Treatment with bortezomib for recurrent proliferative glomerulonephritis with monoclonal IgG deposits in kidney allograft. Case report and review of the literature

被引:0
作者
Rikako Oki
Kohei Unagami
Sekiko Taneda
Toshio Takagi
Hideki Ishida
机构
[1] Tokyo Women’s Medical University,Department of Urology
[2] Tokyo Women’s Medical University,Department of Nephrology
[3] Tokyo Women’s Medical University,Department of Organ Transplant Medicine
[4] Tokyo Women’s Medical University,Department of Surgical Pathology
来源
Journal of Nephrology | 2022年 / 35卷
关键词
Bortezomib; Kidney transplantation; Proliferative glomerulonephritis with monoclonal immunoglobulin; Recurrent glomerulonephritis;
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摘要
Proliferative glomerulonephritis with monoclonal immunoglobulin IgG deposits (PGNMID) is an already described form of renal involvement by monoclonal gammopathy. PGNMID is known to recur in kidney allografts. Bortezomib has shown clinical success in the treatment of multiple myeloma. However, its effect for recurrent PGNMID in kidney allografts has rarely been reported. We present the case of a 61-year-old woman who developed recurrent PGNMID 3 weeks after kidney transplantation. This patient was initially treated with steroid pulses (500 mg/day for 2 days) and two cycles of rituximab therapy (200 mg/body). However, disease progression was observed with mesangial matrix expansion and subendothelial deposits by light microscopy and stronger staining for IgG3 and kappa in the mesangial area by Immunofluorescence (IF) microscopy. Thus, we started treatment with bortezomib therapy (1.3 mg/m2, once weekly, on days 1, 8, 15, and 22 in a 5-week cycle, for a total of six cycles). Bortezomib therapy reduced massive proteinuria, although monoclonal immune deposits on IF and the serum creatinine level did not change during the treatment period. Seven months after completion of the first bortezomib course, we decided to prescribe a second course of bortezomib with the same regimen. Each course resulted in a > 50% reduction of proteinuria. Bortezomib may delay the progress of PGNMID in kidney allograft patients.
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页码:1289 / 1293
页数:4
相关论文
共 42 条
  • [1] Nasr SH(2009)Proliferative glomerulonephritis with monoclonal IgG deposits J Am Soc Nephrol 20 2055-2064
  • [2] Satoskar A(2011)Proliferative glomerulonephritis with monoclonal IgG deposits recurs in the allograft Clin J Am Soc Nephrol 6 122-132
  • [3] Markowitz GS(2018)Clinicopathological analysis of proliferative glomerulonephritis with monoclonal IgG deposits in 5 renal allografts BMC Nephrol 19 173-215
  • [4] Nasr SH(2021)Proliferative glomerulonephritis with monoclonal immunoglobulin deposits: a nephrologist perspective Nephrol Dial Transplant 36 208-888
  • [5] Sethi S(2014)IgG subclasses and allotypes: from structure to effector functions Front Immunol 5 520-666
  • [6] Cornell LD(2009)Bortezomib: a review of its use in patients with multiple myeloma Drugs 69 859-1074
  • [7] Wen J(2009)Proteasome inhibition for antibody-mediated rejection Curr Opin Organ Transplant 14 662-1561
  • [8] Wang W(2012)Proteasome inhibitor-based therapy for antibody-mediated rejection Kidney Int 81 1067-169
  • [9] Xu F(2009)Abrogation of anti-HLA antibodies via proteasome inhibition Transplantation 87 1555-4790
  • [10] Bridoux F(2017)Successful treatment with bortezomib and dexamethasone for proliferative glomerulonephritis with monoclonal IgG deposits in multiple myeloma: a case report BMC Nephrol 18 127-728