Solid organ donor antigens are recognized by the recipient immune system, resulting in acute and chronic rejection. Immunosuppression minimizes the effects of rejection in order to prolong graft function.

A. Highly polymorphic human leukocyte antigens (HLAs) and peptide antigens derived from other cellular proteins are presented by antigen-presenting cells to the immune effector cells of the recipient.

B. Acute rejection: unrestricted activation and proliferation of recipient immune cells. If not treated immediately, permanent graft dysfunction or loss occurs.

C. Chronic rejection: longer term irreversible graft fibrosis.

Rule out other causes of allograft dysfunction. Confirm with biopsy before specific therapy or as soon as possible after empiric therapy is begun.

A. Kidney: decreased urine output, elevated serum creatinine, proteinuria >200 mg/day.

Rule out:

1. Intravascular volume depletion (response to IV saline bolus).

2. Ureteral obstruction or urine leak (ultrasound).

3. Arterial or venous obstruction or thrombosis (Doppler ultrasound).

4. Drug nephrotoxicity.

5. Infection, including adenovirus, cytomegalovirus (CMV), polyomavirus nephropathy.

B. Liver: elevated serum transaminases (aspartate aminotransferase [AST], alanine aminotransferase [ALT]), gamma glutamyltransferase (GGT), alkaline phosphatase, bilirubin.

Rule out:

1. Hepatic artery thrombosis (particularly early postoperatively; Doppler ultrasound).

2. Biliary obstruction (ultrasound).

3. Drug hepatotoxicity.

4. Liver graft infection, most commonly viral, that is, CMV; hepatitis C virus (HCV) or hepatitis B virus (HBV) (primary infection or disease recurrence in the liver graft).

5. Functional cholestasis (e.g., due to sepsis, cholangitis).

6. Intravascular volume depletion.

C. Heart: decreased left ventricular ejection fraction (symptoms of congestive heart failure, echocardiogram), acute myocardial infarction (associated with chronic rejection).

Rule out:

1. Infection (CMV, toxoplasmosis).

2. Posttransplant lymphoproliferative disease (PTLD) (serum Epstein-Barr virus [EBV] PCR and biopsy).

D. Lung: cough, shortness of breath, decreased forced expiratory volume in 1 second (FEV₁) on pulmonary function testing.

Rule out:

1. Infection (pleural fluid analysis and culture, bronchoalveolar lavage, transbronchial biopsy).

2. Airway stenosis at bronchial anastomosis, airway granulation tissue (bronchoscopy).

3. Thromboembolism (ultrasound to rule out deep venous thrombosis, CT angiogram, D-dimer).

4. Recurrence of original disease.

E. Pancreas: elevated serum amylase; decreased urinary amylase excretion (with bladder-drained pancreas grafts). Hyperglycemia is a late manifestation.

Rule out:

1. Vascular thrombosis (Doppler ultrasound).

2. Leak from enteric anastomosis (duodenojejunostomy, enteric-drained grafts) or bladder anastomosis (duodenocystostomy, bladder-drained grafts); diagnosis by ultrasound, CT, or cystography (bladder-drained grafts).

3. Pancreatic duct obstruction magnetic resonance cholangiopancreatography (MRCP).

4. Recurrence of type 1 diabetes mellitus.

F. Intestine: increased stoma output, ileus, fever, abdominal distension and pain, decreased oral intake.

Rule out:

1. Bacterial or fungal sepsis (can also be precipitated by acute rejection).

A. Maintenance of immunosuppression.

1. Corticosteroids decrease antigen presentation and lymphocyte activation.

2. Calcineurin inhibitors (cyclosporine, tacrolimus) block cytokine interleukin (IL)-2 production to inhibit T-cell activation.

3. Antimetabolites (mycophenolate mofetil, azathioprine) inhibit T- and B-lymphocyte proliferation.

4. mTOR inhibitors (sirolimus, everolimus) inhibit initiation of T-cell proliferation.

5. Belatacept inhibits T-cell activation by blocking costimulatory molecule interactions.

6.

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