Saudi Journal of Kidney Diseases and Transplantation

ORIGINAL ARTICLE
Year
: 2009  |  Volume : 20  |  Issue : 5  |  Page : 775--778

Kaposi's sarcoma after renal transplantation


Shahin Abbaszadeh, Saeed Taheri 
 Dr. Taheri Medical Research Group, Baqiyatallah University of Medical Sciences, Tehran, Iran

Correspondence Address:
Saeed Taheri
Dr. Taheri Medical Research Group; Baqiyatallah Research Center for Gastroenterology and Liver Disease Baqiyatallah Hospital, Mullasadra St, P.O. Box 14155-6437, Postal Code 1435915371 Tehran
Iran

Abstract

In this study, we aimed to evaluate the incidence, features and outcome of post trans­plant KS among Iranian recipients of living kidney allograft. We studied 2211 kidney allograft reci­pients who underwent living renal transplantation at our center between January 1984 and August 2007. All patients in our study received cyclosporine based immunosuppressive agents. The diagno­sis of KS was confirmed with pathological evaluations of tissue biopsy specimens. There were 10 of 2211 (0.45%) incident cases of KS kidney transplant population at our center during a mean follow up of 57 ± 38 months. Of the 10 KS patients, 8 were males and two were females with a median age of 52 years. The median time from transplantation to the development of KS was 8 months. Overall, two (20%) patients developed visceral involvement (one eye, one bladder), and eight patients mani­fested only KS restricted to the skin. Immunosuppression was reduced in 5 patients and thoroughly withdrawn in the remainder (including two cases of visceral involvement); KS did not abate in the patient with bladder involvement. All the KS patients remained alive after a mean of 35.6 ± 39.3 months of follow up; two patients lost their allograft and underwent dialysis (one after 3 months and one another after 4 months of KS diagnosis). The KS patients were significantly older at their transplantation time (P= 0.008; [Table 1]). Survival analysis using Kaplan Meier method and log-rank test revealed no difference in graft and patient survival between both groups. In conclusion, we found low incidence of KS in our living renal transplant recipients. The outcome of the KS patients was excellent with low morbidity and mortality. The incidence of KS was significantly associated with an older age at transplantation time for the allograft recipients. Further studies with larger pa­tient population are warranted to confirm our results.



How to cite this article:
Abbaszadeh S, Taheri S. Kaposi's sarcoma after renal transplantation.Saudi J Kidney Dis Transpl 2009;20:775-778


How to cite this URL:
Abbaszadeh S, Taheri S. Kaposi's sarcoma after renal transplantation. Saudi J Kidney Dis Transpl [serial online] 2009 [cited 2022 Nov 28 ];20:775-778
Available from: https://www.sjkdt.org/text.asp?2009/20/5/775/55360


Full Text

 Introduction



Kaposi's sarcoma (KS) is a soft tissue cancer that is related to several intrinsic and environ­mental factors. [1] In the general population, KS is an extremely rare tumor; however, the risk of its development is substantially increased in immunecompromised patients including patients with acquired immune deficiency syndrome (AIDS) and solid organ recipients. [1],[2] Genetic predisposition, [3],[4] seropositivity for human herpes virus type 8 (HHV-8), [5],[6] and increased HHV-8 prevalence in the general population [1],[7] are some proposed factors for the development of KS.

Middle East is reported as a highly prevalent region for the incidence of post transplant KS; [1] reports from Saudi Arabia, [8] Egypt [9] and Turkey [10] indicate a high incidence of this disease.

In this study, we aimed to evaluate the inci­dence, features and outcome of post transplant KS among Iranian recipients of living kidney allograft.

 Methods and Materials



We studied 2211 kidney allograft recipients who underwent living renal transplantation at our center between January 1984 and August 2007. Almost all the transplanted patients were under observation monthly at our outpatient cli­nic within the first year after transplantation and at least every 2-3 months thereafter.

We usually suspect KS when a kidney re­cipient presents with multiple hyperpigmented cutaneous nodules that may be associated with gastrointestinal discomfort and pulmonary symp­toms resistant to conventional therapies. Then a battery of endoscopic, broncoscopic, radiologic, and pathologic tests are used to diagnose KS.

All patients in our study received cyclosporine based immunosuppressive agents. There were two main distinct periods of immunosuppressive regimen: the first period was from 1984-2001 azathioprine (1.5 mg/kg), cyclosporine (6 mg/kg) and prednisolone (50 mg/d), and the second pe­riod was from 2001 onwards during which the patients received triple immunosuppressive the­rapy consisting of Cellcept (2 gr/day), cyclos­porine, and prednisolone at the same dosages mentioned above. Induction therapy using anti­thymocyte globulin (ATG) or antilymphocyte globulin (ALG) was preserved to the high risk patients in the early phase of transplantation or for treatment of acute rejection; OKT-3 was not used in any of the studied populations.

The doses of the immunosuppressive agents were reduced, or the agents were withdrawn upon diagnosis of KS. The method of reduction of immunosuppression and decision on which the agent to be reduced or withdrawn were de­pendent on the individual patient's health con­dition, response to treatment, and his/her phy­sician's judgment.

 Statistical Analysis



Software SPSS v.13.0 was used for data ana­lyses. Statistical differences between patients' groups were performed by using ÷2 and Fishers' exact tests for proportions and the non-parame­tric Mann-Whitney U test for continuous data. Survival analysis was performed using Kaplan­Meier method and log rank test. All statistical tests were considered significant at the level of P [1],[8].[9],[10]

The KS incidence peaks during the first year post transplantation. In our study, 70% of all KS cases were diagnosed in the first 2 years after receiving a renal allograft, which is compatible with previous studies. [11].[12],[13],[14] Several factors have been proposed as explanations for the higher incidence of KS in the early periods post trans­plantation such as a higher prevalence of HHV­8 seroprevalence among the general population. A South African study demonstrated that the prevalence of anti-HHV-8 antibodies in white individuals is substantially lower than that in non-white general population, [15] with a conside­rably higher incidence of KS in the non-white than the white patients. Unfortunately we have no data on the prevalence of HHV-8 infection among our transplant population or the general population, which calls for more studies in our population.

The potency of immunosuppression is a highly relevant factor in the development of KS after transplantation. [16] Patients receiving more intense immunosuppressive protocols are at a signifi­cantly high risk of developing post transplanta­tion KS. [16] Iranian renal transplant recipients re­veal serum levels of cyclosporine substantially lower than recommended (unpublished obser­vations), which may explain the low incidence of KS in our population.

In our study, we found that patients who de­veloped post transplant KS were significantly older at the time of transplantation. This finding contrasts previous reports about high incidence of KS among younger organ recipients. [17] More­over, most previous studies have reported a male preponderance in the incidence of post transplant KS. [18],[19],.[20] In our study, although males constituted 80% of the KS population, the gender compare­son with the non-KS patients showed no sig­nificant difference. This suggests that obser­vations indicating a male predominance in the development of post transplant KS might be re­lated to an overall high proportion of males in the transplant population.

Only 20% of our patients manifested a visceral involvement and just one of them did not expe­rience a complete remission. None of our pa­tients died, while two lost their allograft. How­ever, the graft and patients' survival were equi­valent in KS and non KS patients. This finding can corroborate arguments suggesting KS as a benign hyperplasia rather than a malignancy. [21]

The treatment strategy for our patients was to taper the immunosuppressive drugs. In five cases, we discontinued the immunosuppressive agents in order to achieve remission. One case with a bladder involvement did not respond to treat­ment, although he remained alive with a func­tioning graft for 18 months of follow-up.

The limitations of our study include its re­trospective nature and the use of registry data, which may be incomplete.

In conclusion, we found low incidence of KS in our living renal transplant recipients. The out­come of the KS patients was excellent with low morbidity and mortality. The incidence of KS was significantly associated with an older age at transplantation time for the allograft recipients. Further studies with larger patient population are warranted to confirm our results.

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