and the immunosuppressive regimen. Chronic allograft dysfunction is the main cause of post transplant hypertension. The introduction of calcineurin inhibitors, such as cyclosporine, has increased the prevalence of hypertension. At present, the growing manual of diagnostic and therapeutic tools enables us to adapt better antihypertensive therapy. Tight monitoring, individualization of the immunosuppressive protocol, inclusion of non-pharmacological measures and aggressive antihypertensive treatment should help to minimize the negative implications of post transplant hypertension. Probably, this goal can only be reached by "normalization" of systolic and diastolic blood pressure to below 135/85 mmHg.

Keywords: Cardiovascular morbidity, Graft survival, Hypertension, Patient survival, Renal transplantation, Review.

How to cite this article:
Waiser JE, Budde KT, Neumayer HH. Hypertension in Renal Allograft Recipients. Saudi J Kidney Dis Transpl 1999;10:333-48

How to cite this URL:
Waiser JE, Budde KT, Neumayer HH. Hypertension in Renal Allograft Recipients. Saudi J Kidney Dis Transpl [serial online] 1999 [cited 2023 Feb 4];10:333-48. Available from: https://www.sjkdt.org/text.asp?1999/10/3/333/37241

   Introduction Top

The prevalence of hypertension in patients with end-stage renal disease (ESRD) varies between 10% and 100%, [1] depending on the underlying renal disease. The prevalence of hypertension in renal allograft recipients ranges between 40 and 75%. [2],[5] Most of these patients have been hypertensive before renal transplantation and continue to be so, although there is a small percentage who acquire hypertension or become normotensive after transplantation. Furthermore, renal trans­plantation can normalize the circadian blood pressure profiles in Cyclosporine A­(CsA-) treated renal allograft recipients. [6]

Throughout the past decades, patient survival after renal transplantation has continuously improved. [7] Meanwhile, renal allograft recipients seem to have a substantial survival advantage compared to corresponding ESRD patients on the waiting list. [8] However, cardio­vascular disease remains the most frequent single cause of death following renal transplantation. [9],[10] The mortality rate from cardiovascular events among patients on renal replacement therapy currently ranges between 35 and 50%. [10],[11],[12],[13] This is significantly higher as compared to the general population [14],[15] and contributes to the elevated overall mortality in these patients. [7] Whether hypertension is an independent risk factor for cardio-vascular disease in renal allograft recipients or not, remains controversial. The fact that some studies failed to detect such a correlation, [16] may be due to aggressive antihypertensive treatment that results in normotension in transplant patients. Nevertheless, in context with other relevant risk factors such as diabetes, hyperlipidemia, age, male gender or smoking, post transplant hypertension is an important risk factor for cardiovascular disease. [17],[18]

Hypertension is also an important risk factor for the progression of chronic renal disease. [19] In the US, the high incidence rates of new cases of ESRD is, in part, a consequence of hypertension. [20] Comparably, post transplant hypertension is a risk factor for poor renal allograft survival.[21],[22] So far, it has not been established whether the dele­terious effect of hypertension is causative for graft dysfunction, or whether hyper­tension is a consequence of preexisting renal dysfunction. [23] It is conceivable that hypertension initiates a vicious cycle, where progression of chronic graft dysfunction further elevates blood pressure.

Patients with chronic renal failure tend to accumulate cardiovascular risk factors. [24] Tight monitoring and reasonable treatment of each of these risk factors is essential in order to reduce the risk of cardiovascular morbidity and mortality, and to further improve renal allograft survival. In the following review, we will focus on etiology, pathophysiology, diagnosis and treatment of the most common causes of sustained hypertension in renal allograft recipients.

Etiology, pathophysiology and diagnosis

Etiology and pathogenesis of post transplant hypertension are multifactorial and are summarized in [Table - 1]. Besides common risk factors, [3] such as family history, obesity, regular alcohol consumption and salt intake, renal allograft recipients have additional risk factors. The most important ones are the presence of pre-transplant hypertension, chronic graft dysfunction and the immuno­suppressive medication. In the pre-cyclos­porine era, post-transplant hypertension occurred in 40 to 50% of all kidney transplant recipients. [25],[26],[27] The most common cause was chronic allograft dysfunction. The introduction of calcineurin inhibitors has generally increased the prevalence of hypertension to 60-75%. [26],[27],[28] The varying prevalence rates of post-transplant hypertension in different studies are probably due to different definitions of arterial hypertension.

Cyclosporine A

The negative influence of CsA on the prevalence of hypertension has been documented in numerous investigations. Even the use of low-dose CsA in non-renal conditions such as uveitis [29] or heart transplantation [30],[31] has been shown to result in a significant rise in blood pressure. The introduction of CsA has increased the incidence of hypertension in renal allograft recipients by approximately 20%. Conversely, shifting from CsA to azathioprine has been shown to reduce blood pressure levels. [32],[33]

CsA-dependent hypertension is mainly caused by four mechanisms: renal vaso constriction, [34] an increase in systemic vascular resistance [35] chronic CsA vasculopathy, [36] and the development of hemolytic uremic syndrome [37] Acute CsA nephrotoxicity is characterized by renal vaso-constriction. In healthy volunteers, a single oral dose of CsA (10-12 mg/kg) increased mean arterial blood pressure and renal vascular resistance with a concomitant drop in renal plasma flow and glomerular filtration rate (GFR). [38],[39] A large number of animal studies support the action of CsA as a powerful renal vasoconstrictor, especially of the preglomerular vascular resistance vessels. [34],[35] CsA-induced hypertension persists as long as the patient is on the drug. [40] This initially functional vasoconstriction may progress to fixed structural changes in the renal microvasculature. Histological changes of chronic CsA nephropathy are similar to those observed in chronic graft dysfunction. [41] The longer the duration of the exposure to the drug, the more likely is the presence of irreversible chronic CsA nephropathy. [42] Renal vasoconstriction and hypertension due to CsA have been shown to be reversible up to 10 months after transplantation. [34]

Catecholamines, [44] prostaglandins, [45] endo­thelin, [46] the renin angiotensin aldosterone system (RAAS), [47] and nitric oxide (NO) synthase expression48 have all been implicated as possible mediators of CsA­induced vasoconstriction of the afferent arteriole. CsA-induced hypertension may also be mediated by the renal nervous system. [44],[49],[50]

The fact that renal allografts are primarily denerved may explain, why hypertension and nephrotoxicity are more pronounced in non-renal transplants as compared with renal allograft recipients. [51] In the pre­cyclosporine era, renal transplant recipients had predominantly renin-dependent hyper­tension, which was resistant to low-salt diet. [53] In contrast, hypertensive patients on CsA exhibit a significant fall in blood pressure on low-salt diet. [52] Furthermore, angiotensin converting enzyme (ACE) inhibition by captopril causes a fall in blood pressure in azathioprine-treated patients, but not in CsA-treated patients. [53] These results indicate that CsA-induced hyper­tension is volume-dependent. [54],[55] Plasma volume contraction induced by low-salt diet in combination with furosemide causes a significant decrease in GFR in CsA-treated patients. [56] as he physiological vasodilatory response of the afferent arteriole is inhibited by the vasoconstrictive effect of CsA. When the afferent vasoconstriction is marked, GFR becomes dependent on angio­tensininduced efferent vasoconstriction. This may explain the sometimes-deleterious effect of concomitant medication of CsA and ACE inhibitors,[57],[58]

Concerning the new microemulsion formulation of CsA, "Neoral", we observed a slight improvement in systolic and in mean arterial blood pressure as compared to the conventional CsA preparation, at one year after conversion. [59] However, this may have been the consequence of a dose reduction by about 15%.

FK 506 (Tacrolimus)

The incidence of post-transplant hypertension in the European and US Tacrolimus Multicenter Trials was equal in patients receiving tacrolimus and those receiving CsA. [60],[61],[62] Equivalent results were obtained in liver allograft recipients. [63] However, some studies have reported a lower incidence of hypertension in tacrolimus-treated patients than CsA-treated patients. [64] Tacrolimus and CsA bind to different intracellular binding proteins. Both agents mediate their major immunosuppressive action by a similar mechanism: the inhibition of the phosphatase activity of calcineurin. [65] In rats, both CsA and tacrolimus reduced renal blood flow and GFR, whereas rapamycin did not. In addition, tacrolimus treatment caused similar histological alterations as described for CsA. [67],[68] Treatment with nilvadipine, a calcium channel blocker (CCB) with renal vasodilating activity, prevented both biochemical and histopathological changes. [69] Similarly, nilvadipine improved kidney function in liver transplant recipients who received tacrolimus. [70] In conclusion the side effect profile of tacrolimus and CsA concerning hypertension and renal function seems to be similar. Therefore, antihypertensive therapy in patients treated with either of these drugs should be adjusted according to the same criteria.


Steroids still play an essential role in the immunosuppressive protocols after organ transplantation. Despite the introduction of newly developed immunosuppressive agents, they are still used in induction, maintenance and rejection therapy. However, due to their well-known and quite harmful side-effect profile (such as hypertension and hyperlipidemia), many transplant physicians all-over the world are trying to develop immunosuppressive strategies, which may allow to avoid the use of steroids in the future. According to Fryer et al., the steroid dose at one month after transplantation has a significant impact on the occurrence of post-transplant hypertension. [71] In addition, it was clearly documented that complete steroid withdrawal has a beneficial effect on the prevalence and severity of hypertension. Moreover, withdrawal may reduce additional cardiovascular risk factors, such as plasma lipid profiles and glycemic control. [75] Converting from daily to alternate-day steroid therapy, while maintaining the same total dose, may also improve blood pressure profile, [76] obesity and insulin resistance. [77]

Chronic graft dysfunction

In the pre-cyclosporine era chronic graft dysfunction was the most common cause of hypertension after renal transplantation. [2],[56] This disorder is characterized by a progressive deterioration of renal function (GFR), the development of hypertension and overt Proteinuria, and by typical histological findings. [18],[19] At present, the question whether hypertension causes chronic graft dysfunction or vice versa cannot be answered conclusively.

Frei et al. observed that chronic progressive graft dysfunction was associated with hypertension not only at one year after transplantation, but also at the time of transplantation, indicating that hypertension per se leads to graft damage and initiates chronic progressive graft dysfunction. [80]

Tullius et al. showed that antigen­independent mechanisms cause functional and morphologic changes in rat kidney isografts that resemble those of allografts with chronic allograft dysfunction. [81] These results emphasize that non-immunological factors such as hypertension are important risk factors for chronic graft dysfunction.

Recurrence of the underlying renal disease

Recurrence of the underlying renal disease may also cause post-transplant hypertension. The reported incidence of "recurrent glomerulonephrtis" in large transplant series varies from 6% to 27%. [82] This wide range is probably due to the case mix of the investigated patients. Depending on regional differences and on the age of the recipient, the overall rate of graft failure due to recurrence of the underlying disease ranges between 1% and 7%.[83],[84],[85],[86] Treatment of the recurrent underlying renal disease and concomitant hypertension should be identical to the treatment of the original disease.

Essential hypertension

An increased prevalence of post­transplant hypertension was documented in recipients of cadaveric allografts from donors with a family history of essential hypertension. [3]

Guidi et al. showed that recipients without a family history of hypertension, grafted with a kidney coming from a "hypertensive family", developed hypertension much more frequently than recipients grafted with a kidney coining from a "normotensive family". Furthermore, such recipients have a greater increase of diastolic blood pressure and a greater degree of acute renal damage during acute rejection episodes. [88] This indicates that a kidney graft can transmit net only hypertension, but also the susceptibility to an acute insult. Accordingly, recipients of cadaveric kidneys from donors with a history of familial hypertension required more anti-hypertensive therapy as compared to a matched control group. [89]

Interestingly, the resolution of essential hypertension by transplantation of a kidney graft from a normotensive donor is also possible, in hypertensive rats from a hyper­tension-prone strain, a renal homograft from a hypertension-resistant strain resulted in a sharp fall in blood pressure. [90],[91] These results underline the central role of the kidney in hypertension, indicating that genetically controlled factors operating through the kidney may regulate at least a segment of essential hypertension.

A fall in systemic blood pressure together with an increase in allograft plasma flow after administration of ACE inhibitors indicates the presence of an "endocrine clamp" as a consequence of renin secretion coming from the retained native kidneys. If severe hypertension persists, despite lowering of the CsA dose, bilateral nephrectomy is recommendable. [92] Such surgery is most appropriate in young patients who require multiple anti­hypertensive drugs. Although these patients may be infrequent, it is worth considering this possibility in severe hypertension not explained by allograft renal artery stenosis, chronic rejection or high CsA trough levels

Transplant renal artery stenosis

The incidence of transplant artery stenosis ranges between 1 and 25%. [93] A functionally significant transplant artery stenosis is characterized by either an acute deterio­ration of renal function with sudden onset of hypertension or the deterioration of preexisting hypertension. Sometimes, a bruit near the allograft may be present. The autoregulatory capacity, which maintains GFR, starts to fail. [94] Regulatory mechanisms include dilatation of the preglomerular vessels and angiotensin-dependent constriction of the postglomerular vessels. [95]

Diminished allograft plasma flow together with increased allograft vascular resistance is a common feature of patients with post-transplant hypertension. [96] Functio­nally relevant renal artery stenosis can be detected by demonstration of a reduction in renal blood flow and GFR after admini­stration of an ACE inhibitor. [97] However, this phenomenon is not specific for renal artery stenosis but rather for a situation where maintenance of GFR has become dependent on the intra-renal angiotensin system. [95] Clinical examples include pre­renal failure with reduction of systemic blood pressure below the auto-regulatory range (volume contraction and congestive heart failure), severe preglomerular vasoconstriction (non-steroidal anti­inflammatory agents and CsA) and intra­renal small vessel disease due to chronic graft dysfunction or chronic CsA nephrotoxicity. Moreover, administration of ACE inhibitors can abruptly drop GFR causing functional acute renal failure. Because of these major concerns, ACE inhibitor provocative tests, are not the tools of choice for the diagnosis of transplant renal artery stenosis.

In the last few years, the use of Doppler ultrasound examination as a primary screening tool for transplant artery stenosis has been established. Using color Doppler ultrasound, "aliasing" and perivascular color artefacts are typical signs of transplant artery stenosis. These findings must be confirmed by pulsed-wave- (pw-) Doppler ultrasound, which shows a marked accele­ration of the peak systolic flow (> 200 cm/sec) within the stenotic area and a reduction of the Pourcelot resistive index (RI < 0.50) within the allograft.

Recently, a new technique, gadolinium­enhanced magnetic resonance angiography, was introduced. [99] This technique may be promising in further improving the diagnostic manual for transplant renal artery stenosis, especially as gadolinium is less nephrotoxic as compared to conven­tional iodinated contrast media. [100]

Nevertheless, selective intra arterial angiography remains to be the "gold standard " for the diagnosis of renal artery stenosis.

   Treatment Top

Post-transplant hypertension should be treated aggressively with a reasonable regimen adapted to the underlying cause. In patients with proteinuria >1 g/day, aggressive treatment of hypertension targeting at a "low" mean arterial blood pressure (92 mmHg) is associated with a slower decline in GFR as compared to less aggressive treatment targeting at a "usual" mean arterial blood pressure (107 mmHg). [101]

If serum creatinine exceeds 160umol/L, allograft biopsy should be performed, to exclude chronic graft dysfunction, recurrent disease and de novo glomerulonephritis. Non-pharmacological measures, including weight control, moderate sodium restriction, low saturated fat intake, exercise and cessation of smoking should accompany antihypertensive medication. Sodium restriction may not be well tolerated by all patients, so mild diuretic therapy may be considered.

Today, calcineurin inhibitors are part of most immunosuppressive routine protocols. Therefore, antihypertensive treatment needs to consider adverse effects of these agents. "Low dose" CsA/tacrolimus treatment may be useful, although a good correlation between CsA/tacrolimus trough levels and blood pressure is not proven. [97] In some patients, a "switch" to an alternative immunosuppressive regimen, not containing CsA or tacrolimus, has to be considered. In the case of hemolytic uremic syndrome, CsA or tacrolimus must be discontinued immediately. Severe salt restriction, especially if coupled with diuretic therapy, may cause a decline in GFR, due to impairment of the autoregulatory capacity of the transplanted kidney. [102]

In general, treatment of CsA-/ tacrolimus -associated hypertension should be directed at the reversal of preglomerular vasoco­nstriction. The predominantly preglome­rular vasodilatory effects of CCBs' favor these compounds. [103] Opinions vary, about which classes of CCBs' should be used. Some authors prefer the dihydropyridine­type CCBs' (e.g. felodipine, isradipine, lacidipine, nicardipine, nifedipine and nitrendipine), as these agents, with the exception of nicardipine, do not sub­stantially affect CsA metabolism. Others prefer to use CCBs' such, as verapamil or diltiazem, [104] which increase CsA trough levels by interfering with CsA metabolism and therefore allow a significant dose reduction and cost benefit. [105],[106] Using these agents, it is helpful to monitor monoclonal or even polyclonal CsA trough levels more frequently. Lacidinine can completely prevent acute CsA-induced hypo­perfusion. [107] Similar effects have been observed with amlodipine, [108] felodipine, [109] isradipine, [110] nifedipine, [111] verapamil [112] and diltiazem. [113] Nifedipine also exerts a beneficial long-term effect on renal hemodynamics and function.

In patients, who fail to respond adequately to CCBs', a cardioselective - blocker can be added. Furthermore, this may relieve tachycardia provoked by dihydropyridinetype CCBs'. Alternatively, either a centrally or a peripherally acting vasodilatator, such as moxonidine or doxazosin, can be administered. Long­acting agents are preferred, especially concerning dihydropyridine-type CCBs',

The use of the ACE inhibitors in patients treated with calcineurin inhibitors is still controversial. In short-term crossover experiments, a similar decrease in blood pressure was observed in response to nifedipine as compared to captopril. [115] In contrast to nifedipine, administration of captopril was associated with a significant fall in GFR.

On the other hand, lisinopril has been reported to be effective in controlling blood pressure during 2.5 years of follow-up, without having a detrimental effect on renal function. Lisinopril was also shown to reduce protein excretion in renal transplant recipients with severe proteinuria, while maintaining stable renal function. [117] The main adverse effect was a significantly lower hematocrit, when compared with patients receiving CCBs'.[116],[117],[118],[119]

Enalapril [111] and captopril [58] may cause a significant fall in renal blood flow and GFR. Reversible acute renal failure has also beenreported.[57],[120],[121]

In conclusion, ACE inhibitors should be used with caution in renal allograft recipients treated with calcineurin inhibitors. The question. Whether an ACE inhibitor induced slight reduction in GFR has any impact on long-term renal allograft function needs to be further investigated.

There is no specific treatment for steroid­induced post-transplant hypertension. If possible, complete steroid withdrawal or conversion from daily to alternate day steroidtherapy should be considered. However, the potential benefits of steroid withdrawal must be balanced against an associated risk of precipitating acute allograft rejection. Patients subsequently maintained on CsA and azathioprine or CsA alone have a reported incidence of rejection ranging from 3 to 75%. Hricik et al. demonstrated that late steroid withdrawal (>6 months after transplantation) is more successful than early withdrawal. [122] The rejection rate in patients receiving conventional triple therapy (steroids/CsA/azathioprine) ranges between 20 to 30%. [123],[124] Steroid withdrawal was more successful in patients who received triple immunosuppressive therapy consisting of prednisone, CsA and myco­phenolate mofetil. [125] Since nearly all current immunosuppressive maintenance protocols are based on calcincurin inhibitors or steroids, at least one of these agents should be continued.

In a rat model of chronic renal allograft rejection, all different antihypertensive treatment regimens improved graft function, proteinuria, graft survival and histopathological findings. [126] In contrast to the other regimens, administration of an angiotensin receptor antagonist also reduced graft atherosclerosis. These data indicate that anti-hypertensive treatment can be effective in ameliorating chronic allograft dysfunction.

The question remains, which type of anti­hypertensive treatment is most effective in CsA-treated patients with chronic rejection. ACE inhibitors should be beneficial in treating glomerular hypertension, hyperfiltration and hypertrophy, all of which contribute to the progression of chronic allograft failure. However, in CsA treated patients with sodium retention, RAAS suppression and glomerular ischemia due to afferent arteriolar vasoconstriction, ACE inhibitors may lack any renoprotective action. Instead. CCBs' may be more useful. In future, long-term prospective controlled comparative trials are necessary, in order to assess the effect of these differing therapeutic approaches on chronic allograft dysfunction.

Renin-dependent hypertension may be the underlying cause of native kidney hypertension and is likely to persist despite successful renal transplantation. Usually, such pre-transplant hypertension can be controlled by antihypertensive therapy including volume control. In some cases, it may be the cause for severe hypertension. Bilateral nephrectomy [127] or embolization [128],[129] of the native kidneys may be effective in such patients. However, before surgery, the diagnosis should be confirmed by the eaptopril test [130],[131] If positive, bilateral native kidney nephrectomy has a high probability of effect tiveness. [132] In contrast, bilateral nephrectomy in renal allograft recipients may not be successful without a preceding positive captopril test. [133]

The diagnostic and therapeutic approach to renal artery stenosis after kidney transplantation was recently summarized by Rengel et al. [134] If a functionally relevant transplant renal artery stenosis is confirmed adequately, the primary therapy of choice is percutaneous transluminal angioplasty. In the majority of cases, hypertension can be treated successfully with this intervention. [135] Bypass surgery should be reserved for cases in which this procedure is not successful.

   Conclusion Top

Renal allograft recipients have an increased burden of cardiovascular disease due to multiple interrelated risk factors, which accelerate each other. Post-transplant hypertension needs to be diagnosed and treated aggressively. CCBs seem to be advantageous, especially in patients who receive calcineurin inhibitors. ACE inhibitors and angiotensin receptor antagonists may be helpful when proteinuria is present. However, so far there is not enough evidence to confirm this assumption. Therefore, long-term pros­pective controlled trials are necessary to compare the effect of these various agents on long-term renal allograft survival. Non­pharmacological measures, including a modest salt restriction, should accompany pharmacological treatment. In future, the introduction of new immunosuppressants like rapamycin may extend the existing immunosuppressive manual and help to reduce the incidence of post-transplant hypertension.

   References Top

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Correspondence Address:
Johannes E Waiser
Medizinische Klinik mit Schwerpunkt Nephrologie, Universitatsklinikum Charite, Schumannstrasse 20/21, 10117 Berlin
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