Acute kidney injury presenting a feature of leukemic infiltration during therapy for chronic myelogenous leukemia

Yukio Yuzawa, Waichi Sato, Tomohiro Masuda, Yuzuru Hamada, Miho Tatematsu, Yoshinari Yasuda, Takenori Ozaki, Isao Ito, Masashi Mizuno, Shoichi Maruyama, Yasuhiko Ito, Seiichi Matsuo

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Chronic myelogenous leukemia (CML) is a myeloproliferative disease that originates in abnormal pluripo- tent bone marrow stem cells and it is consistently associated with the Philadelphia chromosome and/or BCR/ ABL fusion gene. Renal infiltration of leukemic cells is relatively rare in CML and is associated with renal impairment. We describe a patient who developed acute renal failure by tubulointerstitial nephropathy during treatment with imatinib mesylate for CML. The acute kidney injury was subsequently found to be due to direct leukemic infiltration. Treatment with hydroxycarbamide and prednisolone resulted in stabilization of the renal function for approximately 4 months. Leukemic infiltration into the kidney should always be considered when a patient with CML presents with renal impairment, regardless of the clinical stage, as the renal failure often responds well to chemotherapy.

Original languageEnglish
Pages (from-to)1139-1142
Number of pages4
JournalInternal Medicine
Volume49
Issue number12
DOIs
Publication statusPublished - 01-07-2010
Externally publishedYes

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Leukemic Infiltration
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Acute Kidney Injury
Kidney
Therapeutics
Philadelphia Chromosome
Gene Fusion
Prednisolone
Bone Marrow Cells
Renal Insufficiency
Stem Cells
Drug Therapy

All Science Journal Classification (ASJC) codes

  • Internal Medicine

Cite this

Yuzawa, Yukio ; Sato, Waichi ; Masuda, Tomohiro ; Hamada, Yuzuru ; Tatematsu, Miho ; Yasuda, Yoshinari ; Ozaki, Takenori ; Ito, Isao ; Mizuno, Masashi ; Maruyama, Shoichi ; Ito, Yasuhiko ; Matsuo, Seiichi. / Acute kidney injury presenting a feature of leukemic infiltration during therapy for chronic myelogenous leukemia. In: Internal Medicine. 2010 ; Vol. 49, No. 12. pp. 1139-1142.
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abstract = "Chronic myelogenous leukemia (CML) is a myeloproliferative disease that originates in abnormal pluripo- tent bone marrow stem cells and it is consistently associated with the Philadelphia chromosome and/or BCR/ ABL fusion gene. Renal infiltration of leukemic cells is relatively rare in CML and is associated with renal impairment. We describe a patient who developed acute renal failure by tubulointerstitial nephropathy during treatment with imatinib mesylate for CML. The acute kidney injury was subsequently found to be due to direct leukemic infiltration. Treatment with hydroxycarbamide and prednisolone resulted in stabilization of the renal function for approximately 4 months. Leukemic infiltration into the kidney should always be considered when a patient with CML presents with renal impairment, regardless of the clinical stage, as the renal failure often responds well to chemotherapy.",
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Yuzawa, Y, Sato, W, Masuda, T, Hamada, Y, Tatematsu, M, Yasuda, Y, Ozaki, T, Ito, I, Mizuno, M, Maruyama, S, Ito, Y & Matsuo, S 2010, 'Acute kidney injury presenting a feature of leukemic infiltration during therapy for chronic myelogenous leukemia', Internal Medicine, vol. 49, no. 12, pp. 1139-1142. https://doi.org/10.2169/internalmedicine.48.2747

Acute kidney injury presenting a feature of leukemic infiltration during therapy for chronic myelogenous leukemia. / Yuzawa, Yukio; Sato, Waichi; Masuda, Tomohiro; Hamada, Yuzuru; Tatematsu, Miho; Yasuda, Yoshinari; Ozaki, Takenori; Ito, Isao; Mizuno, Masashi; Maruyama, Shoichi; Ito, Yasuhiko; Matsuo, Seiichi.

In: Internal Medicine, Vol. 49, No. 12, 01.07.2010, p. 1139-1142.

Research output: Contribution to journalArticle

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AU - Yuzawa, Yukio

AU - Sato, Waichi

AU - Masuda, Tomohiro

AU - Hamada, Yuzuru

AU - Tatematsu, Miho

AU - Yasuda, Yoshinari

AU - Ozaki, Takenori

AU - Ito, Isao

AU - Mizuno, Masashi

AU - Maruyama, Shoichi

AU - Ito, Yasuhiko

AU - Matsuo, Seiichi

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