Allograft dysfunction post renal transplant

Allograft dysfunction post renal transplant

Pat Weiskittel

Patient Profile

K.H. is a 50-year-old white male with end stage renal disease (ESRD) presumed to be caused by diabetes mellitus. He did not have a native kidney biopsy. Significant past medical history included hypertension, hypothyroidism, and hepatitis C, and the liver biopsy indicated cirrhosis and mild inflammatory activity. He successfully completed a course of rebetron and ribavirin and was cleared for renal transplant.

K.H. received a one-haplotype matched kidney from his sister in January 2002. He had an uneventful postoperative course and maintained good renal function. His immunosuppression consisted of mycophenolate mofetil, steroids, and tacrolimus. In April 2002 he presented with an elevated serum creatinine without other clinical signs or symptoms, and an allograft biopsy was performed. The results were consistent with calcineurin inhibitor toxicity. The tacrolimus dose was decreased and a lower therapeutic blood level targeted.

In early August, K.H. again had a rise in creatinine. A renal biopsy diagnosis of acute rejection Banff 97 grade 1A was made, and he was treated with a short course of IV methylprednisilone and an increase in oral steroid dose. Three weeks following this change in therapy, his creatinine remained elevated and he was re-biopsied. The diagnosis was consistent with BK virus nephropathy. Immuno-suppressants were decreased with plans to repeat a biopsy in a few weeks to check for rejection and evaluate the status of the BK virus nephropathy. There was no evidence of BK virus infection on the repeat biopsy, but there was a Banff 97 Grade IB rejection. His tacrolimus dose was increased to treat the rejection. A repeat biopsy three weeks later revealed calcineurin inhibitor toxicity without evidence of rejection or BK virus infection.

Intended Patient Outcomes

1. The patient will maintain adequate renal function.

2. The patient will remain free from allograft dysfunction related to infection, rejection, and drug toxicity.

3. The patient will demonstrate an understanding of allograft dysfunction and participate in its management.


Renal transplant recipients receive close follow-up in the first year after transplant to evaluate renal function and identify the causative agent if renal dysfunction occurs. Patient education focuses on the importance of following the pharmacological regimen and early identification of complications. Education programs focus on the side effects of immunosuppressive agents and the signs and symptoms of infection and rejection. Patients are at the highest risk for posttransplant complications in the first year following the transplant. The differential diagnosis for renal dysfunction includes: hypovolemia, obstruction, vascular complications, rejection, nephrotoxicity, and polyomavirus nephropathy from BK virus infection. Physical assessment of volume status is used to rule out hypovolemia. Radiographic studies such as ultrasound and renal scan are used to rule out the presence of an obstructive process or a vascular complication. The gold standard for diagnosing rejection, nephrotoxicity, and polyomavirus nephropathy is a transplant biopsy.

The signs and symptoms of rejection can include fever, malaise, weight gain, elevated blood pressure, presence of edema, graft swelling and tenderness, decreased urine output, proteinuria, and elevated blood urea nitrogen (BUN) and serum creatinine. However, with the use of the calcineurin inhibitors the patient may not manifest any of the above symptomatology except for laboratory abnormalities. This was the case with K.H. The only clinical sign that he presented with on all occasions was an elevated serum creatinine, and the only definitive diagnostic tool was renal biopsy.

Therapeutic decisions were based on the renal biopsy findings. The presence of calcineurin inhibitor toxicity warranted decreasing the dose of tacrolimus. However, this placed the patient at an increased risk for an acute rejection episode. K.H.’s subsequent rejection episode treated with pulse steroids and an increase in his oral steroids placed him at increased risk for an infectious process. Assessments of cytomegalovirus and Epstein-Barr virus status and prophylaxis with antiviral agents such as ganciclovir, valganciclovir, or acyclovir are instituted routinely during rejection therapy. K.H., however, developed a different viral infection with BK virus, which leads to polyomavirus nephropathy. The only proven therapy for this condition at the present time is to decrease immuno-suppression, which allows clearance of the virus. Decreasing the immunosuppression placed K.H. at higher risk for a subsequent acute rejection episode. This did occur, and the decision to treat was based on past biopsy findings and therapy chosen in an attempt to minimize the potential for recurrence of polyomavirus nephropathy. Therefore, no steroids or antilymphocyte preparations were used. Increasing the tacrolimus dose was the safest treatment. However, doing this also increased the risk of further nephrotoxic damage to K.H.’s kidney. The treatment plan consisted of frequent monitoring of renal function and drug levels with appropriate dose adjustments.

Nursing management of K.H. involved assessment of his physical and emotional status, and review of the treatment plan. Interventions included providing emotional support, preparing him for renal biopsies, and monitoring the effects of the immunosuppressive therapy. In addition, monitoring liver function was important because of K.H.’s hepatitis C history and the potential adverse effects of the immunosuppressants on liver function. During rejection therapy with increased steroid doses, blood glucose control became a major problem. It was necessary to greatly increase his baseline insulin and sliding scale doses until he was on a stable dose of prednisone.

K.H. required several teaching sessions that focused on the causes of graft dysfunction, the duration of the causative factors, treatment options, the need for changes in insulin dosing, and the long-term implications of the causes and the treatments required. This was a complicated sequence of events and required lengthy discussions with K.H. and his wife. It was extremely important for them to be part of the discussions regarding diagnosis and potential treatment and to partner with the transplant team in deciding the most appropriate therapy.

K.H. currently has compromised, but stable, renal function and is free of infection and rejection. His liver function is stable and his hepatitis C antibody PCR remains negative. He is on a stable dose of insulin and maintains good control.


This case illustrates the dilemmas encountered when diagnosing and treating renal allograft dysfunction. Two of the three intended patient outcomes have been achieved. The second outcome is partially achieved in that the patient has stable renal function but still has some allograft dysfunction related to chronic calcineurin inhibitor toxicity. The most important nursing interventions in this case were emotional support, patient education, and involvement of the patient and wife in the therapeutic decisions. Although clinical assessment is very important in the care of posttransplant recipients, the most definitive tool for diagnosing allograft dysfunction is renal biopsy.

The Case Study department of the Nephrology Nursing Journal invites nephrology nurses of all levels and subspecialties to share their clinical experience with their colleagues. Practitioners and educators are encouraged to submit case studies that address their patient-related nursing care and solutions to situations encountered in the care of a patient with renal disease and/or in performing extracorporeal therapies. You may log onto this column at (click on Department link) and email your comments to the Department Editor (see Discussion Area). The opinions and assertions contained herein are the private views of the contributors and do not necessarily reflect the views of the American Nephrology Nurses’ Association.

Additional Readings

Leichtman, A. (1998). Pathogenesis and pathology of early kidney allograft dysfunction. In D. Norman & W. Suki (Eds.), Primer on transplantation (pp. 217-222). Thorofare, NJ: American Society of Transplant Physicians.

Mudge, C., Carlson, L., & Brennan, P. (1998). Transplantation. In J. Parker (Ed.), Contemporary nephrology nursing (pp. 725-748). Pitman, NJ: American Nephrology Nurses’ Association.

Weiskittel, P. (2002). Polyoma virus in renal transplant recipients. Nephrology Nursing Journal, 20(3), 247-249.

Pat Weiskittel, MSN, RN, CNN, CS, is a Clinical Nurse Specialist in the Renal Transplant Department at University Hospital Cincinnati, OH. She is a Past President of ANNA and a member of ANNA’s Tri-State chapter.

COPYRIGHT 2003 Jannetti Publications, Inc.

COPYRIGHT 2007 Gale Group