Correspondence

Renal Transplantation

N Engl J Med 1994; 331:1719-1720December 22, 1994

Article

To the Editor:

Suthanthiran and Strom (Aug. 11 issue)1 “discourage the use of organs from donors seropositive for the hepatitis C virus [HCV] for grafting in recipients who are seronegative for the virus.” In the setting of renal transplantation, in which effective alternative renal-replacement therapy is available, this guideline is not adequate to prevent HCV infection and thus exposes patients to unacceptable risks.

The authors' figure of 5 percent for the prevalence of chronic hepatitis due to HCV after kidney transplantation is optimistically low. Lau et al. found that among 100 patients undergoing kidney transplantation, 18 were seropositive for HCV RNA before transplantation and 28 were positive one year afterward.2 Host seropositivity for anti-HCV antibody provides no assurance that the patient receiving a kidney from an HCV-positive donor will have a lower risk of infection than a seronegative recipient, since the antibody is not protective and repeated exposure to the virus may result in repeated bouts of hepatitis.3 Patients who are already infected with HCV may be the least able to tolerate additional hepatic injury and should not be further exposed to the virus. Immunosuppression may enhance HCV replication,2 whose impact is not yet established.

Besides presenting a risk of chronic liver disease, HCV infection may increase the risk of infection and rejection after transplantation.4 Although in most series HCV infection does not alter short-term graft or recipient survival after kidney transplantation,2,4 among blacks it is a risk factor for graft loss.5 Especially since most patients do quite well with dialysis, kidneys from HCV-infected donors should not be used in transplantation.

Paul D. King, M.D.
University of Missouri-Columbia, Columbia, MO 65212

5 References

1
Suthanthiran M, Strom TB. Renal transplantation. N Engl J Med 1994;331:365-376
Full Text | Web of Science | Medline

2
Lau JY, Davis GL, Brunson ME, et al. Hepatitis C virus infection in kidney transplant recipients. Hepatology 1993;18:1027-1031
CrossRef | Web of Science | Medline

3
Farci P, Alter HJ, Govindarajan S, et al. Lack of protective immunity against reinfection with hepatitis C virus. Science 1992;258:135-140
CrossRef | Web of Science | Medline

4
Roth D, Zucker K, Cirocco R, et al. The impact of hepatitis C virus infection on renal allograft recipients. Kidney Int 1994;45:238-244
CrossRef | Web of Science | Medline

5
Fritsche C, Brandes JC, Delaney SR, et al. Hepatitis C is a poor prognostic indicator in black kidney transplant recipients. Transplantation 1993;55:1283-1287
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To the Editor:

Suthanthiran and Strom have provided an excellent overview of the immunobiologic and clinical aspects of renal transplantation. However, they do not mention avascular bone necrosis, a very important associated condition. We want to bring the attention of readers to this well-described complication, which may cripple a patient who has undergone successful renal transplantation.

The prevalence of avascular bone necrosis in renal-transplant recipients is between 3 percent and 37 percent.1,2 Post-transplantation osteonecrosis is directly related to steroid treatment.3 Of the patients who received renal transplants at Duke University Medical Center from 1965 through 1988, 90 percent (54 of 60) have had osteonecrosis of the femoral head, and bilateral disease has developed in 80 percent.2

Various types of surgery have been advocated for symptomatic patients with avascular bone necrosis of the femoral head, such as drilling of the femoral neck and head, free-fibular grafting, cup arthroplasty, hemiarthroplasty, and cemented and cementless total-hip arthroplasty. Cementless total-hip arthroplasty has been a reasonably successful therapeutic option for steroid-induced end-stage avascular bone necrosis in patients with renal transplants.2,4

Cobi Lidor, M.D., Ph.D.
Thomas P. Vail, M.D.
Duke University Medical Center, Durham, NC 27707

4 References

1
Churchill MA, Spencer JD. End-stage avascular necrosis of bone in renal transplant patients: the natural history. J Bone Joint Surg Br 1991;73:618-620
Web of Science | Medline

2
Murzic WJ, McCollum DE. Hip arthroplasty for osteonecrosis after renal transplantation. Clin Orthop 1994;299:212-219
Web of Science | Medline

3
Fabrega AJ, Lopez-Boado M, Gonzalez S. Problems in the long-term renal allograft recipient. Crit Care Clin 1990;6:979-1005
Web of Science | Medline

4
Alpert B, Waddell JP, Morton J, Bear RA. Cementless total hip arthroplasty in renal transplant patients. Clin Orthop 1992;284:164-169
Web of Science | Medline

Author/Editor Response

The authors reply:

To the Editor: Dr. King has called attention to an important, unresolved issue. In its broadest sense, it concerns the effect of exposing the recipient to viruses carried by the donor organ. It is clear that primary exposure to a virus at the time of transplantation, when high doses of immunosuppressant drugs are used, will result in a far more feeble antiviral response than will secondary exposure to a virus at this time.

The specific question relates to the use of organs from HCV-positive donors. Firm data to support or refute Dr. King's conviction that kidneys from HCV-positive hosts should not be used for transplantation are not available. In the absence of such data, he believes that HCV-positive organs should not be transplanted even into HCV-positive hosts. We disagree. Given the organ shortage and the superior clinical outcome with renal transplantation, as compared with dialysis, in most patients with end-stage renal disease, we believe that HCV-positive organs should be considered for transplantation into HCV-positive recipients. We also believe that the clarification of HCV status (i.e., active vs. latent infection), as well as studies of the clinical outcome in HCV-positive patients treated with dialysis or transplantation and of the role of therapy with interferon alfa, may provide the scientific underpinnings for rational strategies to treat HCV-positive patients.

We thank Drs. Lidor and Vail for emphasizing the occurrence of avascular bone necrosis. Fortunately, this condition is no longer frequently observed in our units. In a previous era, this often devastating complication was widely prevalent. Although the reason for the decline in incidence (noted in many units) is not fully understood, we assume that improvements in pretransplantation care -- such as the use of potent vitamin D preparations, calcium carbonate, and higher calcium concentrations in dialysate, as well as the use of lower doses of glucocorticoids after transplantation -- are responsible. Should efforts to develop steroid-free therapeutic regimens succeed, we would anticipate a further improvement.

Manikkam Suthanthiran, M.D.
New York Hospita–Cornell Medical Center, New York, NY 10021

Terry B. Strom, M.D.
Harvard Medical School, Boston, MA 02115

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