Focal segmental glomerulosclerosis and concurrent glomerular microangiopathy after long-term imatinib administration View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2021-09-09

AUTHORS

Natsumi Morita, Tomomi Ozaki, Soichiro Yokota, Hidenori Sasaki, Maho Watanabe, Koji Takahashi, Naoko Himuro, Kenji Ito, Tetsuhiko Yasuno, Katsuhisa Miyake, Aya Nawata, Toshiyuki Nakayama, Noriko Uesugi, Kosuke Masutani

ABSTRACT

A 79-year-old Japanese man was admitted to our hospital because of proteinuria and kidney dysfunction. He was diagnosed with chronic myeloid leukemia 13 years before and was treated with imatinib. Deep molecular response was achieved but he developed 1+ proteinuria in the first year, which gradually worsened thereafter. Imatinib was discontinued 12 years later but proteinuria and kidney dysfunction were progressive. Percutaneous kidney biopsy revealed mild mesangial hyper-cellularity and matrix increase, swelling of endothelial cells, and partial double contours of glomerular tufts. Subendothelial edema in the interlobular artery was also noted. Immunofluorescence was not remarkable. Electron microscopy revealed endothelial injury with severe sub-endothelial edema. Since imatinib had already been discontinued, conservative therapy with maximal dose of azilsartan was administered. A second biopsy was performed 1 year later because of further deterioration of kidney function, which revealed markedly increased global glomerulosclerosis and severe interstitial fibrosis and tubular atrophy. Segmental glomerulosclerosis with podocyte hyperplasia was also observed. Electron microscopy revealed glomerulosclerotic changes and partially attenuated endothelial injury. Two and a half years later, proteinuria reduced, progression of kidney dysfunction slowed, and he was independent on dialysis therapy. Molecular response of chronic myeloid leukemia was also maintained. The clinical course suggested that endothelial and podocyte injuries were induced by imatinib, and that the nephrotoxic effects lasted for a few years after discontinuation. More... »

PAGES

134-140

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s13730-021-00622-w

DOI

http://dx.doi.org/10.1007/s13730-021-00622-w

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1141003396

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/34505278


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21 schema:description A 79-year-old Japanese man was admitted to our hospital because of proteinuria and kidney dysfunction. He was diagnosed with chronic myeloid leukemia 13 years before and was treated with imatinib. Deep molecular response was achieved but he developed 1+ proteinuria in the first year, which gradually worsened thereafter. Imatinib was discontinued 12 years later but proteinuria and kidney dysfunction were progressive. Percutaneous kidney biopsy revealed mild mesangial hyper-cellularity and matrix increase, swelling of endothelial cells, and partial double contours of glomerular tufts. Subendothelial edema in the interlobular artery was also noted. Immunofluorescence was not remarkable. Electron microscopy revealed endothelial injury with severe sub-endothelial edema. Since imatinib had already been discontinued, conservative therapy with maximal dose of azilsartan was administered. A second biopsy was performed 1 year later because of further deterioration of kidney function, which revealed markedly increased global glomerulosclerosis and severe interstitial fibrosis and tubular atrophy. Segmental glomerulosclerosis with podocyte hyperplasia was also observed. Electron microscopy revealed glomerulosclerotic changes and partially attenuated endothelial injury. Two and a half years later, proteinuria reduced, progression of kidney dysfunction slowed, and he was independent on dialysis therapy. Molecular response of chronic myeloid leukemia was also maintained. The clinical course suggested that endothelial and podocyte injuries were induced by imatinib, and that the nephrotoxic effects lasted for a few years after discontinuation.
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28 administration
29 artery
30 atrophy
31 azilsartan
32 biopsy
33 cells
34 changes
35 chronic myeloid leukemia
36 clinical course
37 conservative therapy
38 contours
39 course
40 deep molecular response
41 deterioration
42 dialysis therapy
43 discontinuation
44 dose
45 double contour
46 dysfunction
47 edema
48 effect
49 electron microscopy
50 endothelial cells
51 endothelial injury
52 fibrosis
53 first year
54 focal segmental glomerulosclerosis
55 function
56 further deterioration
57 global glomerulosclerosis
58 glomerular microangiopathy
59 glomerular tuft
60 glomerulosclerosis
61 glomerulosclerotic changes
62 half years
63 hospital
64 hyperplasia
65 imatinib
66 imatinib administration
67 immunofluorescence
68 increase
69 injury
70 interlobular arteries
71 interstitial fibrosis
72 kidney biopsy
73 kidney dysfunction
74 kidney function
75 leukemia
76 matrix increases
77 maximal dose
78 men
79 microangiopathy
80 microscopy
81 molecular response
82 myeloid leukemia
83 nephrotoxic effects
84 percutaneous kidney biopsy
85 podocyte hyperplasia
86 podocyte injury
87 progression
88 proteinuria
89 response
90 second biopsy
91 segmental glomerulosclerosis
92 severe interstitial fibrosis
93 subendothelial edema
94 therapy
95 tubular atrophy
96 tufts
97 years
98 schema:name Focal segmental glomerulosclerosis and concurrent glomerular microangiopathy after long-term imatinib administration
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