Extracellular vesicle-packaged ILK from mesothelial cells promotes fibroblast activation in peritoneal fibrosis.

Progressive peritoneal fibrosis and the loss of peritoneal function often emerged in patients undergoing long-term peritoneal dialysis (PD), resulting in PD therapy failure. Varieties of cell-cell communications among peritoneal cells play a significant role in peritoneal fibrogenesis. Extracellular vesicles (EVs) have been confirmed to involve in intercellular communication by transmitting proteins, nucleic acids or lipids.

Polarization-dependent phase-modulation metasurface for vortex beam (de)multiplexing.

Vortex beams (VBs) carrying orbital angular momentum (OAM) have shown promising potential in enhancing communication capacity through the possession of multiple multiplexing dimensions involving the OAM mode, polarization, and wavelength. Although many research works on multidimensional multiplexing have been conducted, the (de)multiplexer compatible with these dimensions remains elusive. Following the expanded concept of the Pancharatnam-Berry (PB) phase, we designed a polarization-dependent phase-modulation metasurface to phase-modulate the two orthogonal linearly polarized components of light, and two Dammann vortex gratings with orthogonal polarization responses were loaded to simultaneously (de)multiplex OAM mode and polarization channels.

Proteomic Characterization of Peritoneal Extracellular Vesicles in a Mouse Model of Peritoneal Fibrosis.

Peritoneal fibrosis progression is regarded as a significant cause of the loss of peritoneal function, markedly limiting the application of peritoneal dialysis (PD). However, the pathogenesis of peritoneal fibrosis remains to be elucidated. Tissue-derived extracellular vesicles (EVs) change their molecular cargos to adapt the environment alteration, mediating intercellular communications and play a significant role in organ fibrosis.

Adding/dropping polarization multiplexed cylindrical vector beams with local polarization-matched plasmonic metasurface.

Here we propose a polarization-dependent gradient phase modulation strategy and fabricate a local polarization-matched metasurface to add/drop polarization multiplexed cylindrical vector beams (CVBs). The two orthogonal linear polarization states in CVB multiplexing will represent as radial- and azimuthal-polarized CVBs, which means that we must introduce independent wave vectors to them for adding/dropping the polarization channels. By designing the rotation angle and geometric sizes of a meta-atom, a local polarization-matched propagation phase plasmonic metasurface is constructed, and the polarization-dependent gradient phases were loaded to perform this operation.

SIS3 Alleviates Cisplatin-Induced Acute Kidney Injury by Regulating the LncRNA Arid2-IR-Transferrin Receptor Pathway.

Introduction: TGF-β/Smad3 may be involved in the pathogenesis of acute kidney injury (AKI), but its functional role and mechanism of action in cisplatin-induced AKI are unclear. Here, we established a cisplatin-induced AKI mouse model to demonstrate that Smad3 may have roles in cisplatin nephropathy because of its potential effects on tubular epithelial cell (TEC) death and regeneration.

Methods: Using a cisplatin-induced AKI model, the expression levels of lncRNA Arid2-IR were measured by qRT-PCR and the location detected by FISH.

Sofosbuvir and ledipasvir decreased nephrotic syndrome caused by IgA nephropathy with a membranoproliferative pattern of injury in hepatitis C virus-induced cirrhosis: a case report.

Background: Immunoglobulin (Ig) A nephropathy (IgAN) with a membranoproliferative pattern of injury that manifests as nephrotic syndrome (NS) is rarely reported in hepatitis C virus (HCV)-induced cirrhosis. It is not known whether eradication of HCV by direct-acting antiviral (DAA) drugs can lead to remission of proteinuria and improve the long-term prognosis.

Case Description: We report the case of a 52-year-old woman with HCV cirrhosis for 10 years.

Alteration of N6-Methyladenosine RNA Profiles in Cisplatin-Induced Acute Kidney Injury in Mice.

To identify the alterations of N6-methyladenosine (mA) RNA profiles in cisplatin-induced acute kidney injury (Cis-AKI) in mice. The total level of mA and the expression of methyltransferases and demethylases in the kidneys were measured. The profiles of methylated RNAs were determined by the microarray method.

Expansion of Monocytic Myeloid-Derived Suppressor Cells in Patients Under Hemodialysis Might Lead to Cardiovascular and Cerebrovascular Events.

Background: The specific mechanism of cardiovascular and cerebrovascular vasculopathy in the context of end-stage renal disease has not been elucidated. In the present study, we investigated the clinical impact of myeloid-derived suppressor cells (MDSCs) on hemodialysis patients and their mechanism of action.

Methods: MDSCs were tested among 104 patients undergoing hemodialysis and their association with overall survival (OS) and cardiovascular and cerebrovascular events was determined.

A retrospective cohort study on the pathology and outcomes of type 2 diabetic patients with renal involvement.

Objective: To investigate the association of clinical and histological characteristics and the development of ESRD in T2DM patients with renal involvement.

Methods: We conducted a retrospective analysis of clinical and pathologic data from T2DM patients who underwent renal biopsy (n = 120).

Results: The mean age, duration of diabetes, and eGFR were 50.

Sirt3 modulates fatty acid oxidation and attenuates cisplatin-induced AKI in mice.

Fatty acid oxidation (FAO) dysfunction is one of the important mechanisms of renal fibrosis. Sirtuin 3 (Sirt3) has been confirmed to alleviate acute kidney injury (AKI) by improving mitochondrial function and participate in the regulation of FAO in other disease models. However, it is not clear whether Sirt3 is involved in regulating FAO to improve the prognosis of AKI induced by cisplatin.

The influence of cardiac valvular calcification on all-cause and cardiovascular mortality in maintenance hemodialysis patients.

Objective: To investigate the effect of cardiac valve calcification (CVC) on all-cause and cardiovascular mortality in maintenance hemodialysis (MHD) patients.

Methods: A retrospective cohort study was conducted in 183 long-term hemodialysis patients with complete follow-up data from January 1, 2012, to December 30, 2015. The baseline data between CVC and non-CVC groups were compared.

Low serum uric acid levels increase the risk of all-cause death and cardiovascular death in hemodialysis patients.

Background: Elevated serum uric acid (SUA) is associated with increased cardiovascular (CV) and all-cause mortality risk in the general population, but the impact of UA on mortality in hemodialysis patients is still controversial. The aim of the study was to explore the relationship between SUA and all-cause mortality and CV mortality in hemodialysis patients.

Methods: This retrospective, observational cohort study included 210 HD patients with a mean age of 56.

Circular RNA expression profiles in cisplatin-induced acute kidney injury in mice.

This study was carried out to identify the expression profile and role of circRNAs in cisplatin-induced acute kidney injury (AKI). In this study, an AKI model was established in cisplatin-treated mice, and the expression of circRNAs was profiled by next-generation sequencing. The differential expression levels of selected circRNAs were determined by quantitative real-time polymerase chain reaction.

Advanced glycation end products induce glomerular endothelial cell hyperpermeability by upregulating matrix metalloproteinase activity.

The present study aimed to investigate the effects of advanced glycation end‑products (AGEs) on the permeability of glomerular endothelial cells (GEnCs) and determine whether enhanced permeability was due to degradation of tight junction (TJ) complexes by matrix metalloproteinases (MMPs). Cultured monolayers of GEnCs were exposed to AGEs at different doses and treatment durations in the presence or absence of the organic MMP‑2/9 inhibitor (2R)‑2‑((4‑biphenyl sulfony‑l)amino)‑3‑phenylproprionic acid) (BiPs). Expression of the TJ proteins occludin and claudin‑5 was determined by western blot analysis and immunofluorescence, while the permeability of the GEnCs was measured using transendothelial electrical resistance and by diffusion of 4 kDa fluorescein isothiocyanate (FITC)‑dextran.

High glucose induces activation of the local renin‑angiotensin system in glomerular endothelial cells.

Activation of the intrarenal renin‑angiotensin system (RAS), which has been identified in podocytes and mesangial cells, is a novel mechanism in the progression of diabetic kidney disease (DKD). The present study aimed to identify the local RAS in glomerular endothelial cells (GEnCs). Rat GEnCs were stimulated by culture medium containing 30 mmol/l glucose for 12, 24, 48 and 72 h.

Simvastatin alleviates hyperpermeability of glomerular endothelial cells in early-stage diabetic nephropathy by inhibition of RhoA/ROCK1.

Background: Endothelial dysfunction is an early sign of diabetic cardiovascular disease and may contribute to progressive diabetic nephropathy (DN). There is increasing evidence that dysfunction of the endothelial tight junction is a crucial step in the development of endothelial hyperpermeability, but it is unknown whether this occurs in glomerular endothelial cells (GEnCs) during the progression of DN. We examined tight junction dysfunction of GEnCs during early-stage DN and the potential underlying mechanisms.

Mesangial medium from IgA nephropathy patients induces podocyte epithelial-to-mesenchymal transition through activation of the phosphatidyl inositol-3-kinase/Akt signaling pathway.

Background: Podocyte injury plays an important role in glomerulosclerosis in IgA nephropathy (IgAN). Eepithelial-to-mesenchymal transition (EMT) caused by different factors is the main reason for podocyte damage. This study hypothesized that conditioned mesangial medium may induced EMT process of podocytes and thereby lead to glomerular injury or sclerosis.