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

Journal: Journal Of Nephrology
Treatment Used: Bortezomib
Number of Patients: 1
Published:
MediFind Summary

Summary: This article reviewed the case of a patient with proliferative glomerulonephritis (disorder of the small blood vessels of the kidney) with monoclonal immunoglobulin IgG deposits (PGNMID) after kidney transplantation (surgical procedure to place a healthy kidney from a living or deceased donor into a person whose kidneys no longer function properly) treated with bortezomib.

Conclusion: Bortezomib therapy reduced massive proteinuria (presence of excess proteins in the urine), although monoclonal immune deposits on immunofluorescence and the serum creatinine level did not change during the treatment period. Seven months after completion of the first bortezomib course, it was 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 proliferative glomerulonephritis (disorder of the small blood vessels of the kidney) with monoclonal immunoglobulin IgG deposits after kidney transplantation (surgical procedure to place a healthy kidney from a living or deceased donor into a person whose kidneys no longer function properly).

Abstract

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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