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327
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C. J.Wong andC. D.Blosser
329© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2025
C. J. Wong (ed.), Primary Care of the Solid Organ Transplant Recipient,
https://doi.org/10.1007/978-3-031-98076-3_11
Chapter 11
Metabolic Complications intheAdult Solid
Organ Transplant Recipient
AnnaL.Golob, JenniferWright, andKimO’Connor
11.1 Introduction
Solid organ transplantation is increasing in incidence, its recipients are beneting
from improved long-term survival, and the age of transplant survivors is increasing.
These factors lead to both an increase in the metabolic complications faced by solid
organ transplant recipients and the increased likelihood that these patients will be
cared for in the primary care setting. Primary care providers regularly manage meta-
bolic conditions such as hypertension and diabetes. For the solid organ transplant
recipient, addressing these conditions is often a price of success—with longevity
comes the need for chronic disease management to maintain health. Primary care
providers can and should play a vital role in the screening, prevention, diagnosis,
and treatment of metabolic complications in solid organ transplant recipients.
A. L. Golob (*)
Division of General Internal Medicine, University of Washington, VA Puget Sound
Healthcare System, Seattle, WA, USA
e-mail: zilanna@uw.edu
J. Wright
Division of General Internal Medicine, University of Washington, Seattle, WA, USA
e-mail: sonic@uw.edu
K. O’Connor
Division of General Internal Medicine, Department of Medicine, University of Washington,
Seattle, WA, USA
e-mail: koconnor@uw.edu
330
11.2 Cardiovascular Disease
11.2.1 Epidemiology
Cardiovascular disease (CVD), including atherosclerotic-related heart disease and
structural heart disease, is common after solid organ transplantation, despite
screening for heart disease prior to transplantation (see Chap. 2 for discussion of
pre-transplant testing). In patients who have undergone kidney transplantation,
CVD risk is higher than in the general population and is the most common cause
of death [1]. The rates of myocardial infarction at 12- and 36-months after kidney
transplantation is 5% and 11%—while this rate is lower than in patients with end-
stage renal disease awaiting transplant, it is still 10–30 times higher than in the
general population [2]. Long-term rates of CVD are also high in patients who have
received a liver transplant, with an average rate of 12% for cardiovascular events
that occur after 6months, although studies vary widely in cardiovascular outcomes
measured and duration of follow up [3]. With metabolic dysfunction-associated
steatotic liver disease (MASLD) becoming a leading cause of liver transplantation
(see Chap. 5), it is predicted that cardiovascular disease will become more com-
mon, as transplantation for MASLD is associated with higher rates of cardiovascu-
lar complications compared to other indications [4]. Heart transplant recipients are
not only at risk for conventional cardiovascular disease but also have the unique
risks of cardiac allograft vasculopathy (CAV) of the coronary vessels as well as
graft rejection. Cardiac allograft vasculopathy occurs in 30% of heart transplant
recipients by 5years, and in 50% at 10years [5] (see Chap. 6). Lung transplant
recipients frequently have metabolic risk factors [6
], but long- term survival is most
impacted by graft dysfunction, malignancy, and infectious complications, with car-
diovascular disease representing a comparatively smaller proportion of causes of
death [7].
11.2.2 Pathophysiology
Risk factors for cardiovascular disease in solid organ transplant recipients include
traditional risk factors, organ-related risk factors, and post-transplant factors includ-
ing medications and metabolic changes.
Traditional cardiac risk factors such as hypertension (HTN) and diabetes are
common, particularly in kidney transplant recipients and liver transplant recipients
who had end-stage liver disease due to MASLD.In almost all cases, solid organ
transplant recipients are required to quit smoking prior to transplantation, but
tobacco use can recur after transplantation.
Organ-specic risk factors are less commonly encountered and not necessarily
modiable. These include uremic cardiomyopathy, the term used to describe the
pathologic cardiac hypertrophy that can occur in patients with advanced kidney
A. L. Golob et al.
331
disease [8], and hepatopulmonary syndrome and cirrhotic cardiomyopathy in
advanced liver disease [4]. Heart transplant recipients have a unique set of factors
that contribute to an elevated CVD risk. In the short-term, transplant graft failure is
the most common cause of cardiovascular death in heart transplant recipients. In the
years following transplant, cardiac allograft vasculopathy (CAV), a unique form of
immunologically-mediated coronary artery disease, becomes increasingly common
and problematic, with an incidence of approximately 50% at 10years post- transplant
[5], contributing to >10% of annual deaths after the rst-year post-transplant [9]
(see Chap. 6).
Many of the immunosuppressive medications used after solid organ transplanta-
tion contribute to the development of CVD risk factors (see Table11.1, and Chap. 3).
Observational data not specic to solid organ transplant recipients has found an
increased risk of cardiovascular events in patients treated with high-dose corticoste-
roids, dened as ≥7.5mg of prednisolone or equivalent daily [11]. There are several
mechanisms by which this association likely occurs: Corticosteroids often cause
uid retention which can then cause hypertension; lead to glucose intolerance and
secondary diabetes; and are associated with weight gain which in turn may worsen
a patient’s lipid prole.
Calcineurin inhibitors (CNIs) similarly can lead to the development of several
established cardiovascular risk factors. Hypertension is a common side effect of
CNIs, which cause renal vasoconstriction and direct nephrotoxicity [10]. Post trans-
plant diabetes mellitus (PTDM) is also associated with CNI use (see section on
“Diabetes” below for details).
Sirolimus and everolimus, mammalian target of rapamycin (mTOR) inhibitors,
can lead to increased cholesterol levels. In kidney transplant recipients, sirolimus
has been associated with a higher risk of all-cause mortality despite the lower risk
of malignancy compared to other maintenance immunosuppression regimens;
patients receiving sirolimus had an increased risk of death due to infection and car-
diovascular causes [12]. However, increased mortality has not been demonstrated in
heart or lung transplant recipients [13, 14], suggesting that the potential cardiovas-
cular risk may be outweighed by other factors.
Table 11.1 Immunosuppressive medications and cardiovascular risk factors
Corticosteroids
Calcineurin
inhibitors:
tacrolimus
Calcineurin
inhibitors:
cyclosporine
mTOR Inhibitors:
sirolimus/
everolimus
HTN ++ + ++
Diabetes
(PTDM)
a
++ ++ + +
Dyslipidemia ++ + ++ +++
Renal
impairment
+ + Proteinuria
Weight gain ++
Adapted from Munagala MR, etal., 2016 [10], reprinted with permission.
a
PTDM post-transplant diabetes mellitius
11 Metabolic Complications intheAdult Solid Organ Transplant Recipient
332
11.2.3 Screening
Due to the increased risk of developing hypertension, diabetes and dyslipidemia
following solid organ transplantation, more intensive screening is performed than
what is generally recommended for the general population. See Table11.2 for the
screening recommendations recommended by the Kidney Disease: Improving
Global Outcomes (KDIGO) Transplant Work Group for CVD risk factors in kidney
transplant recipients [15]. These are evidence-based guidelines that may be applied
to other solid organ transplant recipients.
In addition to the above screening, heart transplant recipients are typically
screened aggressively for the development of CAV with coronary angiography,
often starting the rst-year post-transplant [9]. This approach is favored rather than
using symptoms to guide surveillance because the transplanted organs are dener-
vated, resulting in a lack of classic angina symptoms (see Chap. 6).
11.2.4 Prevention andTreatment
• Hypertension: Blood pressure management is overall similar to the approach in
the general population.
– Target blood pressure: In general, blood pressure should be maintained at
<130mm Hg systolic and<80mm Hg diastolic, although this goal should be
adjusted for a patient’s risk factors and tolerance to medications.
– Lifestyle: Dietary modication such as the DASH diet [16], exercise and
maintaining a normal body weight are all important.
– Medications: Studies are lacking to guide a single best approach to pharma-
cotherapy in solid organ transplant recipients.
Table 11.2 KDIGO Screening recommendations for CVD risk factors in kidney transplant
recipients [15]
Cardiovascular risk factor Interval Test/target
Diabetes (post-transplant
diabetes mellitus)
a
Weekly for rst
4weeks
Every 3months for
rst year
Annually thereafter
Fasting glucose, oral glucose tolerance
test, or hemoglobin A1c
a
Hypertension Measure blood pressure
at every visit
Maintain a blood pressure of
<130/<80mmHg
Dyslipidemia 2–3month after
transplant
Annually thereafter
Lipid panel
LDL goal <100mg/dL
a
See below re: use of hemoglobin A1c
A. L. Golob et al.
333
Calcium channel blockers: Because calcineurin inhibitors are a common
cause of blood pressure elevation, though to be at least partly mediated by
renal vasoconstriction, many providers preferentially use dihydropyridine
calcium channel blockers (CCBs) such as amlodipine as the rst-line agent
in treatment. A review of kidney transplant recipients found that CCBs
resulted in less graft loss compared to placebo and fewer side effects such
as hyperkalemia and anemia compared to angiotensin converting enzyme
inhibitor (ACEi) therapy [17] (see Chap. 4). Nondihydropyridine CCBs
should be avoided or discussed with the transplant team before using, as
they may increase the levels of both CNIs and mTOR inhibitors (see
Chap. 3).
Beta-blockers: While no longer rst-line therapy for hypertension in the gen-
eral population, beta-blockers are still often used in the solid organ trans-
plant population because of concerns for adverse effects of other
anti-hypertensive medications. As with non-transplant patients, they
should be used with caution in patients with reactive airways, hypoglyce-
mia unawareness, or baseline bradycardia. Beta-blockers should be used
with caution in heart transplant recipients who often have a high resting
heart rate and may be more sensitive to beta blocker therapy. Anti-
hypertensive therapy is generally managed by the cardiologist for heart
transplant recipients (see Chap. 6).
Angiotensin-converting enzyme-inhibitors (ACE-i) and angiotensin receptor
blockers (ARBs): These medications are often avoided early after trans-
plantation because of the risk of renal insufciency at the higher doses of
calcineurin inhibitors used early post-transplant, as well as the risk of
hyperkalemia with the concomitant use of trimethoprim-sulfamethoxazole
for pneumocystis jirovecii pneumonia prophylaxis. There is limited data to
support the long-term benets of ACE-i therapy in kidney transplant recip-
ients, with a small randomized controlled trial nding long-term cardio-
vascular benet in patients treated with ACE-i compared to placebo, in
addition to other anti-hypertensive medications if needed [18], although
conrmatory studies are lacking. As with non-transplant patients, ACE-Is
and ARBs should be considered in patients with proteinuria. Although
ACE inhibitors and ARBs can often be well tolerated 3–6 months after
transplantation in a stable patient, because of the risk of worsening renal
function it is still advisable to discuss with the transplant team before start-
ing ACE-i or ARB therapy. They should be avoided in kidney transplant
recipients who have known renal artery stenosis.
Diuretics: Although thiazide diuretics are rst-line anti-hypertensive therapy
for the general population, they should be used with caution in solid organ
transplant recipients. Thiazide diuretics can worsen the already-increased
risk of hyperuricemia, dyslipidemia, and hyperglycemia in solid organ
transplant recipients. Acute kidney injury can occur if the patient is at risk
11 Metabolic Complications intheAdult Solid Organ Transplant Recipient
334
for volume depletion. There may be an increased risk of non-melanoma
skin cancer [19] although studies are not conclusive; solid organ transplant
recipients are already at increased risk of these malignancies (see Chap.
10). As with ACE-i and ARB use, it is best to discuss with the transplant
team prior to initiating treatment with thiazide diuretics.
• Dyslipidemia: Management of dyslipidemia is the same as in the general popula-
tion with the exceptions that drug interactions are more common, and treatment
is routine for kidney and heart transplant recipients.
– Patients already on statin therapy prior to transplantation: In general, it is
recommended to reduce statin therapy by 50% prior to initiation of calcineu-
rin inhibitor therapy, unless the patient is already on pravastatin, rosuvastatin,
or uvastatin, which have fewer drug interactions. The other option is to
switch to pravastatin, rosuvastatin, or uvastatin prior to starting a calcineurin
inhibitor (see Chap. 3).
– Indications: All heart transplant recipients should receive statin therapy unless
contraindicated, as early use may decrease the incidence of CAV [20] (see
Chap. 6). Most kidney transplant recipients should be treated with statin ther-
apy (see Chap. 4). Liver and lung transplant recipients should be treated if
they meet other indications for statin therapy.
– Initiation: If lower-intensity therapy is indicated, then pravastatin is the pre-
ferred statin because of fewer drug interactions with calcineurin inhibitors. If
higher-intensity statin therapy is indicated, rosuvastatin is a suitable option,
again because of fewer drug interactions with calcineurin inhibitors.
Fluvastatin is an acceptable choice with regard to drug interactions but is low-
potency and less commonly used. While there is some data for supporting the
use of other statins in reducing CAV in heart transplant recipients, because of
drug interactions other statins are generally avoided. If statins other than
pravastatin or rosuvastatin are considered, it is best to discuss with the trans-
plant team rst.
• Aspirin: Aspirin use for primary prevention of cardiovascular disease in the gen-
eral population is no longer routinely recommended by the American College of
Cardiology/American Heart Association [21], but guidelines vary, and its use
may be considered on a case-by-case basis. Primary prevention studies generally
excluded immunosuppressed patients, however. In the solid organ transplant
population, aspirin is recommended for all heart transplant recipients. Currently
there is minimal data regarding aspirin for primary prevention in other solid
organ transplant recipients. In a post-hoc analysis of a trial of folate therapy in
kidney transplant recipients, aspirin use was not associated with reduction in
cardiovascular outcomes, all-cause mortality or change in kidney function [22].
However, whether this result can be generalized is uncertain, and aspirin is still
used variably in the kidney transplant population [23]. For liver and lung trans-
plant recipients, the use of aspirin for primary prevention should be individual-
A. L. Golob et al.
335
ized. In patients who have known cardiovascular disease, aspirin should be
prescribed for secondary prevention, similar to non-transplant patients, as long
as there are no contraindications. Note that some solid organ transplant recipi-
ents may be receiving aspirin therapy for vascular complications or risks (e.g.,
liver transplant recipients with a history of hepatic artery thrombosis, pediatric
en-bloc kidney transplants)—if uncertain as to the indication, it is recommended
to consult with the transplant team and not assume it is for primary prevention of
cardiovascular disease.
Modication of the immunosuppressive medication regimen by the transplant
team may be considered for management of hypertension, dyslipidemia and diabe-
tes, especially if these metabolic conditions are severe or life-threatening. However,
any reduction in dosing must be balanced against the risk for allograft rejection.
Corticosteroid doses are routinely lowered as much as possible post- transplant.
Switching a patient from tacrolimus to another agent is less commonly done despite
the increased risk of diabetes and hypertension, because tacrolimus has better pres-
ervation of graft function [24].
11.3 Diabetes Mellitus
11.3.1 Epidemiology
Diabetes is common among solid organ transplant recipients and contributes to the
increasing prevalence of cardiovascular disease (CVD) in this population. It encom-
passes pre-transplant diabetes mellitus (present prior to transplantation) and post-
transplant diabetes mellitus (PTDM, occurring after transplantation) [25].
The reported prevalence of PTDM 1 year and 5years after transplantation has
ranged from 9% to 40%, with variation based on type of organ transplant and crite-
ria used to dene diabetes [26, 27].
Consensus guidelines outline several possible natural histories of hyperglycemia
and diabetes in transplant recipients (Fig.11.1):
• Pre-transplant diabetes: These patients have diabetes prior to transplantation and
typically continue to have diabetes post-transplant.
• Transient hyperglycemia in the immediate postoperative period: Transient post-
transplant hyperglycemia caused by surgical stress and high-dose glucocorti-
coids in the rst few weeks (generally dened as 6weeks) after transplant surgery
is common and does not always lead to post-transplant diabetes mellitus.
• Early post-transplant diabetes mellitus: Diabetes diagnosed at 3months post-
transplant may be classied as “early” PTDM.In some patients, it may reverse,
while in others, it may persist as late PTDM.
• Late post-transplant diabetes mellitus: Dened as diabetes that is diagnosed at
1year and afterward. This category may include early PTDM that persists.
11 Metabolic Complications intheAdult Solid Organ Transplant Recipient
336
Fig. 11.1 2022 Consensus guidelines for assessment of post-transplant diabetes mellitus (PTDM).
NGT=normal glucose tolerance; IGT=impaired glucose tolerance; IFG=impaired fasting glucose;
OGTT=oral glucose tolerance test; 2hPG=2h plasma glucose; HbA1c=hemoglobin A1c; BMI=body
mass index. (Reprinted from Sharif etal., Nephrol Dial Transplant 2024 (Open Access) [25])
A. L. Golob et al.