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　10月16日・17日にWeb配信で開催された「日本腎臓学会西部学術大会」で
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演題「地域における腎臓病療養指導士の役割」についての講演を行いました。

　生活習慣病対策　市民公開講座　Web版による「高血圧予防！カラダがよろこぶ減塩のお話」
～専門医と管理栄養士による健康で長生きのための秘訣について～が、
2020年10月1日（木）よりYouTube熊本市公式チャンネルにて配信されています。
「おいしく続ける減塩生活のコツ」を
あけぼのクリニック腎臓病療養指導士　北岡主任管理栄養士が講師として担当しています。

下記のURLからアクセス可能です。
https://www.city.kumamoto.jp/hpKiji/pub/detail.aspx?c_id=5&id=29982&class_set_id=3&class_id=563

　肺炎球菌ワクチンは、肺炎球菌による肺炎の発症を予防し、重症化を防ぎます。
新型コロナウイルス関連の肺炎予防にも、接種をお勧め致します。
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Imafukua T*, Tanaka M*, Tokunaga K, Miyamura S, Kato H, Tanaka S, Nakano T, Hirata K, Kadowaki D, Maeda H, Matsushita K, Otagiri M, Komaba H, Fukagawa M, Watanabe H#, Maruyama T# Effect of cinacalcet on the redox status of albumin in secondary hyperparathyroidism patients receiving hemodialysis. Biol Pharm Bull. in press *equal contribution; # equal corresponding author

Abstract

Chronic kidney disease (CKD) patients with secondary hyperparathyroidism (SHPT) have an increased risk of cardiovascular disease (CVD). Cinacalcet is a calcimimetic that permits impaired endothelial functions to be recovered via inhibiting parathyroid hormone (PTH) production in SHPT patients. However, the underlying mechanism for its action remains unknown. The purpose of this study was to examine the effect of cinacalcet on the redox state of human serum albumin (HSA), a reliable marker for assessing endothelial oxidative damage in SHPT patients who were receiving hemodialysis. Cinacalcet was administered to six SHPT patients for a period of 8 weeks. After 4 weeks of treatment, cinacalcet significantly decreased the oxidized albumin ratio which is a ratio of reduced and oxidized forms of HSA via increasing reduced form of HSA. Moreover, the radical scavenging abilities of HSA that was isolated from SHPT patients were increased by cinacalcet, suggesting the recovery of the impaired vascular anti-oxidant ability. Interestingly, the oxidized albumin ratio in SHPT patients was significantly higher than that in hemodialysis patients. In addition, the changes of intact PTH levels were significantly correlated with the oxidized albumin ratio. It therefore appears that PTH may induce oxidative stress in SHPT patients. In fact, an active analogue of PTH increased the production of reactive oxygen species in human endothelial cells. Thus, cinacalcet exhibits anti-oxidative activity through its pharmacological action. Additionally, cinacalcet itself showed radical scavenging activity. In conclusion, cinacalcet improves the redox status of HSA by inhibiting PTH production and partially by inhibiting its radical scavenging action.

①Kidney360に論文が受理されました。（酸化蛋白質による腎Elovl6発現誘導と脂肪酸組成の変動が腎障害の進展に関与する）

Advanced oxidation protein products contribute to renal tubulopathy via perturbation of renal fatty acids

Tadashi Imafuku, Hiroshi Watanabe§, Takao Satoh, Takashi Matsuzaka, Tomoaki Inazumi, Hiromasa Kato, Shoma Tanaka, Yuka Nakamura, Takehiro Nakano, Kai Tokumaru, Hitoshi Maeda, Motoko Tanaka, Kazutaka Matsushita, Soken Tsuchiya, Yukihiko Sugimoto, Hitoshi Shimano, Masafumi Fukagawa, Toru Maruyama

②Bi J, Watanabe H, Fujimura R, Nishida K, Nakamura R, Oshiro S, Imafuku T, Komori H, Miyahisa M, Tanaka M, Matsushita K, Maruyama T, A downstream molecule of 1,25-dihydroxyvitamin D3, alpha-1-acid glycoprotein, protects against mouse model of renal fibrosis, Sci Rep (2018) Nov 26;8(1):17329.

③Watanabe H*#, Sugimoto R*, Ikegami K, Enoki Y, Imafuku T, Fujimura R, Bi J, Nishida K, Sakaguchi Y, Murata M, Maeda H, Hirata K, Jingami S, Ishima Y, Tanaka M, Matsushita K, Komaba H, Fukagawa M, Otagiri M, Maruyama T#. Parathyroid hormone contributes to the down-regulation of cytochrome P450 3A through the cAMP/PI3K/PKC/PKA/NF-κB signaling pathway in secondary hyperparathyroidism. Biochem Pharmacol. *equal contribution, #equal corresponding author 2017 Dec 1;145:192-201.

④Enoki Y*, Watanabe H*, Arake R, Fujimura R, Ishiodori K, Imafuku T, Nishida K, Sugimoto R, Nagao S, Miyamura S, Ishima Y, Tanaka M, Matsushita K, Komaba H, Fukagawa M, Otagiri M, Maruyama T. Potential therapeutic interventions for chronic kidney disease-associated sarcopenia via indoxyl sulfate-induced mitochondrial dysfunction. J Cachexia Sarcopenia Muscle. *equal contribution 2017 Oct;8(5):735-747.

 ⑤Enoki Y, Watanabe H, Arake R, Sugimoto R, Imafuku T, Tominaga Y, Ishima Y, Kotani S, Nakajima M, Tanaka M, Matsushita K, Fukagawa M, Otagiri M, Maruyama T. Indoxyl sulfate potentiates skeletal muscle atrophy by inducing the oxidative stress-mediated expression of myostatin and atrogin-1. Sci Rep. 6:32084 (2016)