BACKGROUND/OBJECTIVES: Patients with chronic kidney disease (CKD) have a high concentration of uremic toxins in their blood and often experience muscle atrophy. Indoxyl sulfate (IS) is a uremic toxin produced by tryptophan metabolism. Although an elevated IS level may induce muscle dysfunction, the effect of IS on physiological concentration has not been elucidated. Additionally, the effects of ursolic acid (UA) on muscle hypertrophy have been reported in healthy models; however, it is unclear whether UA ameliorates muscle dysfunction associated with chronic diseases, such as CKD. Thus, this study aimed to investigate whether UA can improve the IS-induced impairment of mitochondrial biogenesis.MATERIALS/METHODS: C2C12 cells were incubated with or without IS (0.1 mM) and UA (1 or 2 µM) to elucidate the physiological effect of UA on CKD-related mitochondrial dysfunction and its related mechanisms using real-time reverse transcription-polymerase chain reaction, western blotting and enzyme-linked immunosorbent assay. RESULTS: IS suppressed the expression of differentiation marker genes without decreasing cell viability. IS decreased the mitochondrial DNA copy number and ATP levels by downregulating the genes pertaining to mitochondrial biogenesis (Ppargc1a, Nrf1, Tfam, Sirt1, and Mef2c), fusion (Mfn1 and Mfn2), oxidative phosphorylation (Cycs and Atp5b), and fatty acid oxidation (Pdk4, Acadm, Cpt1b, and Cd36). Furthermore, IS increased the intracellular mRNA and secretory protein levels of interleukin (IL)-6. Finally, UA ameliorated the IS-induced impairment in C2C12 cells. CONCLUSIONS Our results indicated that UA improves the IS-induced impairment of mitochondrial biogenesis by affecting differentiation, ATP levels, and IL-6 secretion in C2C12 cells. Therefore, UA could be a novel therapeutic agent for CKD-induced muscle dysfunction.

We present a successful case of redo-tricuspid valve replacement for tricuspid prosthetic valve endocarditis. A 78-year-old man who underwent tricuspid bioprosthetic valve replacement for severe tricuspid regurgitation thirty-two years earlier was referred to our institution with persistent high fever and back pain. The blood culture was positive for Streptococcus oralis, and echocardiography revealed a mobile vegetation attached to the tricuspid prosthetic valve with moderate tricuspid regurgitation. A clinical diagnosis of prosthetic valve endocarditis was established. Redo-tricuspid bioprosthetic valve replacement was performed following antibiotics therapy. The patient was discharged on postoperative day 49 after 6 weeks of additional antibiotic treatment, and had no recurrence of infection for 6 months after redo-surgery.

A woman in her 50s underwent abdominal total hysterectomy for uterine myoma. She was discharged from the hospital on postoperative day (POD) 6 following an uneventful postoperative course but returned to the outpatient clinic on POD 11 with chief complaints of fever and abdominal pain. Blood tests at presentation showed a C-reactive protein level of 22.95 mg/dL and a white blood cell count of 21300/μL, indicating an increased inflammatory response. Transvaginal ultrasonography and contrast-enhanced computed tomography (CT) revealed a small amount of ascites and a thickened pelvic peritoneum. Based on these findings, pelvic peritonitis was diagnosed and the patient was readmitted to the hospital. After admission, antimicrobial treatment with cefmetazole 3 g/day was started, but transvaginal ultrasonography on POD 13 (3 days after readmission) revealed an intra-pelvic abscess. The abscess was punctured under transvaginal ultrasonographic guidance and the puncture fluid was submitted for microbiological examination, followed by CT-guided drainage. At the same time, the antimicrobial regimen was changed to sulbactam/ampicillin 9 g/day and doxycycline (DOXY) 200 mg/day (100 mg/day from the following day). On POD 18 (8 days after readmission), Mycoplasma hominis was detected in the abscess culture, leading to the decision to increase the dose of DOXY to 200 mg. Subsequently, with improvement of subjective and objective symptoms and reduction of the abscess cavity, the patient was discharged from the hospital on POD 21 (11 days after readmission). Although M. hominis is a common urogenital commensal, it can be a potential pathogen in a patient with a pelvic abscess that occurs as a late postoperative complication and does not respond to beta-lactam antibiotics, so treatment decisions should be made with this organism kept in mind.

The patient was a 36-year-old primipara with no comorbidities such as diabetes or hypertension. At 35 weeks and 3 days of pregnancy, she was admitted for rupture of membranes. She vomited often during the expulsive stage of labor, so a vacuum extraction was performed. Her vital signs were normal throughout the delivery. She vomited repeatedly after the delivery but did not complain of headache or arm weakness and her level of consciousness was Japan Coma Scale I-1. Head CT revealed right caudate hemorrhage and cerebral ventricular rupture. Head MRI showed no obvious cerebrovascular abnormality, so she was followed up with symptomatic treatment. Recovery was uneventful, without neurological sequelae, and she was discharged on postpartum day 27. Cerebral hemorrhage during pregnancy is caused in many cases by comorbidities such as cerebral aneurysm, cerebral artery malformation, and pregnancyinduced hypertension syndrome. Cerebral hemorrhage may occur in pregnant women with no risk factors, even when their vital signs are stable. It is necessary to pay attention to the appearance of new symptoms, such as vomiting, around the time of delivery.