REVIEW ARTICLE
HYPERTENSION IN RENAL TRANSPLANT RECIPIENTS
 1. CORONARY MOTION
2. TREATMENT
3. Renal Artery Stenosis
4. Chronic Allograft Dysfunction
5. Resistant Hypertension
The prevalence of hypertension in patients with
end-stage renal disease ranges between 10 and
100%[1].
It occurs in renal transplant recipients in 40
75%[3,4].
Factors contributing to post-transplant hypertension
include immunosuppressive therapy:
corticosteroids and calcineurin inhibitors; causes
related to the graft:
chronic graft dysfunction, genetic, renal artery
stenosis, recurrence of the original disease and
factors related to the native kidneys.
Investigation of post-transplant hypertension
should be directed to these possible underlying
factors.
Treatment considerationswill depend on the presence
or absence of underlying factors and should observe
interaction between hypotensive medications and
immunosuppressive drugs.
(Heart Views. 2001; 2(2): 57-62) © 2001 Hamad
Medical Corporation.
Key Words:
hypertension
renal transplantation
The prevalence of hypertension in patients with end-stage renal disease varies
widely from as low as 10% to up to 100%[1].
This depends on the aetiology especially the underlying
primary renal disease.
Fluid control and aggressive maintenance dialysis
can lead to normotension in many patients[2].
In renal transplant recipients, the prevalence
of hypertension ranges between 40 and 75%[3-4].
Although many patients are hypertensive before
transplantation, a certain group develop hypertension
post-transplantation.This is partly related to
the timing of transplantation.
The prevalence is higher in the early post-transplant
period and tends to drop later.
Hypertension in renal transplant recipients is
the important risk factor for cardiovascular disease[5-6].
It is a frequent cause of mortality in 35 50%
of patients post-renal transplantation [7-8].
This is significantly high compared to the non-transplant
population[9].
Post transplant hypertension is possibly also
a risk factor for graft dysfunction[10] although
the possibility exists that hypertension could
be the sequence of graft dysfunction[11].
The main factors leading to post-transplant hypertension
are:
1) Immunosuppressive treatment :
Cyclosporin A, FK 506
(Tacrolimus) Corticosteroids
2) Graft related : Chronic allograft
dysfunction, donor-kidney mediated hypertension,
graft
renal artery stenosis
(RAS), recurrence of the original disease, de
Novo renal disease.
3) Pre-existing disease : Native
kidneys mediated hypertension, essential hypertension
The evidence incriminating cyclosporin A (CsA) in the production of hypertension
is overwhelming.
In the pre-CsA era, hypertension occurred in 40
50% of renal allograft recipients[12-13] and
was mostly mediated by the renin-angiotensin system,
either from the native kidneys or a dysfunctioning
graft[14].
The introduction of CsA led to elevation of the
blood pressure in almost all patients and increase
in the post renal transplant hypertension to 60
75%[15-16].
Even in bone marrow and cardiac transplantation,
when native kidneys mediated hypertension is unlikely,
the prevalence of post transplant hypertension
rose from below 10 - 33% to 60% (in bone marrow)
and 70 - 100% (in cardiac) with the use of CsA[17].
Also, shifting from CsA to azathioprine was found
to be associated with reduction in blood pressure
level[18].
CsA induces hypertension by a number of mechanisms.
It causes renal vasoconstriction, especially of
the preglomerular vascular resistance vessels
[19].
Catechlomines[20], prostaglandins[21], endothelin[22]
and the renin-angiotensin system[23] have all
been implicated as possible mediators of CsA renal
vasoconstriction.
Initially this vasoconstriction is reversible
if CsA therapy is discontinued but later it progresses
to fixed structural changes in the renal microvasculature.
The development of permanent damage is directly
related to the duration of CsA therapy[24].
Other mechanisms contributing to CsA induced hypertension
include increase in systemic vascular resistance[25]
and development of haemolytic uraemic syndrome
26]. CsA-induced hypertension is volume-dependent[26],
hence, salt restriction is useful in its treatment[27].
However, plasma volume depletion due to salt restriction
if coupled with loop diuretics treatment can cause
a marked drop in GFR[28].
This is due to blunting of physiological afferent
arteriole vasodilatation caused by CsA vasoconstrictive
effect.
In such patients, GFR can be enhanced by efferent
arteriolar vasoconstriction.
Accordingly, the additional use of Angiotensin
Converting Enzyme (ACE) inhibitors can have unfavourable
effects on renal graft function[29-30].
Transplant recipients treated with calcineurin inhibitor were found to have
a prevalence of hypertension similar to that of
CsA.
This was reported in the European and US Tacrolimus
Multi-center Trials [31,32,33] and in liver transplant
recipients[34].
The mechanism via which FK 506 induces hypertension
are similar to those of CsA.
This condition is characterized by a progressive deterioration of renal function,
development of hypertension, proteinuria, and
typical histological findings.
There is progressive ischaemia and fibrosis with
secondary renin production and may respond to
ACE inhibitors.
It is unclear whether hypertension here is a cause
or an effect creating a chicken-and-egg problem[11].
This condition is characterized by a progressive deterioration of renal function,
development of hypertension, proteinuria, and
typical histological findings.
There is progressive ischaemia and fibrosis with
secondary renin production and may respond to
ACE inhibitors.
It is unclear whether hypertension here is a cause
or an effect creating a chicken-and-egg problem[11].
Some evidence suggests that the grafted kidney may have a role in inducing
or relieving hypertension in the transplant recipients.
Such evidence was obtained from multiple cross
transplantation studies in animal experimental
models of genetic hypertension which showed that
the inherited tendency to hypertension resides
mainly in the kidney[38].
Available studies indicate that this possibly
also applies in humans.
Cutis et al[39] reported normalization of blood
pressure in six recipients with ESRD due to hypertensive
nephrosclerosis when transplanted with kidneys
from normotensive donors with a negative family
history of hypertension.
On the other hand elevation in blood pressure
and increased requirement for hypotensive therapy
occurred more frequently in 85 recipients from
normotensive families when they received grafts
from donors with hypertensive family history[40].
Moreover increased prevalence of post-transplant
hypertension was documented in recipients of cadaveric
allografts from donors with a family history of
essential hypertension[4] .
The prevalence of functionally significant anastomotic graft RAS is about 12%.
It appears to be less in recipients of cadaveric
grafts due to better donor kidney harvesting techniques.
It usually occurs within the first 6 months but
may occur up to 2 years post-transplant and manifests
itself by sudden onset of hypertension with or
without deterioration of renal function or with
worsening of pre-existing hypertension.
It may be associated with diuretic resistant edema.
Arteriography remains the gold standard for the
diagnosis, but a renal graft biopsy should be
performed before arteriography to exclude chronic
graft dysfunction as an underlying cause for the
hypertension.
Because of the invasive nature of arteriography,
non-invasive diagnostic modalities should be performed
first.
Ultrasonography is used as a primary screening
tool and appears to have high accuracy.
In a study comparing doppler ultrasonography (with
RAS defined as > 50% reduction in vessel diameter
giving a peak systolic velocity of ? 2.5 m/sec)
with digital subtraction angiography, it was found
to have a sensitivity and specificity of 100%
and 95% respectively[41] .
Magnetic Resonance Angiography (MRA) is being
increasingly used with a high degree of accuracy.
With the use of gadolinium-enhanced MRA and three-dimensional
phase contrast post-gadolinium, Johnson et al[42]
reported a sensitivity and specificity of 100%
in decting RAS in 9 transplant patients.
In addition, gadolinium is less nephrotoxic as
compared to conventional iodinated contrast media
[43].
This can lead to post-transplant hypertension.
Recurrence of the original disease occurs between
6 and 27%[44] of grafts depending on different
series and the type of glomerulonephritis.
Hypertension is less prevalent among transplant recipients who are anephric
and bilateral native nephrectomy even long after
transplantation can lead to normalization of blood
pressure.
Native kidneys continue to secrete renin.
Several reports have indicated that native nephrectomy
is followed by a consistent fall in blood pressure
and reduction in the vascular resistance of the
allograft.
In addition to the causes of hypertension directly related to transplantation,
renal graft recipients are also prone to the recognized
risk factors for hypertension such as family history,
obesity, alcohol consumption and high salt intake
in the salt sensitive[4].
The timing of the operation is important in relation to the degree of hypertension
control.
In the immediate post-transplant period a level
of 160 mmHg systolic and 90 mmHg diastolic is
aimed for to ensure adequate graft perfusion[45].
Following this period, post-transplant hypertension
should be treated aggressively to protect against
hypertensive graft damage and other target organ
disease.
With normal graft function and absent or mild
proteinuria (<1 gm/day), the target mean arterial
blood pressure accepted is 107 mmHg.
With proteinuria of >1gm/day tighter control is
required with the goal mean BP being 92 mmHg[46].
Treatment should also be directed towards any
possible underlying cause like graft dysfunction,
recurrence of underlying disease or de novo renal
disease.
A graft biopsy is indicated when such conditions
are suspected especially in the presence of abnormal
renal function or deterioration of function.
Non- pharmacological measures such as weight control,
exercise, and abstention from alcohol and smoking
should be addressed as required in individual
patients.
The dose of calcineurin inhibitors and corticosteroids, which contribute to
production of hypertension in post-transplant
patients, should be reduced to the lowest maintenance
level required for effective immunosuppression.
Some studies, though, have not proven a positive
calcineurin inhibitor dose correlation in the
production of hypertension[47].
Hypotensive drug therapy should take into consideration
the immunosuppressive treatment of the patient
and any possible interactions that may occur.
This class of hypotensive medications is preferred in the treatment of patients
with post-transplant hypertension because of its
preglomerular vasodilator effect[48] opposing
the calcineurins vasoconstrictive effect.
The dihydropyridine CCBs felodipine, isradipine,
lacidipine, amlodipine, nifedipine and nitrendipine
have no significant effect on CsA metabolism.
Verapamil and Diltiazem have a potentiating effect
on CsA trough level[49], a property occasionally
considered of cost benefit allowing lower CsA
dose[50] Whether this antagonistic vasodilative
effect of CCBs has long-term beneficial effect
is debatable.
A randomized controlled trial comparing diltiazem
with placebo in 35 patients found no effect of
diltiazem on the incidence of delayed graft function,
the frequency of rejection or long-term graft
survival[51].
A meta-analysis of published studies showed no
evidence for an improvement by CCBs in long-term
graft survival[52]. On the other hand, some trials
showed beneficial long-term effect[53].
The role of ACE inhibitors in the treatment of post-transplant hypertension
is not well defined, especially in patients on
calcineurin inhibitors. Beneficial effects were
reported but potential risks exist.
In one study Lisinopril was reported to be effective
in blood pressure control without harmful effect
on renal function in 2_ years of follow-up[54].
In another study, it was shown to reduce gross
proteinuria with no adverse effect on renal function[55].
Deterioration in renal function and acute renal
failure are potential hazards because of the efferent
vasodilator effect of ACE inhibitors in a vulnerable
single functioning transplant kidney due to the
preglomenular vasoconstriction induced by calcineurin
inhibitors[29,30]. Potential hazards also include
hyperkalemia due to the combined effects of CsA,
causing decreased urinary potassium excretion,
and ACE inhibitors, inhibiting angiotensin II
production and consequently aldosterone secretion.
Furthermore, ACE inhibitors can lower the haemotacrit
by 5 to 10%, an effect enhanced by CsA[56].
This class of drugs is similar to ACE inhibitors in effect.
In addition, the use of angiotensin II receptor
antagonists in animal experiments suggest deceleration
of interstitial fibrosis and myointimal proliferation,
which is observed with chronic allograft nephropathy.
This effect is possibly mediated by inhibition
of cytokines triggers due to blockade of the angiotensin
II receptor[57].
b-blocker can be used especially as add-on therapy to CCBs where they may blunt
the tachycardia induced by CCBs.
Centrally- or peripherally- acting vasodilators
can also be of benefit in patients whose hypertension
is not controlled with mono- or double therapy.
This new class of drugs has shown encouraging results in ameliorating the renal
vasoconstrictive effects of CsA.
In vitro evidence indicates that CsA increases
the release of Endothelin 1 (ET-1) and that
ET-1 is an important factor in the production
of CsA-induced renal vasocontriction[58].
Both ET type A or mixed type A/B receptor antagonists
were found to be capable of ameliorating or even
preventing acute CsA-induced renal vasoconstriction[59].
Human trials of some members of this class have
shown them to be as effective as ACE inhibitors
in the control of hypertension.
Accordingly they may prove a useful class in the
treatment of post-transplant hypertension
.
Available therapeutic options for the treatment of functional RAS are angioplasty and surgery.
Percutaneous transluminal angioplasty is the treatment of choice with a success rate of 80%[60].
However, postangioplasty stenosis develops in 20% of patients[61].
The use of angioplasty with stenting is proving useful but has only been used in small series[62].
Further use and evaluation of this relatively new technique is required.
Surgery should only be reserved for patients in whom angioplasty was not successful or unsuitable and their hypertension is difficult to control.
The fibrosis and scarring around the transplanted kidney makes surgical correction of RAS difficult and not without hazards.
The success rate ranges between 60 and 90% with recurrence rate of 10%, graft loss has been reported in up to 30% of cases[63].
In animal models antihypertensive treatment proved successful in ameliorating
chronic graft dysfunction.
All hypotensive therapeutic regimens were shown
to improve graft function, proteinuria, graft
survival and histopathologic changes[64].
Accordingly, the contribution of graft dysfunction
to production of hypertension can be decreased,
thus blunting the vicious circle.
In patients with resistant hypertension underlying contributing factors like RAS, chronic allograft dysfunction, recurrence of the original disease,
and de novo glomerulonephritis should be thoroughly looked for and treated, if found, as discussed above.
The contributory effect of immunosuppressive therapy should be considered.
In this respect, calcineurin inhibitors have already been discussed.
There is no specific treatment for steroid induced post-transplant hypertension.
Therapeutic manipulations have been tried like steroid withdrawal and alternate day therapy.
The benefit is controversial and has to be weighed against the risk of rejection.
The native kidneys may continue to produce renin dependent hypertension which may be difficult to control.
This diagnosis may be confirmed by captopril test.
If positive, bilateral nephrectomy has a high probability of being of benefit[65].
The technique of bilateral native kidney embolization can also be used to avoid surgery[66].
The prevalence of hypertension is high in renal transplant recipients due to multiple factors including the use of immunosuppressive agents, chronic graft dysfunction, graft renal artery stenosis, genetics and recurrence of the original disease in the graft.
These etiologic factors need to be thoroughly looked for especially when worsening of the hypertension or deterioration of the graft function occurs.
Treatment should be directed to the underlying cause if found.
The CCBs are the preferred antihypertensive drugs because they antagonize the renal vasoconstrictive effect of the calcineurin inhibitors.
The role of ACE inhibitors is controversial.
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