Anti-glomerular basement membrane glomerulonephritis following nintedanib for idiopathic pulmonary fibrosis: a case report

Abstract

BackgroundWe report a previously unrecognized and unreported case of a patient with anti-glomerular basement membrane glomerulonephritis following nintedanib, an orally active small molecule tyrosine kinase inhibitor.Case presentationA 59-year-old Caucasian woman with a history of idiopathic pulmonary fibrosis presented with severe acute kidney injury (creatinine 285 umol/L) secondary to anti-glomerular basement membrane glomerulonephritis disease 4 months after commencement of nintedanib. She had hematuria with red blood cell casts, nephrotic range proteinuria (3.5g/24 hours) and significantly elevated anti-glomerular basement membrane glomerulonephritis titers at 860 chemiluminescent units. A kidney biopsy confirmed severe crescentic glomerulonephritis with linear immunoglobulin G deposition in glomerular basement membrane. Despite the commencement of treatment with plasma exchange and cyclophosphamide, she remained dialysis dependent. Nintedanib was discontinued.ConclusionsOnset of acute anti-glomerular basement membrane glomerulonephritis was found to be associated with recent nintedanib use suggesting that nintedanib may be a potential trigger for anti-glomerular basement membrane glomerulonephritis. This case highlights the importance of close monitoring of patients receiving new targeted therapies. Management of novel targeted agents in patients receiving dialysis is challenging because of the scarcity of specific data.

Slowly Progressive ANCA-associated Glomerulonephritis with Strong Mesangial MPO Deposits Following a Diagnosis of Interstitial Lung Disease

“…Endothelial dysfunction is hypothesized to be a potential cause of proteinuria ( 6 ). While there have been a few reports of nintedanib being used to treat idiopathic pulmonary fibrosis, inducing anti-glomerular basement membrane disease, and renal thrombotic microangiopathy ( 7 , 8 ), the renal pathology in our patient did not exhibit either of these conditions.…”

Pembrolizumab-Induced Anti-GBM Glomerulonephritis: A Case Report

“…First, anti-GBM glomerulonephritis has rarely been described as a paraneoplastic disease, but in the reported cases, serum antineutrophil cytoplasmic antibody levels are positive. 12 , 13 Second, there has been a case report of anti-GBM glomerulonephritis associated with nintedanib, 14 but not with bevacizumab. Whereas nintedanib is a small molecule that targets vascular endothelial growth factor receptors-1,2,3, platelet-derived growth factor receptors-α/β, and fibroblast growth factor receptors-1,2,3 pathways, bevacizumab is a recombinant humanized monoclonal antibody that binds to vascular endothelial growth factor-A.…”

Identification of biomarkers and drug repurposing candidates based on an immune-, inflammation- and membranous glomerulonephritis-associated triplets network for membranous glomerulonephritis

“…Some previous studies reported that the treatment effect of tamoxifen on MGN [27]. In addition, a previous study suggests that nintedanib may be a potential trigger for MGN [28]. Nintedanib is a multiple tyrosine kinase inhibitor that works on key angiogenesis pathways including platelet-derived growth factor, vascular endothelial growth factor, and basic fibroblast growth factor.…”