Open AccessA case of early recurrent immunoglobulin A nephropathy and T-cell-mediated rejection in a transplant patient with Wiskott–Aldrich syndrome
Author(s) -
K Yamaguchi,
Mineaki Kitamura,
Yuki Kawaguchi,
Kengo Hayashi,
Kumiko Muta,
Minato Nakazawa,
Tsuyoshi Matsuda,
Toru Onita,
Masaharu Nishikido,
Hideki Sakai,
Hiroshi Mukae,
Tomoya Nishino
Publication year - 2021
Publication title -
cen case reports
Language(s) - English
Resource type - Journals
ISSN - 2192-4449
DOI - 10.1007/s13730-021-00631-9
Subject(s) - medicine , nephrology , transplantation , wiskott–aldrich syndrome , kidney transplantation , nephropathy , gastroenterology , immunology , renal function , kidney , kidney disease , endocrinology , biology , biochemistry , gene , diabetes mellitus
Wiskott-Aldrich syndrome (WAS) is an X-chromosome recessive immunodeficiency disease characterized by the triad of thrombocytopenia, eczema, and susceptibility to infection owing to WAS protein gene abnormalities. Kidney transplantation is rarely offered to WAS patients with end-stage renal disease because of concerns that thrombocytopenia and immune disorders may affect the clinical outcome. Here, we report the case of a 20-year-old kidney transplant patient who developed end-stage renal disease owing to immunoglobulin (Ig)A nephropathy caused by WAS. Despite recurrent IgA nephropathy and T-cell-mediated rejection 7 months after transplantation, two rounds of steroid pulse therapy attenuated his renal function and urinary abnormality. His serum creatinine level was maintained at approximately 1.5 mg/dL 1 year after transplantation. No other WAS-related complications were observed throughout the clinical course. Although WAS can cause poor prognosis in kidney transplant patients, careful follow-up may allow kidney transplantation to be performed.