An inflammatory cytokine signature predicts IgA nephropathy severity and progression.

IgA nephropathy (IgAN) is the most prevalent primary glomerulonephritis, resulting in end-stage renal disease and increased mortality rates. Prognostic biomarkers reflecting molecular mechanisms for effective IgAN management are urgently needed. Analysis of kidney single-cell transcriptomic sequencing data demonstrated that IgAN expressed high-expression levels of inflammatory cytokines TNFSF10, TNFSF12, CCL2, CXCL1, and CXCL12 than healthy controls (HCs).

Ultrasound molecular imaging for early detection of acute renal ischemia-reperfusion injury.

Background: Microcirculatory perfusion disorder and inflammatory response are critical links in acute kidney injury (AKI). We aim to construct anti-vascular cell adhesion molecule-1(VCAM-1) targeted microbubbles (TM) to monitor renal microcirculatory perfusion and inflammatory response.

Methods: TM carrying VCAM-1 polypeptide was constructed by biological coupling.

Influences of renal anemia on the pathology of IgA nephropathy: a study based on propensity score matching.

Objective: This study aims to investigate the influences of renal anemia on the pathogenesis of IgA nephropathy using propensity score matching (PSM).

Methods: Renal biopsies from 462 patients with IgA nephropathy were enrolled in this study. PSM was used to balance intergroup covariates, and matching results were verified using a dot-plot of standardized mean differences and histograms of the propensity score distribution and distance distribution.

Pericentrin expression in pancreatic β cells is associated impaired glucose tolerance.

Objective: To explore the role and mechanism of pericentrin (PCNT) in impaired glucose tolerance.

Methods: Mouse model of specific PCNT reduction in β-cells (PCNTβPCNT) was built using a Tet-on induction system; mouse model of impaired glucose tolerance was built by high-fat feeding. MIN6 cells were divided into control and Si-PCNT groups.

The role and difference of TLR2 and TLR4 in rhabdomyolysis induced acute kidney injury in mice.

To investigate the role of toll like receptors (TLRs) 2 and 4 in rhabdomyolysis (RM)-related acute kidney injury (AKI). Wild-type (WT) mice and TLR2 knockout (TLR2) or TLR4 knockout (TLR4) mice were injected with either saline (sham) or glycerin (to induce RM-related AKI). Samples were collected for detection of 0 h 24 h (Cr) creatinine, urea nitrogen (BUN), creatine kinase (CK), and PAS staining of renal tissues.

Adenovirus-expressing miR-153-3p alleviates aortic calcification in a rat model with chronic kidney disease.

Background: Patients with chronic kidney disease (CKD) have abnormal calcification in vascular tissue that is a risk factor for cardiovascular disease. However, the specific molecular mechanisms for vascular calcification remain largely unknown. The present study aimed to determine the differentially expressed miRs and the underlying molecular mechanisms of miR-153-3p in vascular calcification induced by adenine.

The renal level of a novel cytokine IL-35 is related to sepsis-associated acute kidney injury in mice.

Interleukin-35 (IL-35) is a novel immunosuppressive and anti-inflammatory cytokine. IL-35 is mainly secreted by regulatory T cells (Tregs), and exerts its effects through inducing proliferation of Tregs and reducing activity of helper T cells Th17. However, the effect of IL-35 on sepsis-associated acute kidney injury (SA-AKI) remains unclear.

Differences in gene expression profiles and signaling pathways in rhabdomyolysis-induced acute kidney injury.

Purpose: Rhabdomyolysis is a threatening syndrome because it causes the breakdown of skeletal muscle. Muscle destruction leads to the release of myoglobin, intracellular proteins, and electrolytes into the circulation. The aim of this study was to investigate the differences in gene expression profiles and signaling pathways upon rhabdomyolysis-induced acute kidney injury (AKI).

Long term effects on mineral and bone metabolism by low versus standard calcium dialysate in peritoneal dialysis: a meta-analysis.

Background: Low calcium dialysate with 1.25 mmol/l calcium concentration has been proposed to replace standard calcium dialysate in peritoneal dialysis patients taking calcium-containing phosphate binder to prevent hypercalcaemia. We conducted a meta-analysis to evaluate long term effects on mineral and bone metabolism by low versus standard calcium dialysate in peritoneal dialysis.