The 5 Minute Urology Consult 3rd Ed.

TRANSPLANT REJECTION, RENAL

Eric Langewisch, MD

Jason C. Hedges, MD, PhD

BASICS

DESCRIPTION

• The hallmark of renal transplant rejection is immunologic damage to the transplanted kidney due to donor-specific response by recipient immune system

• Classification of rejection:

– Hyperacute (immediately after revascularization of the kidney graft)

Kidney becomes mottled and cyanotic usually in the OR

– Accelerated (days to weeks after transplantation)

– Acute (weeks to months after transplantation)

– Chronic (months to years after transplantation)

EPIDEMIOLOGY

Incidence

15% rejection rate in 1st yr for those rejection-free at hospital discharge after transplantation

Prevalence

N/A

RISK FACTORS

• Presence of preformed human leukocyte antigen (HLA) antibodies

• Positive crossmatch between donor and recipient

• Previous transplant, pregnancy, blood transfusion

• Prior rejection episodes

• Delayed graft function

• African American race

• Noncompliance with immunosuppressant medications

Genetics

Greater degree of HLA mismatch between donor and recipient increases risk of rejection

PATHOPHYSIOLOGY (1)

• Hyperacute rejection: Mediated by preformed cytotoxic antibodies against kidney graft (develop after prior transfusion, transplantation, and child birth)

• Acute rejection: Most cases are acute cellular rejection (ACR) mediated by T-cell recognition of donor major histocompatibility (MHC) proteins that are presented by antigen-presenting cells (APCs) and T-cell activation. This results in mononuclear cell infiltration of interstitium, tubules (tubulitis), and endothelium (vasculitis)

• Acute antibody-mediated rejection (AMR) is mediated by circulating donor-specific antibodies (DSAs) to foreign donor HLA. Recipient antibodies bind to donor HLA, activate complement, and recruit inflammatory mediators.

• Chronic rejection: Fibrosis and atrophy from chronic allograft damage. Limited viable allograft with active inflammation.

ASSOCIATED CONDITIONS

Common causes of end-stage renal disease: Diabetes, hypertension, glomerulonephritis, cystic renal disease

GENERAL PREVENTION

• Avoid incompatible donors for kidney transplant recipient. Avoid transplants across a positive crossmatch or with preformed DSAs.

• Induction immunosuppression with lymphocyte-depleting agents, especially for high immunologic risk recipients

• Compliance with immunosuppressant medications

• Monitor renal function and maintain therapeutic immunosuppressant drug levels

• Minimize sensitizing events (eg, blood transfusions and pregnancies)

DIAGNOSIS

HISTORY

• Medication noncompliance or tapering off immunosuppression for a failed allograft

• Often asymptomatic with plasma creatinine elevation as sole abnormality.

• Severe rejection may result in decreased urine output and pain over kidney transplant.

• Fluid retention/weight gain

PHYSICAL EXAM

• May be normal

• Increased blood pressure

• Volume overload

• May have tenderness over kidney transplant

DIAGNOSTIC TESTS & INTERPRETATION

Lab

• Rising BUN/plasma creatinine

– Otherwise unexplained plasma creatinine rise >20% over baseline is suggestive of rejection.

• Urinalysis and urine culture

– Rule out pyelonephritis.

• Determine drug levels (tacrolimus or cyclosporine)

– 12-hr trough level (usually before morning dose)

– Suspect calcineurin inhibitor (CNI: Tacrolimus or cyclosporine) toxicity if abnormally high levels

– Target levels vary by patient and assay

• If antibody-mediated rejection (AMR) is suspected, test for donor-specific antibodies (DSAs)

Imaging

• Renal ultrasound

– Rule out obstructive uropathy or stone.

– Assess for diminished renal blood flow.

Color flow Doppler evaluates vascular status

– Detect graft swelling (with acute rejection; graft may be small with chronic rejection).

• Nuclear medicine renal scan:

– Rejection: Decreased renal blood flow/glomerular filtration rate

– Arterial or venous thrombosis: Decreased or absent perfusion. With complete obstruction, a reniform photopenic area can be seen

– Acute rejection/acute tubular necrosis: Marked parenchymal retention with normal or mildly reduced perfusion. Rejection will show progressive decrease in function over time.

Diagnostic Procedures/Surgery

• Needle biopsy of transplant kidney (confirmation of rejection)

– Usually under ultrasound guidance

– Automated biopsy gun device, needle sizes 14–18 gauge

– Adequate sample

≥2 cores of cortex, ≥7 glomeruli, and ≥2 arteries required

Pathologic Findings

• Acute cellular rejection

– Interstitial mononuclear cell infiltrate

– Tubulitis

– Vasculitis (in more severe cases)

• Acute antibody-mediated rejection

– Pathology variable

– Acute tubular necrosis (ATN)

– Glomerulitis

– Peritubular capillaritis

– Fibrin thrombi

– C4d staining (C4d is a complement split product that covalently binds to tissue indicating antibody-mediated complement activation)

• Chronic rejection

– Interstitial fibrosis

– Tubular atrophy

DIFFERENTIAL DIAGNOSIS

• Prerenal: volume depletion or hypotension

• CNI (calcineurin inhibitor) toxicity (tacrolimus or cyclosporine)

• Pyelonephritis

• ATN

• Technical complications

– Arterial or venous thrombus,

– Arterial stenosis

– Ureteral obstruction or urine leak (early posttransplant)

• Obstructive uropathy

• Recurrence of original renal disease

TREATMENT

GENERAL MEASURES

• Attempt to reverse rejection with medical therapy

• Graft removal may be necessary in severe rejection eg, hyperacute rejection.

MEDICATION

First Line

• Acute cellular rejection: High-dose glucocorticoids

– Methyl prednisolone IV or high-dose oral prednisone (eg, 5 mg/kg) for 3–5 days followed by taper to maintenance dosing

• Antibody-mediated rejection: Plasmapheresis and intravenous immune globulin (IVIG) ± rituximab in attempt to remove, neutralize, or prevent the production of DSAs, respectively

• Chronic rejection: No effective therapy.

• Hyperacute rejection: Remove transplanted kidney (2)[A]

– Can result in DIC if not removed promptly

Second Line

• Acute cellular rejection: Lymphocyte-depleting agents such as antithymocyte globulin (ATG) or alemtuzumab may be given for severe rejection or rejection refractory to high-dose glucocorticoid therapy (3)[A].

– Significant reactions possible with 1st doses including anaphylaxis, pulmonary edema, fever, hemodynamic instability

– Must be inpatient for initiation of therapy

– Pretreat with glucocorticoids, diphenhydramine, and acetaminophen

– Monitor CBC for therapy-related leukopenia or thrombocytopenia (may be severe)

– Consider prophylaxis against cytomegalovirus (CMV) (eg valganciclovir)

– Continue maintenance immunosuppression

SURGERY/OTHER PROCEDURES

• Allograft nephrectomy

– Remove a symptomatic, irreversibly rejected kidney transplant.

– Remove an asymptomatic, chronically rejected kidney to withdraw immunosuppression and prevent further development of anti-HLA antibodies

ADDITIONAL TREATMENT

Radiation Therapy

N/A

Additional Therapies

Severe rejection and graft failure may require acute dialysis

Complementary & Alternative Therapies

N/A

ONGOING CARE

PROGNOSIS

• Repeated episodes of acute rejection reduce allograft survival

• Relative risk of graft failure is 1.8 for patients who have had 1 episode of rejection compared to none (4)

COMPLICATIONS

• DIC can accompany hyperacute rejection

• Graft loss can result from untreated or unrecognized rejection episode

• Cyclosporin toxicity can resemble mild acute rejection.

• Need to resume dialysis

FOLLOW-UP

Patient Monitoring (5)

• Compliance with anti rejection critical

• Therapeutic drug levels: Including monitoring of CNI toxicity

• Plasma creatinine

• Monitor for recurrence of native kidney disease (ie, diabetes, hypertension, etc.)

• Protocol transplant biopsies (optional)

Patient Resources

National Kidney Foundation. http://www.kidney.org/atoz/content/kidneytransnewlease.cfm

REFERENCES

1. Sunthanthiran M. Acute rejection of renal allografts: Mechanistic insights and therapeutic options. Kidney Int. 1997;51:1289–1304.

2. Sunthanthiran M, Strom TB. Mechanisms and management of acute renal allograft rejection. Surg Clin North Am. 1998;78(1):77–94.

3. Solez K, Colvin RB, Racusen LC, et al. Banff 07 classification of renal allograft pathology: Updates and future directions. Am J Transplant. 2008;8(4):753–760.

4. Pallardó Mateu LM, Sancho Calabuig A, Capdevila Plaza L, et al. Acute rejection and late renal transplant failure: risk factors and prognosis. Nephrol Dial Transplant. 2004;19:iii38–iii42.

5. Kidney Disease: Improving Global Outcomes (KDIGO) Transplant Work Group. KDIGO clinical practice guideline for the care of kidney transplant recipients. Am J Transplant. 2009;9(suppl 3):S1–S155.

ADDITIONAL READING

• Brown ED, Chen MY, Wolfman NT, et al. Complications of renal transplantation: Evaluation with US and radionuclide imaging. Radiographics. 2000;20(3):607–622.

• Danovitch G. Handbook of Renal Transplantation. 5th ed. Lippincott Williams & Wilkins; 2009.

See Also (Topic, Algorithm, Media)

• Acute Kidney Injury, Adult (Renal Failure, Acute)

• Acute Kidney Injury, Pediatric (Renal Failure, Acute)

• Chronic Kidney Disease, Adult (Renal Failure, Chronic)

• Chronic Kidney Disease, Pediatric (Renal Failure, Chronic)

• Pyelonephritis, Adult

CODES

ICD9

996.81 Complications of transplanted kidney

ICD10

• T86.11 Kidney transplant rejection

• T86.12 Kidney transplant failure

CLINICAL/SURGICAL PEARLS

• Don’t confuse kidney transplant rejection with pyelonephritis.

• Cyclosporin toxicity can resemble mild acute rejection.



If you find an error or have any questions, please email us at admin@doctorlib.org. Thank you!