Kaposi's sarcoma in recipients of renal transplants

Abstract

The purpose of this study was threefold; to ascertain if immunosuppression may be a factor in the causation of Kaposi's sarcoma, to find out if there is a correlation between abnormalities in in vitro studies of cellular immune function and the extent of the disease, and to analyze the literature on Kaposi's sarcoma arising in renal transplant recipients to determine a management policy for these patients. The charts of 44 patients with Kaposi's sarcoma seen in a 20 year period at The Princess Margaret Hospital were reviewed in a search for evidence of immunosuppression as a possible risk factor. Such evidence was found in seven patients. Four of these seven patients were renal transplant recipients, two had generalized lymphomas and were receiving chemotherapy whereas one had a glioblastoma multiforme and was receiving chemotherapy. Studies of cellular immunity using phytohemagglutinin, conconavalin A, pokeweed mitogen, the mixed leukocyte reaction and dinitrochlorobenzene skin testing, in eight patients with Kaposi's sarcoma, three of whom had previous renal transplants, indicate that a correlation exists between the degree of immunologic deficiency and the extent of the Kaposi's sarcoma. Our seven patients were all of Jewish or Mediterranean ancestry. The four cases of Kaposi's sarcoma arising in renal transplant recipients developed in a population of 100 renal transplant recipients of similar ethnic background (4 per cent). This incidence, when compared with our experience of 40 cases arising in 500,000 people of similar ancestry in the Toronto area, represents a 400 to 500 fold greater incidence in renal transplant recipients than in the control population. A literature review has yielded 12 additional cases of Kaposi's sarcoma developing in renal transplant recipients. On the basis of this review and our own experience we have proposed a management policy for these patients. It is proposed that the etiology of Kaposi's sarcoma is multifactorial and that a combination of immunosuppression and/or immunologic stimulation combined with a hereditary predisposition to the disease are responsible for the major increase in its incidence.