Yoshimitsu Hayashi

Background About 146,000 people were forced into long-term evacuation due to the nuclear power plant accident caused by the Great East Japan Earthquake in 2011. Disaster is known to induce hypertension in survivors for a certain period, but it is unclear whether prolonged disaster stress influences chronic kidney disease (CKD). We conducted an observational cohort study to elucidate the effects of evacuation stress on CKD incidence. Methods Participants were individuals living in communities near the Fukushima nuclear power plant, aged 40–74 years without CKD as of their 2011 general health checkup (non-evacuees: n = 9780, evacuees: n = 4712). We followed new-onset CKD [estimated glomerular filtration rate (eGFR) 2 or proteinuria] using general annual health checkup data from 2012 to 2014. Association between evacuation and CKD incidence was analyzed using the Cox proportional hazard model. Results Mean age of the participants at baseline was 65 years, 46.7% were men, and baseline eGFR was 75.7 ml/min/1.73 m². During the mean follow-up period of 2.46 years, CKD incidence rate was 80.8/1000 and 100.2/1000 person-years in non-evacuees and evacuees, respectively. Evacuation was a significant risk factor of CKD incidence after adjusting for age, gender, obesity, hypertension, diabetes, dyslipidemia, smoking, and baseline eGFR [hazard ratio (HR): 1.45; 95% confidence interval (CI) 1.35–1.56]. Evacuation was significantly associated with the incidence of eGFR 2 (HR: 1.48; 95% CI 1.37–1.60), but not with the incidence of proteinuria (HR: 1.21; 95% CI 0.93–1.56). Conclusion Evacuation was a risk factor associated with CKD incidence after the disaster.

Methylglyoxal (MG), one of the uremic toxins, is a highly reactive alpha-dicarbonyl compound. Recent clinical studies have demonstrated the close associations of cognitive impairment (CI) with plasma MG levels and presence of kidney dysfunction. Therefore, the present study aims to examine whether MG is a direct causative substance for CI development. Eight-week-old male Sprague-Dawley (SD) rats were divided into two groups: control (n = 9) and MG group (n = 10; 0.5% MG in drinking water), and fed a normal diet for 12 months. Cognitive function was evaluated by two behavioral tests (object exploration test and radial-arm maze test) in early (4–6 months of age) and late phase (7–12 months of age). Serum MG was significantly elevated in the MG group (495.8 ± 38.1 vs. 244.8 ± 28.2 nM; p < 0.001) at the end of study. The groups did not differ in cognitive function during the course of study. No time-course differences were found in oxidative stress markers between the two groups, while, antioxidants such as glutathione peroxidase and superoxide dismutase activities were significantly increased in the MG group compared to the control. Long-term MG administration to rats with normal kidney function did not cause CI. A counter-balanced activation of the systemic anti-oxidant system may offset the toxicity of MG in this model. Pathogenetic significance of MG for CI requires further investigation.

Oxidative stress (OS) related to glucose degradation products such as methylglyoxal is reportedly associated with peritoneal deterioration in patients treated with peritoneal dialysis (PD). However, the use of general antioxidant agents is limited due to their harmful effects. This study aimed to clarify the influence of the novel antioxidant molecular hydrogen (H2) on peritoneal OS using albumin redox state as a marker.

Glomerular hypertension aggravates glomerular sclerosis by inducing growth factors, e.g., transforming growth factor-β (TGF-β) to mesangial matrix expansion. Smads are intracellular proteins that transmit signals from TGF-β to nucleus, and Smads are also negatively regulated by inhibitory Smads (I-Smads), Smad6 and Smad7. However, little is known about the role of I-Smads in glomerular hypertension. We studied I-Smad expression in cultured mesangial cells subjected to mechanical stretch as an in vitro model of glomerular hypertension.