Abstract: PO1886
Filgrastim-Induced Crescentic Glomerulonephritis
Session Information
- Cancer and Kidney Diseases: Nephrotoxins, RCC, and More
November 04, 2021 | Location: On-Demand, Virtual Only
Abstract Time: 10:00 AM - 12:00 PM
Category: Onco-Nephrology
- 1500 Onco-Nephrology
Authors
- Zheng, Danyi, The University of Texas Health Science Center at Houston John P and Katherine G McGovern Medical School, Houston, Texas, United States
- Glass, William F., The University of Texas Health Science Center at Houston John P and Katherine G McGovern Medical School, Houston, Texas, United States
- Abudayyeh, Ala, University of Texas MD Anderson Cancer Center, Housotn, Texas, United States
Introduction
Proliferative glomerulonephritis with monoclonal immunoglobulin deposits (PGNMID) is caused by deposition of monoclonal immunoglobulins in the glomeruli. It is one of renal disorders included in the spectrum of monoclonal gammopathy of renal significance (MGRS). IgG3 with kappa light chain is the most common type. Autologous stem cell transplantation (SCT) provides a durable remission and better renal outcomes. Granulocyte colony stimulating factor (GCSF) is a recombinant glycoprotein used for mobilization of bone marrow in SCT. GCSF has been implicated as a cause of crescentic transformation of an acute glomerulonephritis in one prior case with a monoclonal deposits in a kidney transplant patient. In this case, we report the clinical and pathologic findings of GCSF induced exacerbation and crescentic transformation of pre-existing PGNMID with successful treatment and SCT.
Case Description
A 48-year-old male with recent diagnosis of MGRS presenting as MPGN and monoclonal IgG Kappa with C3 deposits on biopsy and treated with Velcade, cyclophosphamide and dexamethasone with a plan for SCT. Patient was admitted after acute increase in creatinine from 2.87 m/dl to 6.6mg/dl with hematuria and proteinuria after receiving GCSF during stem cell mobilization. Timing of acute renal injury correlated with increase in WBC after GCSF injections with a peak of 69 K/ul. Repeat kidney biopsy was significant for crescentic membranoproliferative (62% crescents) glomerulonephritis with monoclonal IgG/Kappa deposits. Patient received 5 sessions of plasmapheresis, one dose of renally adjusted IV Cytoxan, and pulse steroids followed with a taper. After a month he undergone an Autologous SCT (creatinine at baseline1.6mg/dl). His kidney function continued to improve and after 16 months post SCT his creatinine is at 1.4mg/dl.
Discussion
GCSF enhances neutrophils activation in large counts and induces its endothelial activation. In the presence of pre-existing renal pathology, MGRS and MPGN with IgG kappa and C3 deposits in this case, the localized immunoglobin and complement deposits in the glomeruli can attract activated neutrophils leading to its infiltration and degranulation in the glomerular microenvironment, and resulting in rupture of glomeruli basement membrane and formation of crescent. Therefore, GCSF induced kidney injury should be suspected due to its potential risk for exacerbating pre-existing glomerulonephritis.