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Successful treatment of nephrotic syndrome caused by recurrent IgA nephropathy with chronic active antibody‐mediated rejection three years after kidney transplantation
Author(s) -
Yaginuma Tatsuhiro,
Yamamoto Hiroyasu,
Mitome Jun,
Kobayashi Akimitsu,
Yamamoto Izumi,
Tanno Yudo,
Hayakawa Hiroshi,
Miyazaki Youichi,
Yokoyama Keitaro,
Utsunomiya Yasunori,
Miki Jun,
Yamada Hiroki,
Furuta Nozomu,
Yamaguchi Yutaka,
Hosoya Tatsuo
Publication year - 2011
Publication title -
clinical transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 76
eISSN - 1399-0012
pISSN - 0902-0063
DOI - 10.1111/j.1399-0012.2011.01456.x
Subject(s) - medicine , mizoribine , transplantation , nephrotic syndrome , gastroenterology , kidney transplantation , nephropathy , chronic allograft nephropathy , rituximab , glomerulonephritis , renal function , kidney disease , kidney , urology , antibody , immunology , endocrinology , diabetes mellitus
Yaginuma T, Yamamoto H, Mitome J, Kobayashi A, Yamamoto I, Tanno Y, Hayakawa H, Miyazaki Y, Yokoyama K, Utsunomiya Y, Miki J, Yamada H, Furuta N, Yamaguchi Y, Hosoya T. Successful treatment of nephrotic syndrome caused by recurrent IgA nephropathy with chronic active antibody‐mediated rejection three years after kidney transplantation.
Clin Transplant 2011: 25 (Suppl. 23): 28–33.
© 2011 John Wiley & Sons A/S. Abstract: Here, we report the successful treatment of a 38‐yr‐old Japanese man diagnosed with recurrent immunoglobulin A nephropathy (IgAN) with chronic active antibody‐mediated rejection (CAAMR), three yr after undergoing living‐related donor kidney transplantation. Immediately after transplantation, the allograft function was well maintained with a serum creatinine (S‐Cr) level of <1.8 mg/dL. About three yr after transplantation, urine protein excretion had reached 4.59 g/d, and the S‐Cr level had increased to more than 2.0 mg/dL. Based on the allograft biopsy, we diagnosed nephrotic syndrome because of recurrence of IgAN with CAAMR. Subsequently, we performed a tonsillectomy, administered three sessions of steroid pulse therapy, and added losartan for the recurrence of IgAN. We also changed his immunosuppressant from mizoribine to mycophenolate mofetil to treat the CAAMR. The nephrotic syndrome improved with the multiple therapeutic approaches; however, the S‐Cr level did not decrease below 2.0 mg/dL. We possibly could have performed additional treatments such as rituximab and intravenous immunoglobulin for the CAAMR, but therapeutic strategies for CAAMR have not yet been established.