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The world today is facing a pandemic caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which mainly causes a respiratory disease known as coronavirus disease 2019 (COVID-19). Therefore, its pathogenesis and complications should be identified and understood. SARS-CoV-2 infects the host using the angiotensin-converting enzyme 2 (ACE2) as its receptor, which is expressed in several organs including the lungs, heart, kidneys, and intestines. Kidney complications are relatively common, and acute kidney injury (AKI) is a life-threatening complication in patients with COVID-19. In this review, the renal histological patterns of COVID-19 are described in detail, and its potential mechanisms associated with AKI are discussed.

d-serine administration prevents kidney damage in murine models of acute kidney injury, and risperidone inhibits the activity of d-amino acid oxidase, which regulate plasma d-amino acid levels. This pilot randomized controlled trial investigated the effects of risperidone on glucose, amino acid metabolism, and kidney function in healthy adults. Healthy adults with a homeostasis model assessment of insulin resistance (HOMA-IR) of ≥ 1.6 and estimated glomerular filtration rate (eGFR) of ≥ 60 mL/min/1.73m2 were randomly assigned to the risperidone and control groups. The risperidone group received 0.5 mg/day risperidone for 4 days. The primary outcome was mean change in HOMA-IR on day 5, and the secondary outcomes were changes in d-amino acid levels, eGFR, and urinary albumin. Seven participants were randomized to the risperidone and control groups. The changes in HOMA-IR, eGFR, and urinary albumin on day 5 were not significantly different between the two groups (all p > 0.05). Mean changes in plasma d-serine level and urinary d-serine/creatinine ratio were significantly higher in the risperidone group than in the control group (0.2 vs. -0.3 nmol/mL, p = 0.03 and 38.2 vs. -25.8 nmol/mL, p = 0.01, respectively). Short-term risperidone affects d-serine metabolism without instigating acute adverse effects on kidney or glucose homeostasis in healthy individuals. Clinical Trial Registry number: This study was registered with the Japan Registry for Clinical Trials (jRCTs041210165).

Background This study assessed the association of pathological kidney lesions with cardiovascular events in biopsy-proven diabetic kidney disease (DKD) with type 2 diabetes. Methods This multicenter, retrospective study involved 244 patients with no previous cardiovascular events before biopsy, estimated glomerular filtration rate (eGFR) ≥ 30 mL/min/1.73 m 2 at biopsy (baseline), and ≥ 1 year of observation after biopsy. The outcomes were the first occurrence of cardiovascular events (cardiovascular death, non-fatal myocardial infarction, coronary intervention, or non-fatal stroke), and non-cardiovascular deaths before cardiovascular events were considered competing events. The association between the severity of each pathological lesion and cardiovascular events was investigated. Results During follow-up (median: 6.4 years), 43 patients experienced cardiovascular events. The baseline clinical characteristics did not differ according to cardiovascular events. The cumulative incidence of cardiovascular events was higher in patients with mesangiolysis, global glomerulosclerosis ≥ 50%, moderate/severe interstitial inflammation, and moderate/severe arteriolar hyalinosis than in those having less advanced each lesion. Fine–Gray regression models revealed that global glomerulosclerosis ≥ 50% (subdistribution hazard ratio [SHR]: 3.85; 95% confidence interval [95% CI] 1.28–11.52), moderate/severe interstitial inflammation (SHR: 2.49; 95% CI 1.18–5.29), and moderate/severe arteriolar hyalinosis (SHR: 3.51; 95% CI 1.15–10.69) were linked to increased risk of cardiovascular events, after adjusting for clinical variables including RAAS inhibitors use at baseline. Adding the severity of these lesions to clinical variables improved the predictive value for cardiovascular events. Conclusions In DKD with type 2 diabetes, advanced glomerulosclerosis, interstitial inflammation, and arteriolar hyalinosis were associated with cardiovascular events, adding predictive value to clinical features.

Introduction The number of patients with end stage kidney disease (ESKD) are increasing world-side. While interstitial fibrosis (IF) is a common step for the progression to ESKD, therapeutic options for IF is still limited in clinical settings. We have reported that bone marrow-derived fibrotic cell, fibrocyte, is involved in the pathogenesis of kidney fibrosis. Also recent studies revealed that erythropoietin has protective effect on kidney diseases. However, it is unknown whether erythropoietin (EPO) inhibits fibrosis in progressive kidney injury. Therefore, we explored the impacts of EPO on kidney fibrosis with focusing on fibrocyte. Method Fibrocyte was differentiated from peripheral mononuclear cells of healthy donor. Fibrocyte was stimulated with transforming growth factor beta (TGF) - β with/without EPO treatment. Moreover, the therapeutic effect of EPO was evaluated in murine unilateral ureteral obstruction (UUO) model. Result TGF-β stimulation increased the expression of COL1 mRNA in fibrocyte. EPO signal reduced the expression of COL1 mRNA in dose dependent manner. EPO reduced mitochondrial oxidative stress and ameliorated mitochondrial membrane depolarization induced by TGF-β stimulation. Moreover, EPO reduced the mRNA expression of mitochondria related molecules, TRAF6 , in fibrocyte. In addition, the count of CD45+/αSMA + double-positive fibrocyte was decreased in the EPO-administered UUO kidneys. Conclusion EPO signals function to prevent kidney fibrosis, particularly in fibrocyte. Regulating the renal accumulation of fibrocyte is a part of the anti-fibrotic functions of EPO.

Loss of Kif26b function causes renal agenesis or hypoplasia in mice, and a KIF26B mutation resulting in deletion of the C‐terminal region has been identified in a human patient with a congenital kidney disorder. However, the role of this region during kidney development is unclear; thus, to investigate this, we generated mice lacking the C‐terminal region of KIF26B (Kif26b‐C) using CRISPR/Cas9. Homozygous Kif26b‐C mice showed bilateral renal agenesis, resembling Kif26b knockout mice. Histological analysis revealed loss of the nephrogenic zone and impaired nephron progenitor condensation at embryonic day 18.5. In situ hybridization showed reduced Gdnf in the metanephric mesenchyme and reduced Wnt11 in ureteric buds, indicating disruption of the Gdnf‐Wnt11 signaling loop. These findings suggest a key role for the KIF26B C‐terminal region in kidney morphogenesis.

Background Oxidative stress (OS) plays an important role in the progression of chronic liver disease and hepatocarcinogenesis. However, the role of OS in the progression of hepatocellular carcinoma (HCC) is unclear. The aim of this study was to assess whether OS promotes angiogenesis in HCC. Methods The expressions of vascular endothelial growth factor (VEGF), VEGF receptor2 (VEGFR2), and phosphorylated Akt were assessed, and microvessel density (MVD) and the cancer-associated fibroblast (CAF) population were examined by immunohistological staining in 55 HCC samples. The OS level in these tissues was assessed using 8-hydroxy-2′-deoxyguanosine (8-OHdG) and 4-hydroxy-2-nonenal (4-HNE) immunostaining, and an 8-OHdG enzyme-linked immunosorbent assay (ELISA). The expression and activation of angiogenic factors and the effect of growth stimulation of human umbilical vein endothelial cells (HUVECs) were also assessed in vitro, using HLE hepatoma-derived cells and conditioned medium with or without treatment with hydrogen peroxide (H 2 O 2 ); a phosphoinositide 3-kinase (PI3K) inhibitor, wortmannin ; and an anti-oxidative agent, N -acetyl- l -cysteine (NAC). Results A higher OS grade was significantly associated with higher MVD, VEGF expression, Akt activity , and OS grade of CAFs, but not with the percentage of the CAFpopulation in HCC tissues. Additionally, cancer cells constituted a major population of OS marker-positive cells in HCC tissues. In vitro, H 2 O 2 treatment induced up-regulation of VEGF at both the mRNA and protein levels, activated Akt, and resulted in the proliferation of HUVECs; the addition of wortmannin and NAC counteracted the effects of OS. Conclusions OS enhances the malignant potential of HCC through the stimulation of angiogenesis by activation of the Akt-VEGF pathway.

Hexagonal YMnO3 has a ferroelectric property with an optimal remanent polarization along the c-axis. The c-axis oriented YMnO3 thin films with a small leakage current were prepared by the sol-gel dipping method. The c-axis orientation of the films was promoted by the addition of diethanolamine to the Mn precursor solution. A heat treatment with multiple steps led to a dense film structure with fine grains. The dense structure resulted in the decrease of the leakage current. Furthermore, when the films were heat-treated in a vacuum, the leakage current became considerably small and the ferroelectricity of the YMnO3 thin films was observed even at room temperature.

Thin films of YMnO3 are proposed as a new candidate for non-volatile ferroelectric memory devices. They were prepared via solutions through two different processes: thermal decomposition and reflux using yttrium acetate tetrahydrate and manganese acetate tetrahydrate as starting materials. For coatings prepared by thermal decomposition process, the starting materials were dissolved in ethanol containing diethanolamine, and single phase YMnO3 was obtained with heat-treatment at 900°C. When the starting materials were refluxed using 2-ethoxyethanol as a solvent, single phase YMnO3 was obtained with heat-treatment at 800°C. Scanning electron microscopy showed that the 300 nm thick films with a stoichiometric Y/Mn ratio had many pinholes, and a very large dielectric loss, 0.83 at 100 kHz. Inclusion of 5–10% excess of Y in the coating solution produced dense structures with improved dielectric properties. The dielectric constant and loss tangent of the thin films with Y/Mn ratio of 1.00/0.90 were about 20 and 0.05 at 100 kHz, respectively.