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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
CASE REPORT  
Year : 2017  |  Volume : 28  |  Issue : 4  |  Page : 942-944
Native kidney posttransplant lymphoproliferative disorder in a renal transplant recipient


1 Department of Nephrology, Dr. Ram Manohar Lohia Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
2 Department of Nephrology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
3 Department of Pathology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
4 Department of Anaesthesiology, Integral Institute of Medical Science and Research, Lucknow, Uttar Pradesh, India

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Date of Web Publication21-Jul-2017
 

   Abstract 


Compared with the general population, cancer risk in kidney transplant recipients is much higher. In the present study, we report a patient who was diagnosed with posttransplant lymphoproliferative disorder (PTLD) and had a fulminant course, dying within few days of diagnosis. This case report highlights the importance of timely detection and treatment of PTLD as it is associated with high mortality rate.

How to cite this article:
Chandra A, Kaul A, Aggarwal V, Srivastava D. Native kidney posttransplant lymphoproliferative disorder in a renal transplant recipient. Saudi J Kidney Dis Transpl 2017;28:942-4

How to cite this URL:
Chandra A, Kaul A, Aggarwal V, Srivastava D. Native kidney posttransplant lymphoproliferative disorder in a renal transplant recipient. Saudi J Kidney Dis Transpl [serial online] 2017 [cited 2019 Sep 15];28:942-4. Available from: http://www.sjkdt.org/text.asp?2017/28/4/942/211359



   Introduction Top


Posttransplant lymphoproliferative disorders (PTLDs) are potentially life-threatening complications after solid organ transplantation. PTLD after renal transplantation mostly originates from recipient lymphoid cells. We present a novel case of PTLD in the native kidneys of a renal transplant recipient.


   Case Report Top


A 53-year-old male underwent a live related renal transplant at the age of 39 years with his sister being the donor. He remained on maintenance hemodialysis (HD) for one year before transplant. At the time of transplant, cyto-megalovirus recipient status was IgG positive, and donor status was also IgG positive. Epstein-Barr virus (EBV) IgG status of recipient was not known. Posttransplant baseline serum creatinine was 1.2 mg/dL. Initial immunosuppression consisted of azathioprine and prednisolone. Twenty-four months posttransplant, he developed an acute rise in serum creatinine from 1.2 to 2.2 mg/dL with worsening of hypertension. Renal biopsy revealed acute cellular rejection which was successfully treated with methylprednisolone and serum creatinine dropped to 1.2 mg/dL with the blood pressure controlled with nifedipine and atenolol. It was planned to start calcineurin inhibitor and mycophenolate mofetil (MMF). However, because of financial constraints, he was continued on double immunosuppression of azathioprine and prednisolone. During follow-up, his renal functions remained stable at around 1.2–1.3 mg/dL.

Thirteen years posttransplant, he presented with fever for the past four months with a weight loss of 3 kg over the last three months. On evaluation, his laboratory values revealed a drop in hemoglobin to 7.2 g/dL, serum creatinine of 1.2 mg/dL, and urine examination showed trace proteinuria with bland urinary sediments. His ultrasound, however, showed a hypoechoic space occupying lesion of 1.5 cm × 1.4 cm at lower pole of the right native kidney. Contrast-enhanced computed tomography of the abdomen confirmed the presence of a 2.2 cm × 2.0 cm peripherally enhancing space occupying lesion at the lower pole of the right native kidney with no evidence of lymphadenopathy. There was no overt evidence of a lymphoproliferative or plasma cell disorder on the bone marrow aspirate and biopsy. With the possibility of renal cell carcinoma, he underwent a right open radical nephrectomy. Postoperatively, his general condition deteriorated with steadily rising total leukocyte counts. Blood culture was negative. He was started on broad spectrum antibiotics and was kept on mechanical ventilation requiring an increasing dose of vasopressors.

He expired on postoperative day 2. Histologic findings of the kidney tissue showed a cellular tumor composed of sheets of atypical lymphoid cells with areas of necrosis. The atypical lymphoid cells showed oval to irregular moderately pleomorphic nuclei, coarse chromatin, prominent nucleoli, and scant cytoplasm [Figure 1]. On immunohistochemistry, these cells were CD45 and CD3 positive and CD20 negative. Immunohistochemistry for EBV was negative. A diagnosis of monomorphic T-cell PTLD was made.
Figure 1: Section from the renal biopsy shows atypical lymphoid cells with oval to irregular moderately pleomorphic nuclei, coarse chromatin, prominent nucleoli, and scant cytoplasm.

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   Discussion Top


A wide range of lymphoproliferative disorders is seen in solid organ transplant recipients ranging from infectious mononucleosis to malignant lymphoma. PTLD stands second to skin cancer in adults transplant recipients,[1],[2] with a mortality rate exceeding 50%.[3]

In the US and Europe, EBV is responsible for most of the PTLD cases which are of B cell lineage. In far East, T-cell lineage assumes greater percentage owing to higher prevalence of oncogenic human T-cell leukemia virus virus.

In immunosuppressed individuals, like organ transplant recipients, impaired cytotoxic T lymphocyte function allows EBV-infected B cell to transform into latent infected memory cell.[5]

In renal transplant recipients, the incidence of PTLD ranges from 1% to 2.3%.[6] Although PTLD may occur at any time posttransplant, the risk seems to be highest in the 1st year possibly due to the intensity of immunosuppression. In our case, it appeared about 13-year posttransplant.

Risk factors associated with PTLD are intensity and length of immunosuppression, weak immune system as in the elderly,[3] EBV seronegativity at the time of transplant, analgesic nephropathy,[7] previous history of renal cell carcinoma, and acquired renal cystic disease,[8] longer duration of HD before transplantation and male gender.[9] Our patient exhibited risk factors which includes older age and long period of immunosuppression although he was only on dual immunosuppression. Among these none seems to be significantly modifiable. The only possibility of saving him could have been an early detection and intervention. Some immunosuppressive agents may have direct oncogenic properties through damaged DNA and production of oncogenic cytokines. Depleting antibodies used for immunosuppressive induction increase the incidence of PTLD.[10] Data are inconclusive to compare difference in the incidence of PTLD in tacrolimus versus cyclosporine usage.[11] Mtor inhibitors carry a low risk of malignancy in renal transplant patients owing to their anti-proliferative property. Data are conflicting when PTLD risk is compared between MMF and azathioprine.[11] Clinical presentation varies from fever (50%), lymphadenopathy (35%), and weight loss.[12] In some, it may present as intestinal perforation or systemic dissemination. PTLD may involve nodal or extranodal sites. Given the fact that the kidney does not contain lymphoid tissue, hematogeneous spread of EBV immune complex could have been the mechanism of involvement in our patient.[13]

In view of the aggressive nature of malignant lesion in renal transplant recipients, screening in high risk population through ultrasound and CT scan can be useful.[14] For diagnosis, histological examination, EBV detection by immunostaining or in situ hybridization, establishment of clonality of cellular infiltrates with relevant phenotypic markers are required.

Conflict of interest: None declared.



 
   References Top

1.
Feng S, Buell JF, Chari RS, DiMaio JM, Hanto DW. Tumors and transplantation: The 2003 Third Annual ASTS State-of-the-Art Winter Symposium. Am J Transplant 2003;3:1481-7.  Back to cited text no. 1
[PUBMED]    
2.
Boubenider S, Hiesse C, Goupy C, Kriaa F, Marchand S, Charpentier B. Incidence and consequences of post-transplantation lymphoproliferative disorders. J Nephrol 1997;10:136-45.  Back to cited text no. 2
[PUBMED]    
3.
Opelz G, Döhler B. Lymphomas after solid organ transplantation: A collaborative transplant study report. Am J Transplant 2004;4:222-30.  Back to cited text no. 3
    
4.
Hoshida Y, Li T, Dong Z, et al. Lymphoproliferative disorders in renal transplant patients in Japan. Int J Cancer 2001;91:869-75.  Back to cited text no. 4
[PUBMED]    
5.
Burns DM, Crawford DH. Epstein-Barr virus-specific cytotoxic T-lymphocytes for adoptive immunotherapy of post-transplant lymphoproliferative disease. Blood Rev 2004;18:193-209.  Back to cited text no. 5
[PUBMED]    
6.
Taylor AL, Marcus R, Bradley JA. Post-transplant lymphoproliferative disorders (PTLD) after solid organ transplantation. Crit Rev Oncol Hematol 2005;56:155-67.  Back to cited text no. 6
[PUBMED]    
7.
Penn I. Primary kidney tumors before and after renal transplantation. Transplantation 1995;59: 480-5.  Back to cited text no. 7
[PUBMED]    
8.
Heinz-Peer G, Schoder M, Rand T, Mayer G, Mostbeck GH. Prevalence of acquired cystic kidney disease and tumors in native kidneys of renal transplant recipients: A prospective US study. Radiology 1995;195:667-71.  Back to cited text no. 8
[PUBMED]    
9.
Kasiske BL, Vazquez MA, Harmon WE, et al. Recommendations for the outpatient surveillance of renal transplant recipients. American Society of Transplantation. J Am Soc Nephrol 2000;11 Suppl 15:S1-86.  Back to cited text no. 9
[PUBMED]    
10.
Cherikh WS, Kauffman HM, McBride MA, Maghirang J, Swinnen LJ, Hanto DW. Association of the type of induction immunosuppression with posttransplant lymphoproliferative disorder, graft survival, and patient survival after primary kidney transplantation. Transplantation 2003;76:1289-93.  Back to cited text no. 10
[PUBMED]    
11.
Flechner SM. Cancer and renal transplantation. Adv Stud Med 2007;7:411-9.  Back to cited text no. 11
    
12.
Kahan BD, Ponticelli C, Montagnino G, Malignancy. In: Kahan BD, Ponticelli C, editors. Principles and Practice of Renal Transplantation. Martin Dunitz; 2000.  Back to cited text no. 12
    
13.
Araya CE, Mehta MB, González-Peralta RP, Hunger SP, Dharnidharka VR. Native kidney post-transplant lymphoproliferative disorder in a non-renal transplant patient. Pediatr Transplant 2009;13:495-8.  Back to cited text no. 13
    
14.
Wong G, Howard K, Webster AC, Chapman JR, Craig JC. Screening for renal cancer in recipients of kidney transplants. Nephrol Dial Transplant 2011;26:1729-39.  Back to cited text no. 14
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Correspondence Address:
Abhilash Chandra
Department of Nephrology, Dr. Ram Manohar Lohia Institute of Medical Sciences, Lucknow, Uttar Pradesh
India
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PMID: 28748904

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