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Abstract: PO1494

Filgrastim-Induced ANCA-Associated Glomerulonephritis in the Presence of Membranous "Full House Nephropathy"

Session Information

Category: Glomerular Diseases

  • 1202 Glomerular Diseases: Immunology and Inflammation


  • Angel-Korman, Avital, Assuta Ashdod Hospital, Ashdod, South, Israel
  • Leiba, Adi, Assuta Ashdod Hospital, Ashdod, South, Israel

G-CSF is commonly used to stimulate progenitor cell collection for bone marrow transplantation .
We present a seemingly healthy altruistic bone marrow donor who developed glomerulonephritis secondary to G-CSF treatment .

Case Description

A 34-year old man presented after altruistic bone marrow donation. During G-CSF treatment he developed headache, epistaxis, painless macrohematuria and AKI (creatinine- 2.91mg/dL).
Seven years and one year prior to this event he had similar presentations of macrohematuria, AKI and proteinuria .
In between episodes he had persistent microhematuria .
At this admission, Myeloperoxidase antibodies (MPO) were found to be elevated to 97 IU/ml . all other serologies were unremarkable.
A kidney biopsy revealed glomeruli with cellular crescents (Figure 1). Capillary loop “spikes” were seen on silver staining (Figure 2).
On immunofluorescence, there was a “full house” granular pattern . PLA2R and IgG4 stains were negative.
Electron Microscopy revealed mainly subepithelial electron dense deposits.
His current creatinine, without immunosupression, is 1.19 mg/dL.


G-CSF induced ANCA associated glomerulonephritis developed on top of silent membranous “full house nephropathy ”.
Bone marrow donors should be asked about prior glomerulopathies and screened for proteinuria and hematuria before bone marrow donation is authorized.

A glomerulus showing a cellular crescent (PAS stain x100)

By silver stain, spikes are identified (Silver stain x400)