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Fujimoto K, Kikuchi M, Nakai M, Konta T, Iseki K, Tsuruya K, Yamagata K, Narita I, Moriyama T, Shibagaki Y, Kasahara M, Kondo M, Asahi K, Watanabe T, Kaikita K, Fujimoto S
American journal of hypertension 38 ( 7 ) 476 - 484 2025年3月
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：American Journal of Hypertension
BACKGROUND Rapid decline in estimated glomerular filtration rate (eGFR) is linked to increased mortality and morbidity in chronic kidney disease (CKD). Few studies have focused on the risk of rapid eGFR decline. This study evaluates the association between antihypertensive drug use, blood pressure (BP) levels, and rapid eGFR decline in Japanese CKD patients. METHODS Data from 100,746 Japanese individuals aged 40-74 years with CKD were analyzed. Rapid eGFR decline was defined as an annual reduction > 25%. Logistic regression was used to assess associations between antihypertensive drug use, BP levels, and rapid eGFR decline, stratified by eGFR and urinary proteinuria. RESULTS Rapid eGFR decline occurred in 5.8% of participants. Higher BP levels increased the risk compared to normal BP: high-normal + elevated BP (odds ratio [OR], 1.26; 95% CI: 1.12-1.41) and high BP (OR, 1.79; 95% CI: 1.59-2.02). Controlling BP to high-normal or elevated levels in patients receiving antihypertensives reduced this risk. Overall, antihypertensive drug users had approximately twice the risk of rapid eGFR decline compared to nonusers. However, in proteinuric patients with preserved eGFR, the risk increase was lower (1.27 times) in the high-normal + elevated BP group compared to that in the overall cohort. CONCLUSIONS The risk of rapid eGFR decline increased with increasing BP and decreased with controlling BP. Antihypertensive treatment was associated with a higher risk of rapid eGFR decline at all BP levels. For CKD patients with proteinuria, maintaining BP in the high-normal or elevated range may further mitigate this risk.
DOI： 10.1093/ajh/hpaf041
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Fujimoto K, Hisanaga S, Kuroda S, Kodama K, Sugiyama F, Kikuchi M, Kita T, Yamashita A, Nagai T, Kamimura T, Kaikita K, Imamura T, Fujimoto S
CEN case reports 13 ( 1 ) 1 - 8 2023年4月
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：CEN Case Reports
A 42-year-old man showed marked hypokalemia after kidney transplantation. He was diagnosed with hypertension and suffered from acute myocardial infarction at 33 and 38 years of age. At 40 years of age, hemodialysis was introduced. A left adrenal tumor was noted and suspected as a non-functional adrenal adenoma at that time. Therefore, he received a living-donor kidney transplant at 42 years of age. After kidney transplantation, the serum creatinine level dropped. His blood pressure remained high, and the serum potassium level decreased. The PRA and PAC were elevated, and ARR was not elevated. Based on the results of various confirmatory tests and vein sampling, he was diagnosed with excessive secretion of renin from the native kidneys that was complicated by primary aldosteronism (PA), and left nephrectomy and adrenalectomy were performed. The overproduction of aldosterone in the resected adrenal adenoma and over secretion of renin in the kidney with arteriolosclerosis were immunohistologically confirmed. After surgery, the PAC decreased, but the PRA did not decrease. The postoperative serum potassium level improved, and the blood pressure was well controlled with a small dose of medication. This is the first reported case of PA with hyperreninemia after kidney transplantation. It should be noted that PA in dialysis patients and kidney transplant recipients may not fulfill the usual diagnostic criteria of an elevated ARR. In such patients, PA should be suspected based on the absolute value of the PAC and responsiveness to ACTH stimulation, and adrenal and renal vein sampling is required for a definitive diagnosis.
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Seronegative Full-house Nephropathy with Crohn's Disease
Uedono H., Tsuda A., Ueno N., Natsuki Y., Nakaya R., Nishide K., MacHiba Y., Fujimoto K., Nakatani S., Mori K., Emoto M.
Internal Medicine 61 ( 23 ) 3553 - 3558 2022年12月
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：一般社団法人 日本内科学会
Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disease. Lupus nephritis (LN) is a major risk factor for mortality in SLE, and glomerular "full-house" immunofluorescence staining is a well-known characteristic of LN. However, some cases of non-lupus glomerulonephritis can also present with a "full-house" immunofluorescence pattern. We recently encountered a patient with full-house nephropathy (FHN) during adalimumab administration for Crohn's disease. IgA nephropathy or idiopathic FHN was diagnosed, and treatment with steroids was started, after which there was improvement in proteinuria. The prognosis of FHN has been reported to be poor; therefore, aggressive treatment is required for such patients.
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Long-Term Effects of High-Dose Tolvaptan for Autosomal Dominant Polycystic Kidney Disease Patients 査読あり
Nakatani S., Ishimura E., Machiba Y., Fujimoto K., Uedono H., Tsuda A., Mori K., Emoto M., Inaba M.
Case Reports in Nephrology and Dialysis 10 ( 1 ) 9 - 17 2020年
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：Case Reports in Nephrology and Dialysis
Tolvaptan, a vasopressin V2 receptor antagonist, was initially approved in Japan for treatment of autosomal dominant polycystic kidney disease (ADPKD). Recently, a retrospective study showed that the effect of tolvaptan on kidney function could be sustained for a long period. However, the long-Term efficacy and safety of high-dose tolvaptan (120 mg/day) in individual cases remain unknown. We report here 2 Japanese ADPKD patients (males, 36 and 29 years old) treated with tolvaptan (120 mg/day) for 9 years, during which time determinations of estimated glomerular filtration rate (eGFR) and total kidney volume (TKV) were performed. In these 2 patients, eGFR prior to therapy was 57.3 and 76.3 mL/min/1.73 m2, respectively, and 30.2 and 43.5 mL/min/1.73 m2, respectively, after 9 years of tolvaptan treatment, for a relatively constant annual decline of-3.01 and-3.64 mL/min/1.73 m2, respectively. As compared to the predicted (calculated) eGFR without tolvaptan treatment, eGFR actually measured was higher by 15.3 and 12.6 mL/min/1.73 m2, respectively, after the 9-year therapy period. In addition, the rate of TKV increase was gradual, 2.4 and 4.7%, respectively, per year during the initial 3-year period, to 6.5 and 12.5%, respectively, per year in the following 6-year period. During the 9 years of treatment, neither patient showed tolvaptan-related adverse events. Our findings suggest that long-Term administration of tolvaptan at a high dose is both safe and effective to preserve kidney function, though a gradual increase in TKV was seen in both of the present cases, particularly during the later phase.
DOI： 10.1159/000506118
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Oncostatin M induces C2C12 myotube atrophy by modulating muscle differentiation and degradation 査読あり
Miki Y., Morioka T., Shioi A., Fujimoto K., Sakura T., Uedono H., Kakutani Y., Ochi A., Mori K., Shoji T., Emoto M., Inaba M.
Biochemical and Biophysical Research Communications 516 ( 3 ) 951 - 956 2019年8月
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：Biochemical and Biophysical Research Communications
Oncostatin M (OSM) is a cytokine of the interleukin-6 family and plays a role in various disorders such as cancer and inflammatory diseases, which are often accompanied by skeletal muscle atrophy, or sarcopenia. However, the role of OSM in the regulation of skeletal muscle mass remains to be identified. In this study, we investigated the effect of OSM on C2C12 myotube formation in vitro. C2C12 myoblasts were induced to differentiate into myotubes for 3 days and then treated with OSM for 24 or 48 h. The diameter of differentiated C2C12 myotubes were reduced by 18.7% and 23.3% compared to control cells after treatment with OSM for 24 and 48 h, respectively. The expression levels of MyoD and myogenin were decreased, while those of atrogin-1, CCAAT/enhancer binding protein δ, and OSM receptor were increased in C2C12 myotubes treated with OSM for 24 h compared to control cells. Furthermore, the inhibitory effect of OSM on myotube formation was significantly attenuated by pretreatment with an inhibitor of signal transducer and activator of transcription (STAT) 3 or by knockdown of Stat3. Finally, the OSM-induced changes in the expression levels of MyoD, myogenin, and atrogin-1 were reversed by pretreatment with an inhibitor of STAT3 or by Stat3 knockdown in C2C12 myotubes. In conclusion, OSM induces C2C12 myotube atrophy by inhibiting myogenic differentiation and activating muscle degradation in a STAT3-dependent manner.