- 著者
- Tetsuhiko Yasuno Koji Takahashi Kazuhiro Tada Hiroto Hiyamuta Maho Watanabe Kenji Ito Hisatomi Arima Kosuke Masutani
- 出版者
- The Japanese Society of Internal Medicine
- 雑誌
- Internal Medicine (ISSN:09182918)
- 巻号頁・発行日
- pp.1602-23, (Released:2023-06-21)
- 参考文献数
- 23
- 被引用文献数
- 1
Background The gut bacterial microbiota is altered in patients with chronic kidney disease (CKD). However, the bacterial composition at each stage of CKD is unclear in these patients, including those receiving renal replacement therapy. We herein report the changes in the gut microbiota among patients with CKD. Methods A total of 93 individuals were recruited for the study. Seventy-three patients had stage 3-5 CKD, including those receiving renal replacement therapy (CKD group), and 20 were age- and sex-matched controls (CKD stage 1-2). The gut microbiome composition was analyzed using a 16S ribosomal RNA gene-based sequencing protocol. Results At the genus level, the butyrate-producing bacteria Lachnospira, Blautia, Coprococcus, Anaerostipes, and Roseburia were more abundant in the control group (linear discriminant analysis score of >3) than in the CKD group. Lachnospira was more abundant in the control group than in patients with CKD stage 3a. Compared to the control group, multiplex butyrate-producing bacteria were deficient in patients with CKD stage 3b-5D, including in patients receiving renal replacement therapy. Conclusion Our findings highlight the fact that the gut bacterial composition, including butyrate-producing bacteria, deteriorates from CKD stage 3b. Even after renal replacement therapy, the bacterial composition did not change.
- 著者
- Kazuhiro Tada Kenji Ito Aki Hamauchi Koji Takahashi Renya Watanabe Ai Uchida Yasuhiro Abe Tetsuhiko Yasuno Katsuhisa Miyake Yoshie Sasatomi Hitoshi Nakashima
- 出版者
- 一般社団法人 日本内科学会
- 雑誌
- Internal Medicine (ISSN:09182918)
- 巻号頁・発行日
- vol.55, no.8, pp.969-973, 2016 (Released:2016-04-15)
- 参考文献数
- 26
- 被引用文献数
- 1 6
Clopidogrel was administered to a 67-year-old Japanese man to prevent the recurrence of cerebral infarction. Twelve weeks later, he was admitted to our hospital with acute renal failure, hemolytic anemia and thrombocytopenia, and was diagnosed with clopidogrel-induced thrombotic microangiopathy. Clopidogrel was immediately discontinued and corticosteroid and plasma exchange therapy were administered simultaneously. Thereafter, the patient's condition gradually improved. The patient had a decreased serum complement C3 level. This suggests that the activated alternative pathway is related to thrombotic microangiopathy (TMA). TMA is a critical drug-associated adverse reaction that clinicians should always be vigilant about, because clopidogrel is widely prescribed.