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Abstract: PO1497

Granulocyte Colony Stimulating Factor-Associated Vasculitis: Adding Fuel to the Fire

Session Information

Category: Glomerular Diseases

  • 1202 Glomerular Diseases: Immunology and Inflammation


  • Patel, Nilam, Rush University Medical Center, Chicago, Illinois, United States
  • Siddiqui, Ahmed, Rush University Medical Center, Chicago, Illinois, United States
  • Baxi, Pravir V., Rush University Medical Center, Chicago, Illinois, United States

Granulocyte colony-stimulating factor (G-CSF) is commonly used with chemotherapy to stimulate bone marrow production and prevent neutropenia. Although usually well tolerated, G-CSF can exacerbate underlying autoimmune diseases with the development or progression of glomerulonephritis (GN). We present a case of pauci-immune necrotizing GN that developed in a patient with rheumatoid arthritis (RA) after receiving G-CSF therapy.

Case Description

A 61 y/o man with ampullary adenocarcinoma and RA without prior renal involvement presented with AKI. One week prior to admission he had received his 5th cycle of FOLFOX and a first dose of G-CSF. His creatinine (Cr) was 4.8 mg/dL from a baseline of 0.9 mg/dl. His urinalysis was notable for hematuria and urine protein-creatinine ratio (UPC) of 5.2 g/g. Workup showed: +p-ANCA (1:320), +anti-histone Ab, + SSA and +ANA (1:1280 speckled pattern). A renal biopsy revealed necrotizing GN with necrosis or crescents in 75% of the glomeruli (Fig 1). There was no evidence of immune-deposits c/w pauci-immune GN. He received steroids and rituximab for induction. His Cr peaked at 6.0 mg/dl but improved down to 1.1 and UPC improved to 0.6 g/g after 3 months.


G-CSF is used to prevent neutropenia and reduce infection risk by activating mature neutrophils and preventing neutrophil apoptosis. G-CSF can also have inflammatory effects including the release of proinflammatory cytokines and tissue infiltration by activated neutrophils with the potential of end-organ damage. In patients with a preexisting GN or an autoimmune disease (eg RA, SLE), G-CSF administration can exacerbate or even initiate a de-novo GN. Pauci-immune GN is a rare but well established complication of RA. In our case, the almost immediate temporal relationship between the development of the GN and the G-CSF administration supports G-CSF as etiologic. This case demonstrates the importance of considering the possible renal complications and need for close monitoring while giving G-CSF in patients with autoimmune diseases.

Figure 1: A) H&E Stain B) IF stain