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<p>Bosutinib is known to increase serum creatinine levels, and its mechanism of action is believed to involve a decrease in tubular creatinine excretion due to inhibition of tubular transporters and organic cation transporter 2. This study aimed to determine whether discontinuation of bosutinib could reverse bosutinib-induced elevation of serum creatinine levels. Serum creatinine levels were compared immediately before and after bosutinib administration and after bosutinib discontinuation in 11 patients with chronic myeloid leukemia. The median serum creatinine concentration significantly increased from 0.66&#xa0;mg/dL before bosutinib to 0.76&#xa0;mg/dL after bosutinib (<i>P</i> = 0.003) and decreased from 0.79&#xa0;mg/dL before discontinuation of bosutinib to 0.66&#xa0;mg/dL after discontinuation of bosutinib at 3&#xa0;months (<i>P</i> = 0.005). This study revealed that bosutinib-induced elevation of serum creatinine, which was more pronounced in patients with the <i>SLC22A2</i> 808G/G genotype, does not indicate chronic kidney disease, but rather is simply a laboratory abnormality. If bosutinib-induced chronic kidney disease is suspected, renal function should be assessed by urinalysis and cystatin C levels to differentiate from simple elevation of serum creatinine.</p>

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Stopping bosutinib reverses bosutinib-induced elevation of serum creatinine in patients with chronic myeloid leukemia

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年2月25日

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  • Maiko Abumiya,
  • Ayano Saito,
  • Yuki Fujioka,
  • Masatomo Miura,
  • Naoto Takahashi

摘要

Bosutinib is known to increase serum creatinine levels, and its mechanism of action is believed to involve a decrease in tubular creatinine excretion due to inhibition of tubular transporters and organic cation transporter 2. This study aimed to determine whether discontinuation of bosutinib could reverse bosutinib-induced elevation of serum creatinine levels. Serum creatinine levels were compared immediately before and after bosutinib administration and after bosutinib discontinuation in 11 patients with chronic myeloid leukemia. The median serum creatinine concentration significantly increased from 0.66 mg/dL before bosutinib to 0.76 mg/dL after bosutinib (P = 0.003) and decreased from 0.79 mg/dL before discontinuation of bosutinib to 0.66 mg/dL after discontinuation of bosutinib at 3 months (P = 0.005). This study revealed that bosutinib-induced elevation of serum creatinine, which was more pronounced in patients with the SLC22A2 808G/G genotype, does not indicate chronic kidney disease, but rather is simply a laboratory abnormality. If bosutinib-induced chronic kidney disease is suspected, renal function should be assessed by urinalysis and cystatin C levels to differentiate from simple elevation of serum creatinine.