A case of long-term dasatinib-induced proteinuria and glomerular injury

• Published in: CEN case reports 2020-11, Vol.9 (4), p.359-364
• Main Authors: Koinuma, Kana, Sakairi, Toru, Watanabe, Yoshikazu, IIzuka, Azusa, Watanabe, Mitsuharu, Hamatani, Hiroko, Nakasatomi, Masao, Ishizaki, Takuma, Ikeuchi, Hidekazu, Kaneko, Yoriaki, Hiromura, Keiju
• Format: Article
• Language: English
• Subjects: Case Report; Medicine; Medicine & Public Health; Nephrology; Urology
• ISSN: 2192-4449; 2192-4449
• DOI: 10.1007/s13730-020-00484-8

A 52-year-old woman was diagnosed with chronic myeloid leukemia. Treatment with dasatinib, a second-generation Bcr–Abl tyrosine kinase inhibitor, was initiated, and complete cytogenetic remission was achieved. Two years later, proteinuria occurred, and the urinary protein level increased gradually in the next 3 years. Moreover, the serum creatinine level increased mildly during this period. The urinary protein level reached 2.18 g/gCr; hence, a renal biopsy was conducted. Light microscopy revealed mild proliferation of mesangial cells, and immunofluorescence analysis revealed IgG and C3 depositions in the mesangial area. Electron microscopy revealed electron-dense deposition in the paramesangial area, partial podocyte foot process effacement, and segmental endothelial cell swelling with a slight expansion of the subendothelial space. Dasatinib was discontinued, and within 3 weeks, the proteinuria disappeared, with improvements in her renal function. After switching to bosutinib, a new second-generation of tyrosine kinase inhibitor, the proteinuria remained negative. The rapid cessation of proteinuria following dasatinib discontinuation indicated that proteinuria was induced by the long-term administration of dasatinib. Proteinuria and renal function should be regularly monitored during dasatinib therapy.