LETTER TO THE EDITOR
Year : 2013 | Volume
: 24 | Issue : 4 | Page : 793--794
Renal transplantation in idiopathic thrombocytopenic purpura
Kamal V Kanodia1, Aruna V Vanikar1, Pankaj R Shah2, HL Trivedi2,
1 Department of Pathology, Laboratory Medicine, Transfusion Services and Immunohematology, Dr H L Trivedi Institute Of Transplantation Sciences (ITS)-Smt Gulabben Rasiklal Doshi and Smt Kamlaben Mafatlal Mehta Institute off Kidney Diseases and Research Centre (IKDRC), Civil Hospital Campus, Asarwa, Ahmedabad - 380 016, Gujarat, India
2 Department of Nephrology and Clinical Transplantation, Dr H L Trivedi Institute Of Transplantation Sciences (ITS)-Smt Gulabben Rasiklal Doshi and Smt Kamlaben Mafatlal Mehta Institute off Kidney Diseases and Research Centre (IKDRC), Civil Hospital Campus, Asarwa, Ahmedabad - 380 016, Gujarat, India
Kamal V Kanodia
Department of Pathology, Laboratory Medicine, Transfusion Services and Immunohematology, Dr H L Trivedi Institute Of Transplantation Sciences (ITS)-Smt Gulabben Rasiklal Doshi and Smt Kamlaben Mafatlal Mehta Institute off Kidney Diseases and Research Centre (IKDRC), Civil Hospital Campus, Asarwa, Ahmedabad - 380 016, Gujarat
|How to cite this article:|
Kanodia KV, Vanikar AV, Shah PR, Trivedi H L. Renal transplantation in idiopathic thrombocytopenic purpura.Saudi J Kidney Dis Transpl 2013;24:793-794
|How to cite this URL:|
Kanodia KV, Vanikar AV, Shah PR, Trivedi H L. Renal transplantation in idiopathic thrombocytopenic purpura. Saudi J Kidney Dis Transpl [serial online] 2013 [cited 2021 Jan 23 ];24:793-794
Available from: https://www.sjkdt.org/text.asp?2013/24/4/793/113890
To the Editor ,
Chronic kidney disease (CKD) in idiopathic thrombocytopenic purpura (ITP) is uncommon. Poor platelet function secondary to uremic coagulopathy adds up to the risk of transplantation surgery. Kidney transplantation may be challenging in such patients for the platelet dysfunction due to the original disease. We report a case of kidney transplantation with ITP and the preparation for this event.
A 27-year-old woman with CKD was evaluated for kidney transplantation from her mother aged 56 years and HLA 3/6 match as potential donor. The patient underwent splenectomy three years earlier for ITP of 25 years duration resistant to steroids and IV immunoglobulins (IvIg). Her hypertension was controlled with calcium channel and beta blockers and hypothyroidism was controlled with thyroxine. On examination, she was pale with a pulse rate of 100/min and a blood pressure of 130/80 mmHg. Systemic examination was unremarkable except for splenectomy scar. Her hemoglobin was 7.4 g/dL, total leucocyte count was 13,200/cmm, platelet count (PC) was 35,000/cmm, urine albumin was 300 mg/24 h and microscopy was 10-12 red blood cells/ high-power field. Serum creatinine (SCr) was 6.25 mg/dL, serum proteins was 6.1 g/dL, albumin/globulin was 4.0/2.1 and electrolytes and thyroid-stimulating hormone were within normal range. Ultrasonography revealed right kidney 10.3 cm × 3.7 cm and left kidney 9.5 cm × 4.1 cm with bilateral increased echo genicity and altered cortico-medullary differentiation. Chest X-ray was unremarkable. She was subjected to one donor-specific leucocyte transfusion and two peripheral blood stem cell (PBSC) infusions for stimulation of donor-specific clones pre-transplantation. In PBSC, a total of 171 mL cells with CD34 count 0.06 and 7.26 × 10 8 /kg body weight of patient were infused to the patient. No deletion of donor-specific antibodies (DSA) was performed as she was splenectomized. She was transplanted under the cover of anti-B-cell antibody Rituximab 600 mg IV, IV immunoglobulin 10 g × 5 days and methylprednisolone 500 mg × 3 days tapered to 75 mg over 7 days, and it was switched to prednisolone 20 mg/day orally subsequently. The patient was maintained on cyclosporine (CyA) 3 mg/kg BW/day for ITP. Her platelet count was increased to 117,000/ cmm after PBSC infusion, and this was sustained for two weeks. No platelet infusion was administered during the peri-/post-transplant period. She was discharged on the 37 th post-transplant day with SCr 1.1 mg/dL and platelet count 97,000/cmm. She maintained adequate stable graft function with no rejection after 23 months post-transplant, with SCr 1.24 mg/dL and platelet count 40,000/cmm on prednisolone 5 mg/day and CyA 125 mg/day.
ITP is a clinical syndrome with thrombocytopenia manifesting as bleeding tendency, purpura and petechiae. In about 60% of the cases, IgG antibodies are detected against platelet membrane glycoprotein IIb-IIIa or Ib-IX. , Platelet coating with IgG renders them susceptible to opsonization and phagocytosis by splenic macrophages. Abnormal T-helper cells reacting with platelet antigens on the surface of antigen-presenting cells provide stimulus for autoantibody production.  Maintenance of hemodialysis in chronic ITP is not easy because of the difficulty in creating and maintaining arteriovenous fistula, extravasation and hematomas complicating vascular access. We believe that spleen is the major organ for effector humoral responses, and splenectomy in our patient unburdened the memory reservoir response, which rendered transplantation with minimum immunosuppression safe and effective.
ITP with CKD is an uncommon entity. Renal transplantation with minimum immunosuppression in ITP post-splenectomy is safe and effective.
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