[Status Quo and Research Progress in Diagnosis and Treatment of Patients With Diabetes Mellitus and Chronic Kidney Disease].

As the incidence of diabetes mellitus is rapidly increasing worldwide,that of related complications,such as diabetic kidney disease(DKD),also increases,conferring a heavy economic burden on the patients,families,society,and government.Diabetes mellitus complicated with chronic kidney disease(CKD)includes DKD and the CKD caused by other reasons.Because of the insufficient knowledge about CKD,the assessment of diabetes mellitus complicated with CKD remains to be improved.

A novel immune-related gene signature for predicting immunotherapy outcomes and survival in clear cell renal cell carcinoma.

Clear cell renal carcinoma (ccRCC) is one of the most common cancers worldwide. In this study, a new model of immune-related genes was developed to predict the overall survival and immunotherapy efficacy in patients with ccRCC. Immune-related genes were obtained from the ImmPort database.

Schistosoma japonicum infection associated with membranous nephropathy: a case report.

Background: Schistosomiasis is one of the most contagious parasitic diseases affecting humans; however, glomerular injury is a rare complication mainly described with Schistosoma mansoni infection. We report a case of membranous nephropathy associated with Schistosoma japonicum infection in a Chinese man.

Case Presentation: A 51-year-old Chinese male with a long history of S.

Involvement of hydrogen sulfide in the progression of renal fibrosis.

Objective: Renal fibrosis is the most common manifestation of chronic kidney disease (CKD). Noting that existing treatments of renal fibrosis only slow disease progression but do not cure it, there is an urgent need to identify novel therapies. Hydrogen sulfide (H2S) is a newly discovered endogenous small gas signaling molecule exerting a wide range of biologic actions in our body.

Fluorofenidone protects against renal fibrosis by inhibiting STAT3 tyrosine phosphorylation.

Signaling through the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway, especially JAK2/STAT3, is involved in renal fibrosis. Fluorofenidone (FD), a novel pyridone agent, exerts anti-fibrotic effects in vitro and in vivo. Herein, we sought to investigate whether FD demonstrates its inhibitory function through preventing JAK2/STAT3 pathway.

Fluorofenidone attenuates oxidative stress and renal fibrosis in obstructive nephropathy via blocking NOX2 (gp91phox) expression and inhibiting ERK/MAPK signaling pathway.

Background/aims: We evaluated the therapeutic effects of fluorofenidone (AKF-PD), a novel pyridone agent, targeting oxidative stress and fibrosis in obstructive nephropathy.

Methods: AKF-PD was used to treat renal interstitial fibrosis in unilateral ureteral obstruction (UUO) obstructive nephropathy in rats. The expression of NOX2 (gp91phox), fibronectin and extracellular signal regulated kinase (ERK) were detected by western blot.

Losartan inhibits LPS + ATP-induced IL-1beta secretion from mouse primary macrophages by suppressing NALP3 inflammasome.

Objectives: IL-1beta is a potent proinflammatory, pro-fibrogenetic and pro-athrosclerosis cytokine which has been shown to play an important role in an expanding number of noninfectious, chronic inflammatory conditions including cardiovascular disease, renal fibrosis, rheumatoid arthritis and even type 2 diabetes. Losartan is an angiotensin II receptor antagonist widely used for the treatment of hypertension, diabetic nephropathy and congestive heart failure. In this study, we attempted to clarify whether losartan has an inhibitory effect on IL-1beta.

Fluorofenidone inhibits nicotinamide adeninedinucleotide phosphate oxidase via PI3K/Akt pathway in the pathogenesis of renal interstitial fibrosis.

Aim: Oxidative stress plays an important role in the progression of renal interstitial fibrosis. The nicotinamide adeninedinucleotide phosphate (NADPH) oxidase (Nox) family is considered one of the major sources of reactive oxygen species (ROS). In the present study, we investigated the inhibitory effects of a novel anti-fibrotic agent, Fluorofenidone (AKF-PD), upon Nox-mediated oxidative stress and deposition of extracellular matrix (ECM) in the development of renalinterstitial fibrosis.

[Discrimination of eleven genera of Chinese herbs in Geraniaceae by FTIR spectroscopy and clustering analysis].

A fast identification method of eleven genera of Chinese herbs in Geraniaceae was developed by the combination of Fourier transform infrared spectroscopy with clustering analysis. FTIR spectroscopy was employed to identify and analyze eleven genera of Chinese herbs in Geraniaceae. On the basis of a principal component analysis (PCA) model, three genera of Chinese herbs were rapidly classified by using the method of SIMCA clustering analysis.

[Analysis and identification of Geranium by two-dimensional correlation infrared spectroscopy].

Tri-step infrared spectroscopy (Fourier transform infrared spectroscopy (FTIR) combined with second derivative spectra and two-dimensional correlation infrared spectroscopy (2D-COS)) was employed to identify and analyze the main components of Heilongjiang (HLJG), Jilin (JLG), Liaoning (LNG) genuine Herba Geranium. The emergence of several characteristic absorption peaks of tannins including 1 730 and 1 337 cm(-1) and peaks around 1 618 and 1 318 cm(-1) belonging to calcium oxalate suggested that Herba Geranii contained tannins and calcium oxalate. Differences near 1 370 and 1 230 cm(-1) were found among the three Herba Geranii.

Fluorofenidone attenuates diabetic nephropathy and kidney fibrosis in db/db mice.

Background/aims: Fluorofenidone [1-(3-fluorophenyl)-5-methyl-2-(1H)-pyridone, AKF-PD], a novel pyridone agent, showed potent antifibrotic properties. The aim of the present study was to investigate the effects of AKF-PD on diabetic nephropathy and kidney fibrosis, and to obtain an insight into its mechanisms of action.

Methods: We administered AKF-PD to diabetic db/db mice for 12 weeks.

Fluorofenidone attenuates renal interstitial fibrosis in the rat model of obstructive nephropathy.

Fluorofenidone (FD) is a novel pyridone agent with significant antifibrotic effects in vitro. The purpose of this study is to investigate the effects of FD on renal interstitial fibrosis in rats with obstructive nephropathy caused by unilateral ureteral obstruction (UUO). With pirfenidone (PD, 500 mg/kg/day) and enalapril (10 mg/kg/day) as the positive treatment controls, the rats in different experimental groups were administered with FD (500 mg/kg/day) from day 4 to day 14 after UUO.

Fluorofenidone inhibits Ang II-induced apoptosis of renal tubular cells through blockage of the Fas/FasL pathway.

Objectives: The present study was designed to investigate the inhibitory effects of fluorofenidone on Ang II-induced apoptosis in renal tubular cells and the related signaling pathway.

Methods: Rat proximal tubular epithelial cells (NRK-52E) were used to examine the anti-apoptosis effects of fluorofenidone. Cell proliferation was assessed by methyl thiazolyl tetrazolium assay.

Fluorofenidone inhibits TGF-beta1 induced CTGF via MAPK pathways in mouse mesangial cells.

Objectives: The development of novel antifibrotic agent candidates for the treatment of diabetic nephropathy. The present study was designed to investigate the potential mechanism of fluorofenidone involving the downregulation of CTGF expression induced by TGF-beta1 and the related signaling pathway in mouse mesangial cells (MMCs).

Methods: Mouse mesangial cells were applied to explore the involvement of MAPK in TGF-beta1 signal pathway to CTGF, and the regulation of fluorofenidone.

Fluorofenidone attenuates collagen I and transforming growth factor-beta1 expression through a nicotinamide adenine dinucleotide phosphate oxidase-dependent way in NRK-52E cells.

Aim: Fluorofenidone (1-(3-fluorophenyl)-5-methyl-2-(1H)-pyridone) is a novel pyridone agent. The aim of the present study is to investigate the effects of fluorofenidone on angiotensin (Ang)II-induced fibrosis and the involved molecular mechanism in rat proximal tubular epithelial cells.

Methods: NRK-52E cells, a rat proximal tubular epithelial cell line, were incubated with medium containing AngII, with or without nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor diphenylene iodonium (DPI), losartan, fluorofenidone (2, 4 and 8 mmol/L) and pirfenidone (8 mmol/L) for 24 h.

[Losartan inhibits high glucose-induced CTGF expression via ERK1/2 MAPK pathways in mouse mesangial cells].

Aim: To investigate the effects and mechanism of losartan on expression of CTGF induced by high glucose.

Methods: Mouse mesangial cells (MMCs) were cultured in vitro, initially, MMCs were stimulated by high glucose(25 mmol/L glucose) for 24 h, 48 h, 72 h, the phosphorylation of ERK1/2 was assessed by Western blot. Then MMCs were randomly divided into 5 groups: (1) Low glucose group (5.