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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5258_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Contents
- •1.1 Why Primary Care?
- •2.2.10 Infections
- •2.1 Introduction
- •2.2 Pre-transplant Evaluation
- •2.2.1 Overview
- •2.2.3 Laboratory Testing
- •2.2.4 Cardiopulmonary Screening
- •2.2.6 Dental Evaluation
- •2.2.7 Family Planning
- •2.2.11 Cancer Screening
- •2.2.12 Surgical Evaluation
- •2.2.13 Psychosocial Evaluation
- •2.2.13.1 Financial Evaluation
- •2.2.13.2 Psychiatric Evaluation
- •2.2.13.3 Medication Adherence
- •2.2.13.4 Substance Use
- •2.5.1 Transplanted Organ
- •2.5.2 Time Course
- •2.5.3 Graft Function
- •2.5.4 Complications
- •2.5.5 Medications
- •2.5.6 Serologic Status
- •2.5.7 Metabolic Complications
- •2.5.8 Examination
- •2.8 Conclusion
- •References
- •3.1 Introduction
- •3.2 Typical Immunosuppressant Course
- •3.4 Monitoring
- •3.5 Drug-Related Complications
- •3.6 Drug Interactions [18, 19]
- •3.6.1 COVID-19 Drug-Related Concerns
- •3.9 Conclusion
- •References
- •4.1 Kidney Transplant Recipients
- •4.1.1 Introduction
- •4.1.2 Pre-transplant Course
- •4.1.2.2 Pre-Transplant Treatment
- •4.1.2.3 Waiting List
- •4.1.2.4 Allocation
- •4.1.3 Anatomy
- •4.1.4 Immunosuppression Regimen
- •Alternative Immunosuppressive Strategies
- •4.1.6 Graft Function Surveillance
- •4.1.6.2 Clinical Evaluation
- •4.1.6.4 Biopsies
- •4.1.7 Allograft Dysfunction
- •4.1.7.1 Surgical Complications
- •4.1.7.2 Acute Rejection
- •4.1.7.3 Chronic Allograft Nephropathy
- •4.1.8.1 BK Nephropathy
- •4.1.8.2 Urinary Tract Infection
- •4.1.8.3 Cardiovascular Disease
- •4.1.8.4 Hyperlipidemia
- •4.1.8.5 Hypertension
- •4.1.8.6 Diabetes
- •4.1.8.7 Weight Gain
- •4.1.8.8 Post-Transplant Malignancies
- •4.1.8.9 Chronic Kidney Disease-Metabolic Bone Disease (CKD-MBD)
- •4.1.8.10 Electrolyte Abnormalities
- •4.1.8.11 Hematologic Abnormalities
- •4.2 Pancreas Transplant Recipients
- •4.2.1 Introduction
- •4.2.4 Anatomy
- •4.2.5 Immunosuppression
- •4.2.6 Pancreas Transplant Follow-Up Care
- •4.3 Conclusion
- •References
- •5.1 Introduction
- •5.2 Liver Transplant Anatomy
- •5.3.1 Typical Immunosuppressive Course
- •5.3.2 Infections
- •5.3.3 Graft Dysfunction
- •5.3.4 Vascular Complications
- •5.3.5 Biliary Complications
- •5.3.6 Allograft Rejection
- •5.4.2 Typical Immunosuppressive Course
- •5.4.4 Chronic (Ductopenic) Rejection
- •5.4.6 Late Surgical Complications
- •5.5.1 Immunosuppression Management
- •5.5.2 Immunizations
- •5.5.3 Cancer Screening
- •5.6.2 Diabetes Mellitus
- •5.6.3 Systemic Hypertension
- •5.6.4 Dyslipidemia
- •5.6.5 Chronic Kidney Disease
- •5.6.6 Infectious Disease
- •5.6.7 Mental Health
- •5.6.8 Pain Management
- •5.8 Summary
- •References
- •6.1 Introduction
- •6.2 Pre-Transplant Course
- •6.2.1 Common Indications
- •6.4 Typical Anti-Rejection Course
- •6.4.1 Induction
- •6.4.2 Maintenance
- •6.4.3 Long-Term Dose Adjustments
- •6.5 Rejection
- •6.5.1 Pathophysiology
- •6.5.2 Clinical Presentation
- •6.5.3 Evaluation
- •6.6 Rejection Surveillance
- •6.6.1 Cellular Rejection
- •6.6.2 Antibody-Mediated Rejection
- •6.3 Anatomy
- •6.3.1 Anastomoses (Bicaval Method)
- •6.3.2 Denervation
- •6.3.2.1 Pericardium
- •6.6.3 Overall Rejection Surveillance Strategies
- •6.7 Graft Function Surveillance
- •6.8.1 Cardiac Allograft Vasculopathy (CAV)
- •6.8.2 De Novo Coronary Atherosclerosis
- •6.8.3 Arrhythmias
- •6.8.4 Valvular Disease
- •6.9.2 Cardiovascular Disease
- •6.9.3 Chronic Kidney Disease
- •6.9.4 Cancer
- •6.9.5 Hypertension
- •6.9.6 Diabetes
- •6.9.7 Infectious Endocarditis Prophylaxis
- •6.9.8 Pregnancy
- •6.9.10 Diet
- •6.10 Case Studies
- •6.10.2 Case Study
- •6.10.4 Case Study
- •6.10.6 Case Study
- •6.10.8 Case Study
- •6.10.10 Case Study
- •6.11 Conclusion
- •References
- •7.1 Introduction
- •7.2 Lung Transplant Anatomy
- •7.3.1 Induction
- •7.3.2 Maintenance
- •7.4.1 Monitoring/Spirometry
- •7.4.2 Monitoring/Surveillance Bronchoscopy
- •7.5 Post-Lung Transplant Pulmonary Complications
- •7.5.1 General Issues
- •7.5.2 Acute Rejection
- •7.5.3 Airway Complications
- •7.5.4 Infections
- •7.5.6 Chronic Lung Allograft Dysfunction (CLAD)
- •7.6.1 General Issues
- •7.6.3 Malignancy
- •7.7 Conclusions
- •References
- •8.1 Introduction
- •8.3 Respiratory Infections
- •8.3.1 Diagnostic Considerations
- •8.3.2 Respiratory Viral Illnesses
- •Clinical Presentation
- •Treatment
- •Prevention
- •Clinical Presentation
- •Diagnosis
- •Treatment
- •Prevention
- •8.3.2.3 Other Respiratory Viral Infections
- •Herpes Viruses
- •8.3.2.4 Bacterial Pneumonia
- •8.3.2.5 Mycobacterial Infections
- •8.3.2.6 Fungal Pneumonia
- •8.4 Gastrointestinal Infections
- •8.4.1 Diagnostic Considerations
- •8.4.2.1 Epidemiology
- •8.4.2.2 Diagnosis
- •8.4.3 Cytomegalovirus
- •8.4.3.1 Risk Factors
- •8.4.3.2 Diagnosis
- •8.4.3.3 Treatment
- •8.4.5 Parasites
- •8.4.6 Non-infectious Causes
- •8.4.7 Esophagitis
- •8.5 Urinary Tract Infections
- •8.5.2 Risk Factors
- •8.5.5 Diagnostic Considerations
- •8.5.6 Therapeutic Considerations
- •8.5.8 Sexually Transmitted Infections (STIs)
- •8.7.1 Diagnostic Considerations
- •8.7.3 Necrotizing Skin Infections
- •8.7.4 Infectious Vesicular Eruptions
- •8.7.6 Sexually Transmitted Infections
- •8.8 Prevention
- •8.9 Conclusion
- •References
- •9.1 Introduction
- •9.2 Respiratory Symptoms
- •9.2.1 General Approach: Cough
- •9.2.1.1 Assess Clinical Stability
- •9.2.1.2 History
- •9.2.1.3 Examination
- •9.2.2 General Approach: Dyspnea
- •9.2.2.1 Assess Clinical Stability
- •9.2.2.2 History
- •9.2.2.3 Examination
- •9.2.3 Key Points
- •9.3 Urinary Symptoms
- •9.3.1 General Approach: Urinary Symptoms
- •9.3.1.1 Assess Clinical Stability
- •9.3.1.2 History
- •9.3.1.3 Examination
- •9.3.1.4 Differential Diagnosis
- •9.3.2 Key Points
- •9.4 Gastrointestinal Symptoms: Diarrhea
- •9.4.1 General Approach
- •9.4.1.1 Assess Clinical Stability
- •9.4.1.2 History
- •9.4.1.3 Examination
- •9.4.2 Key Points
- •9.5.1 Malignancy
- •9.5.1.1 Nonmelanoma Skin Cancers (NMSC)
- •9.5.1.2 Melanoma
- •9.5.1.3 Kaposi Sarcoma
- •9.5.1.4 Merkel Cell Carcinoma (MCC)
- •9.5.2 Infection
- •9.5.3 Graft-Versus-Host Disease (GVHD)
- •9.5.4 Cosmesis
- •9.5.5 Key Points
- •9.6 Musculoskeletal Symptoms
- •9.6.1 Joint Pain: General Approach
- •9.6.1.1 Assess Clinical Stability
- •9.6.1.2 History
- •9.6.1.3 Physical Examination
- •9.6.1.4 Differential Diagnosis
- •9.6.1.5 Additional Testing
- •9.6.2 Other Musculoskeletal Symptoms
- •9.7 Constitutional Symptoms
- •9.8 Conclusion
- •References
- •10.1 Introduction
- •10.2 Epidemiology
- •10.2.1 Cancer Incidence
- •10.2.2 Cancer Mortality
- •10.2.3 Timing
- •10.3 Risk Factors
- •10.3.1 Age
- •10.3.2 Gender
- •10.3.3 Immunosuppression
- •10.3.3.1 Calcineurin Inhibitors (CNIs)
- •10.3.3.3 mTOR Inhibitors
- •10.3.3.4 Induction Immune Suppression
- •10.3.6 Oncogenic Infections
- •10.4.1 Donor Transmitted Cancer
- •10.4.2 Skin and Lip Cancer
- •10.4.3 PTLD (Post-transplant Lymphoproliferative Disorder)
- •10.4.3.1 Epidemiology
- •10.4.3.3 Risk Factors
- •10.4.3.4 Presentation
- •10.4.3.5 Treatment
- •10.4.3.6 Prognosis
- •10.4.3.7 Prevention
- •10.4.4 Lung Cancer
- •10.4.6 HPV-Associated Cancer
- •10.4.8 Thyroid Cancer
- •10.4.9 Hepatobiliary Cancer
- •10.4.10 Colorectal Cancer
- •10.4.11 Kaposi’s Sarcoma
- •10.5.1 Non-HPV Associated Gynecologic Cancers
- •10.5.2 Breast Cancer
- •10.5.3 Prostate Cancer
- •10.9 Conclusion
- •References
- •11.1 Introduction
- •11.2 Cardiovascular Disease
- •11.2.1 Epidemiology
- •11.2.2 Pathophysiology
- •11.2.3 Screening
- •11.3 Diabetes Mellitus
- •11.3.1 Epidemiology
- •11.3.2 Pathophysiology
- •11.3.3 Screening
- •11.4 Chronic Kidney Disease
- •11.4.1 Epidemiology
- •11.4.2 Pathophysiology
- •11.4.3 Screening
- •11.5.1 Epidemiology
- •11.5.2 Pathophysiology
- •11.6 Gout
- •11.6.1 Epidemiology
- •11.6.2 Pathophysiology
- •11.6.3 Screening/Surveillance
- •11.6.5 Treatment
- •11.6.6 Prevention
- •11.7 Osteoporosis
- •11.7.1 Epidemiology
- •11.7.2 Pathophysiology
- •11.7.3 Screening
- •11.7.4 Prevention
- •11.7.5 Treatment
- •11.8 Conclusion
- •References
- •12.1 Pre-transplant Mental Health
- •12.1.4 Pre-transplant Pharmacology Considerations
- •12.3 Mental Health Disorders Post-transplant: Management
- •12.3.1.1 Before Transplant
- •12.3.1.2 Early Post-transplant
- •12.3.1.3 Many Years Post-transplant
- •12.11 Conclusion
- •References
- •13.1 Introduction
- •13.2 Pre-conception Counseling
- •13.2.1 Pregnancy Timing
- •13.2.3 Medication Management
- •13.2.4 Cytomegalovirus (CMV) Infection Prevention
- •13.3 Contraception
- •13.5 Pregnancy
- •13.6 Menopause
- •13.7 Osteoporosis
- •13.8 Gynecologic Cancers
- •13.9 Conclusion
- •References
- •14.1.1 Skin Cancer Screening
- •14.1.2 Cervical Cancer Screening
- •14.1.3 Anal Cancer Screening
- •14.1.5 Colorectal Cancer Screening
- •14.3 Metabolic Bone Disease
- •14.3.1 All Solid Organ Transplant Recipients—History
- •14.5 Safe Living Practices
- •14.5.1.1 Immunizations
- •14.5.1.2 Travel Precautions
- •14.6.1 Behavioral Health
- •14.6.2 Substance Use
- •14.7 Conclusion
- •References
- •15.1 Introduction
- •15.2 The Continuity Care Provider
- •15.3 Vaccination
- •15.3.1 Post-Transplant Vaccination
- •15.4.1 Cytomegalovirus (CMV)
- •15.4.2 Epstein Barr Virus (EBV)
- •15.4.3 Polyomaviruses
- •15.6 Development
- •15.9 Conclusion
- •References
- •16.3 Advance Care Planning
- •16.3.1 Advance Directives
- •16.4.1 Pain
- •16.4.2 Dyspnea, Cough
- •16.4.4 Edema
- •16.6 Transplant Failure
- •16.7 Conclusion
- •References
- •17.1 Introduction
- •17.1.1 Epidemiology
- •17.1.2 Terminology
- •17.3.1 Estrogen
- •17.3.1.2 Drug Interactions
- •17.3.1.4 Timing
- •17.3.3 Progestins
- •17.3.3.2 Drug Interactions
- •17.3.4 Gonadotropin-Releasing Hormone (GnRH) Agonists
- •17.3.4.2 Drug Interactions
- •17.3.5 Testosterone
- •17.3.5.2 Drug Interactions
- •17.6 Mental Health
- •17.7 Conclusion
- •References
- •Index

96
A fourth group involves isolated pancreatic islet cell transplantation, a treatment
option for select patients. However, this procedure is less widely available, and its
details are beyond the scope of this discussion.
4.2.2 Benets ofPancreas Transplantation
The long-term benets of pancreas transplantation for insulin-dependent diabetes
mellitus remain a subject of debate. While it is widely accepted that pancreas trans-
plantation signicantly enhances quality of life, data regarding survival benets are
less denitive, partly due to ethical constraints that limit the feasibility of conduct-
ing randomized controlled trials comparing SPK transplants to kidney transplants
alone [130, 131]. However, evidence suggests that patient survival improves across
all pancreas transplant categories—SPK, PAK, and PTA—when compared to indi-
viduals who remain on the waitlist [132]. That said, the survival benet is most
consistently observed in SPK recipients, while studies on PAK and PTA have shown
mixed results regarding long-term survival outcomes [128, 129, 133].
There is some evidence that pancreas transplantation can reduce the severity of
end-organ complications associated with diabetes, including nephropathy, neuropa-
thy, and atherosclerotic cardiovascular disease, particularly in instances in which
the allograft is functioning properly and able to maintain euglycemia for more than
5years [134–136]. This risk-benet discussion will continue as medical treatments
for diabetes are continually advancing.
4.2.3 Eligibility Criteria andPre-transplant Considerations
forPancreas Transplantation
Simultaneous pancreas-kidney (SPK) and pancreas after kidney (PAK) transplants
are primarily indicated for patients with Type 1 diabetes and advanced kidney dis-
ease. In these cases, C-peptide levels are often measured to conrm the absence of
endogenous insulin production. However, select insulin-dependent patients with
Type 2 diabetes may also qualify if their body mass index (BMI) is below 30kg/m
2
and they require less than 1.5units of insulin per kilogram per day [137, 138].
In cases where kidney transplantation is not indicated, the American Diabetes
Association (ADA) suggests that pancreas transplant alone (PTA) should only be
considered for patients who meet the following criteria [139]:
• A history of frequent, severe, and acute metabolic complications (e.g., hypogly-
cemia, marked hyperglycemia, ketoacidosis) that necessitate medical
intervention.
• Severe clinical and emotional issues related to exogenous insulin therapy, to the
point of being incapacitating.
• Persistent failure of insulin-based management to prevent acute complications.
B. Boonpheng and I. C. De Castro

97
Pancreas transplantation is associated with an elevated risk of mortality, particu-
larly in the early post-transplant period, with cardiovascular events being the lead-
ing cause of death. Patients with peripheral vascular disease (PVD) tend to
experience notably poorer outcomes, with a threefold increased risk of death from
all causes and a six-fold increased risk of cardiovascular-related mortality within
10years, compared to those without PVD [140]. Additionally, vascular calcica-
tions in these patients can complicate the procedure by limiting the availability and
quality of suitable sites for vessel anastomosis, leading to increased surgical com-
plexity and a higher risk of graft dysfunction. As a result, individuals with signi-
cant cardiovascular disease or PVD are generally not considered suitable candidates
for pancreas transplantation.
4.2.4 Anatomy
Surgical technique for pancreas transplantation is the same, regardless of whether or
not the patient is receiving a dual organ transplantation. The pancreas is removed
from the donor complete with a small segment of duodenum (surgically closed at
each luminal end) and placed in the pelvis of the recipient. In the USA, it is common
to use systemic venous drainage with anastomosis to a branch of the iliac vein, as
opposed to portal venous drainage (Fig.4.5). In theory, portal venous drainage is
more physiologic and avoids the risks associated with systemic hyperinsulinemia,
however, it has been associated with a higher risk of thrombosis and thus more than
90% of pancreas transplants in the USA use systemic venous drainage [142].
Drainage of pancreatic exocrine secretions is accomplished either by attaching the
small duodenal segment to the bladder or to the small bowel in a side to side fash-
ion. Historically, bladder drainage was preferred as it has the advantage of allowing
for early detection of rejection via monitoring of urinary amylase levels, however
this technique has been associated with increased rates of multiple complications
including the development of metabolic acidosis, recurrent urinary tract infections,
pancreatic leaks and allograft pancreatitis [143]. Allograft survival rates appear to
be similar regardless of drainage type. However, given the reduction in associated
complications more than 80% of pancreas transplantations performed in the USA
are enteric drained [144].
4.2.5 Immunosuppression
Immunosuppression strategies for pancreas transplantation closely mirror those for
kidney transplantation. Nearly all transplant centers advocate induction immuno-
suppression for every pancreas transplantation, with the vast majority of pancreas
recipients (more than 85%) receiving T-cell depleting antibodies such as rATG
[128]. The remainder will typically receive IL-2 receptor antibodies such as
4 Primary Care of the Adult Kidney Transplant and Kidney-Pancreas Transplant…

98
Fig. 4.5 Pancreas transplant anatomy. From Dillman and Elsayes [141] reprinted with permission.
Surgical techniques vary. In this illustration, the arterial anastomosis is created by using a “Y graft”
(YG), using the donor’s iliac common, internal, and external artery, to connect the donor superior
mesenteric artery (dSMA) and the donor splenic artery (dSA) into a single vessel that connects
end-to-side to the recipient common iliac artery (rCIA). The donor superior mesenteric vein
(dSMV) and the donor splenic vein (dSV) join the donor portal vein (dPV) intact, and the donor
portal vein is anastomosed end-to-side to the recipient common iliac vein (rCIV) (venous anasto-
moses vary). The portion of the donor duodenum (dD) attached to the donor pancreas is anasto-
mosed directly to the recipient small bowel (rSB). Other variations, such as bladder drainage of the
exocrine pancreas, are not shown
basiliximab, although basiliximab has been associated with an increased rate of
acute rejection within the rst year when compared to rATG, so its use is generally
reserved for those patients with strong contraindications to rATG [145].
Most patients undergoing SPK or PAK will be maintained on a three-drug main-
tenance immunosuppression regimen including a calcineurin inhibitor, an anti-
metabolite (typically mycophenolate), and prednisone. As with kidney
transplantation, there is signicant variability between centers, particularly with
respect to the long-term use of glucocorticoids. Approximately three fourths of pan-
creas transplant recipients will remain on triple immunosuppression for the life of
the allograft [146]. Tacrolimus is the rst-line calcineurin inhibitor of choice due to
decreased rates of acute rejection and increased allograft survival at 1 year when
compared with cyclosporine [147]. The popularity of alternate agents such as
B. Boonpheng and I. C. De Castro

99
mTOR inhibitors has declined considerably in recent years, likely related to con-
cerns about side effects such as proteinuria, poor wound healing, and dyslipidemia
in patients with diabetes, such that fewer than 10% of pancreas recipients receive an
mTOR inhibitor within the rst year [128]. Belatacept represents a potentially valu-
able alternative for immunosuppression in pancreas transplants, particularly for
patients at risk of nephrotoxicity. However, the higher risk of acute rejection and
limited long-term data means that its use needs to be carefully weighed against
traditional therapies [148].
4.2.6 Pancreas Transplant Follow-Up Care
4.2.6.1 Monitoring andDetection ofPancreas Allograft Dysfunction
Freedom from insulin dependence is the hallmark of pancreas allograft survival.
However, the development of hyperglycemia may be a late sign of pancreas allograft
dysfunction. Given the often clinically silent nature of pancreatic dysfunction, rou-
tine laboratory monitoring is essential for surveillance. Patients are typically fol-
lowed once or twice weekly for the rst several months, then every 2–4 weeks
thereafter for the rst year. Most transplant programs perform serial monitoring of
lipase, amylase, and fasting serum glucose. HBA1c is checked every 3–6months.
Additionally, transplant centers often monitor donor-specic antibodies (DSAs), a
practice common in kidney transplant recipients.
When recipients with a history of type 1 diabetes develop hyperglycemia or
show other signs of allograft dysfunction, further testing for anti-insulin, anti-islet
cell, and anti-glutamic acid decarboxylase antibodies is commonly performed to
assess for recurrent autoimmune disease.
4.2.6.2 Clinical Presentation andDifferential Diagnosis ofPancreas
Allograft Dysfunction
Most instances of pancreas allograft dysfunction, including acute rejection, are
asymptomatic. Occasionally, patients may report tenderness at the allograft site or
experience nonspecic symptoms such as fever, malaise, or nausea. The most com-
mon laboratory abnormality is a new elevation in pancreatic enzyme levels, with or
without the onset of hyperglycemia. The differential diagnosis for elevated pancre-
atic enzymes should include acute rejection, vascular thrombosis or stenosis of the
allograft, and other intra-abdominal conditions such as ileus, enzyme leak, small
bowel obstruction, uid collection, native pancreatitis, chemical or alcohol-induced
pancreatitis, hyperlipidemia, and infection, including cytomegalovirus (CMV) pan-
creatitis or abscesses.
4 Primary Care of the Adult Kidney Transplant and Kidney-Pancreas Transplant…

100
4.2.6.3 Workup forSuspected Acute Rejection
When acute rejection is suspected based on laboratory ndings or patient history,
further evaluation is warranted. This typically begins with abdominal imaging,
including a Doppler ultrasound of the pancreas allograft and a contrast-enhanced
CT scan of the abdomen and pelvis. If imaging is inconclusive, a biopsy is indicated
[149]. In simultaneous pancreas-kidney (SPK) transplant recipients, a kidney biopsy
is often performed rst, as it is less technically challenging and carries fewer risks.
However, there is a reported discordance rate of up to 30% between kidney and
pancreas biopsy results [149]. Therefore, a pancreas biopsy is still necessary if the
kidney biopsy does not provide a suitable explanation for pancreatic dysfunction.
4.2.6.4 Acute Rejection inPancreas Transplant Recipients
Acute rejection is more common in pancreas transplant recipients compared to kid-
ney transplant recipients, with 15–20% experiencing an episode of acute rejection
within the rst year [150, 151]. There are no randomized controlled trials compar-
ing treatment strategies for acute rejection in pancreas transplantation; treatment
protocols are generally based on those used for kidney transplants. Acute cellular
rejection is typically treated with corticosteroids and antithymocyte globulin (ATG),
while acute antibody-mediated rejection is managed with plasmapheresis, intrave-
nous immunoglobulin (IVIG), and rituximab. Treatment outcomes are generally
better when dysfunction is detected early, and response to therapy correlates with
the extent of injury observed on biopsy.
4.3 Conclusion
The care of kidney and kidney-pancreas transplant recipients requires a comprehen-
sive understanding of their transplant history, familiarity with typical post- transplant
protocols, and awareness of the potential adverse effects of immunosuppressive
medications. Careful patient evaluations, combined with timely and effective com-
munication with the transplant team, are essential for optimal outcomes. Primary
care providers play a crucial role in collaborating with nephrologists to manage a
wide range of issues, including metabolic and cardiovascular complications, and
addressing new medical concerns as they arise. Ongoing collaboration between
transplant specialists and primary care providers is critical, as it fosters continuous
research and advances in clinical care, ultimately enhancing both the longevity and
quality of life of kidney transplant recipients.
Acknowledgement We would like to express our heartfelt gratitude to Dr. Cary Paine for his
contributions to this chapter in the previous edition. His insights and expertise laid a strong founda-
tion for this chapter.
B. Boonpheng and I. C. De Castro

101
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