A Case of Late Mixed Acute Humoral and Cellular Rejection Successfully Treated with Rituximab, Plasmapheresis and IVIg.
10.4285/jkstn.2011.25.2.116
- Author:
Seong Min KIM
1
;
Joon Seok OH
;
Jee Min JUN
;
Yong Kee PARK
;
Yong Hun SIN
;
Joong Kyung KIM
;
Kill HUH
;
Yong Jin KIM
Author Information
1. Department of Internal Medicine, Bong Seng Memorial Hospital, Busan, Korea. syhpmj@hanmail.net
- Publication Type:Case Report
- Keywords:
Transplantation;
Graft rejection;
Rituximab;
Plasmapheresis
- MeSH:
Antibodies, Monoclonal, Murine-Derived;
Appointments and Schedules;
Biopsy;
Calcineurin;
Creatinine;
Cyclosporine;
Female;
Follow-Up Studies;
Graft Rejection;
Humans;
Immunoglobulins;
Immunoglobulins, Intravenous;
Kidney Transplantation;
Methylprednisolone;
Middle Aged;
Mycophenolic Acid;
Plasma Exchange;
Plasmapheresis;
Proteinuria;
Rejection (Psychology);
Renal Insufficiency, Chronic;
Retreatment;
Rituximab;
Steroids;
Tacrolimus;
Transplants;
Unrelated Donors
- From:The Journal of the Korean Society for Transplantation
2011;25(2):116-122
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Acute antibody-mediated rejection (AMR) developing simultaneously with acute cellular rejection has been rarely reported as a long-term complication of renal transplantation, and it can present on top of another chronic pathology affecting the graft. A 51-year-old female patient with chronic kidney disease of unknown etiology received renal transplantation 12 years ago from a living unrelated donor with 3 HLA mismatches. She received induction therapy with methylprednisolone and was maintained on steroids, mycophenolate mofetil and cyclosporine A (CsA). For a period of twelve years post-transplantation, she was clinically and biochemically stable. She presented with a rise in serum creatinine (SCr.) from 1.3 mg/dL to 2.4 mg/dL but did not have proteinuria. Graft biopsy revealed findings suggestive of acute cellular rejection on top of antibody-mediated rejection (type II) and chronic calcineurin inhibitor toxicity. Panel reactive antibody (PRA) test levels were 3.6%, 91.7% for class I and II respectively. The patient was treated with high-dose methylprednisolone for 3 days but serum creatinine was not fully normalised. After 2 weeks from initial methyl-PDS pulse therapy, she received intravenous immunoglobulin, plasma exchange and anti-CD20 (rituximab). Cyclosporine was changed to tacrolimus. She achieved a complete response, and SCr. was maintained at 1.3 mg/dL without proteinuria. Follow-up PRA test levels were 0%, 75% for class I and II. Current therapies have had considerable success in reversing mixed, acute humoral and cellular rejection since it is being identified quickly and treated aggressively. The best use of rituximab to treat AMR should be evaluated in controlled trials using dosing strategies that include longer courses or retreatment schedules.
