Erythropoiesis-stimulating agents (ESAs) have been widely used to maintain optimal hemoglobin levels in patients with CKD. However, the use of ESAs should be avoided in patients with a history of stroke according to the TREAT study, as both a history of stroke and ESAs treatment are independent risk factors for new stroke. Here we report a renal anemia patient with a history of cerebral infarction and malignant hypertension who was not suitable for the use of ESAs. On admission, the patient had mild anemia with a hemoglobin of 95 g/L. Iron status biomarkers were detected, and there was no obvious iron deficiency (iron 9.53 μmol/L, total iron binding capacity 39.53 μmol/L and transferrin saturation 24%). A standard dosage of roxadustat (100 mg for ≥60 kg) thrice a week were given to correct anemia, the patient responded well, and the hemoglobin gradually increased to the target level. However, an uncorrected reduction in roxadustat caused further aggravation of anemia (hemoglobin level 90 g/L). At the same time, we found that the patient had absolute iron deficiency (iron 4.62 μmol/L, total iron binding capacity 64.82 μmol/L and TAST 7%). Therefore, roxadustat can be effectively and safely used in patients with cerebral infarction, but the serum iron level should be monitored in application.

错误:搜索内容不能为空,请输入英文关键词
错误:关键词超出字数限制,请精简
高级检索

Treatment of Anemia in a Patient with Chronic Kidney Disease and Cerebral Infarction

  • Wen Zheng,
  • Dong-Wei Liu,
  • Zhang-Suo Liu

摘要

Erythropoiesis-stimulating agents (ESAs) have been widely used to maintain optimal hemoglobin levels in patients with CKD. However, the use of ESAs should be avoided in patients with a history of stroke according to the TREAT study, as both a history of stroke and ESAs treatment are independent risk factors for new stroke. Here we report a renal anemia patient with a history of cerebral infarction and malignant hypertension who was not suitable for the use of ESAs. On admission, the patient had mild anemia with a hemoglobin of 95 g/L. Iron status biomarkers were detected, and there was no obvious iron deficiency (iron 9.53 μmol/L, total iron binding capacity 39.53 μmol/L and transferrin saturation 24%). A standard dosage of roxadustat (100 mg for ≥60 kg) thrice a week were given to correct anemia, the patient responded well, and the hemoglobin gradually increased to the target level. However, an uncorrected reduction in roxadustat caused further aggravation of anemia (hemoglobin level 90 g/L). At the same time, we found that the patient had absolute iron deficiency (iron 4.62 μmol/L, total iron binding capacity 64.82 μmol/L and TAST 7%). Therefore, roxadustat can be effectively and safely used in patients with cerebral infarction, but the serum iron level should be monitored in application.