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Definition, diagnosis, and management of rejection in the second to sixth months posttransplant--an overview
Insights
Cyclosporine A (CsA) reduces graft loss but rejection remains a major issue. Differentiating rejection from CsA nephrotoxicity is key for effective kidney transplant management.
Area of Science:
- Nephrology
- Immunology
- Transplantation
Background:
- Cyclosporine A (CsA) immunosuppression has decreased graft loss in kidney transplantation.
- However, graft rejection episodes persist as the primary cause of graft loss in CsA-treated patients.
- CsA itself complicates the diagnosis of renal dysfunction post-transplant.
Purpose of the Study:
- To outline strategies for differentiating renal dysfunction causes post-transplant.
- To discuss management approaches for acute and steroid-resistant rejection episodes.
- To highlight the role of CsA in the differential diagnosis of renal dysfunction.
Main Methods:
- Clinical presentation assessment.
- Renal scan and sonography.
- Monitoring CsA levels.
- Percutaneous allograft biopsy.
- Therapeutic trials (e.g., dose adjustment).
Main Results:
- Rejection can typically be differentiated from CsA nephrotoxicity using a combination of clinical, imaging, and laboratory findings.
- Acute rejection often responds to increased steroid doses.
- Steroid-resistant rejection may respond to anti-lymphocyte globulin (ALG).
Conclusions:
- Accurate diagnosis of renal dysfunction post-transplant is crucial for appropriate management.
- Treatment strategies vary based on the cause of dysfunction and rejection type.
- Combination therapy (prednisone, azathioprine, CsA) can stabilize patients with recurrent renal dysfunction.
Abstract:
CsA immunosuppression has resulted in decreased graft loss from rejection. However, rejection episodes do occur and, in fact, rejection remains as the major cause of graft loss in the CsA-treated patient. CsA, itself, has added to the differential diagnosis of renal dysfunction following transplantation. In the majority of circumstances, rejection can be differentiated from CsA nephrotoxicity as well as other causes of renal dysfunction by a combination of clinical presentation, renal scan and sonography, CsA levels, and percutaneous allograft biopsy. In some circumstances, a therapeutic trial of lowering the CsA dose may be indicated before extensive laboratory study. Most acute rejection episodes will respond to increased steroid doses. In patients with low CsA levels, increasing the CsA dose may be advised. Steroid-resistant rejection frequently responds to ALG. Patients with repeated episodes of renal dysfunction may be stabilized by using the combination of prednisone, azathioprine, and CsA.