Introduction:
Aplastic anemia causes pancytopenia, which poses challenges for renal transplant. Aplastic anemia is often autoimmune in etiology. Optimum immunosuppression can help maintain normal renal allograft function, while avoiding side effects from the medications and also help maintain remission of aplastic anemia.
Methods:
A 42 year old woman presented to us for renal transplant. She had history of hypertension, hypothyroidism and chronic kidney disease since November 2018. She had small kidneys at the time of diagnosis of CKD, so no renal biopsy was done. She was on thrice weekly hemodialysis via left brachiocephalic AV fistula since January 2019. Routine investigations from April 2021 have shown leucopenia and thrombocytopenia. Complete blood counts at presentation – Hb 11.4, Total counts 2290, P61, L31, M3.8, E4, Platelets 139000.
Bone marrow aspiration showed normocellular bone marrow aspirate with mild megaloblastic erythroid maturation and just adequate megakaryocytes. Bone marrow biopsy showed mildly hypocellular marrow, grade 1 fibrosis, megakaryocytes unremarkable. She was diagnosed to have hypoplastic anemia. She as initiated on cyclosporine 100mg/day and eltrombopag 100mg/day. After 3 months of immunosuppression, she tested positive for cytomegalovirus DNA PCR, which resolved spontaneously after 1 month. She underwent renal transplant 4 months after the diagnosis of aplastic anemia with her son as voluntary renal donor (HLA haplomatch). Basiliximab induction was used and she was continued on cyclosporine, mycophenolate and prednisolone post transplant. Immediate post-transplant, she had good urine output and steady decline in creatinine until day 6 when it reached a nadir of 1.5mg/dl. Post op day 6 onwards, she had increase in creatinine and slight reduction of urine output. A graft renal biopsy showed features of antibody-mediated rejection (g1, ptc2, i1, t1, v1, c4d0) with class 2 DSA positive. She was treated with rituximab 500mg, 5 sessions of plasma exchange and 50gm of IvIg. Post treatment, serum creatinine reached 1.1 mg/dl. CNI was changed to tacrolimus. Eltrombopag was continued.
Results:
Presently, the patient continues to have normal allograft function with normal total counts and normal platelet counts and improving haemoglobin.
Conclusions:
In this patient, use of cyclosporine probably provide inadequate immunosuppression, hence precipitating ABMR. Tacrolimus also appears to be effective in maintaining remission of aplastic anemia.
I have no potential conflict of interest to disclose.
I did not use generative AI and AI-assisted technologies in the writing process.