Comparative N-Glycoproteomics Analysis of Clinical Samples Via Different Mass Spectrometry Dissociation Methods.

Site-specific N-glycosylation characterization requires intact N-glycopeptide analysis based on suitable tandem mass spectrometry (MS/MS) method. Electron-transfer/higher-energy collisional dissociation (EThcD), stepped collision energy/higher-energy collisional dissociation (sceHCD), higher-energy collisional dissociation-product-dependent electron-transfer dissociation (HCD-pd-ETD), and a hybrid mass spectrometry fragmentation method EThcD-sceHCD have emerged as valuable approaches for glycoprotein analysis. However, each of them incurs some compromise, necessitating the systematic performance comparisons when applied to the analysis of complex clinical samples (e.

Lipoprotein glomerulopathy resulting from compound heterogeneous mutations of APOE gene: A case report.

Rationale: Lipoprotein glomerulopathy (LPG) is a rare glomerular disease characterized by the deposition of lipoprotein thrombi in glomerular capillaries. The disease is characterized by proteinuria, progressive renal failure, and characteristic lipoprotein thrombosis in glomerular capillaries. Rare mutations in the apolipoprotein E (APOE) gene mainly contribute to disease pathogenesis.

Dimethyl fumarate attenuates LPS induced septic acute kidney injury by suppression of NFκB p65 phosphorylation and macrophage activation.

Septic acute kidney injury (AKI) always accounts for high mortality of septic patients in ICU. Due to its not well understood mechanism for infection and immune-regulation in kidney dysfunction, there is a lack of effective therapy without side effects. Dimethyl fumarate (DMF) as an immunomodulatory molecule has been approved for treatment to multiple sclerosis.

Isoliquiritigenin attenuates septic acute kidney injury by regulating ferritinophagy-mediated ferroptosis.

Defined differently from apoptosis, necrosis, and autophagy, ferroptosis has been implicated in acute kidney injury (AKI) such as ischemia-reperfusion injury induced AKI, folic acid caused AKI and cisplatin induced AKI. However, whether ferroptosis is involved in LPS induced AKI could be remaining unclear and there is still a lack of therapies associated with ferroptosis in LPS induced AKI without side effects. This study aimed to elucidate the role of isoliquiritigenin (ISL) in ferroptosis of LPS-induced AKI.

Causal effects of life course adiposity on chronic kidney disease: a Mendelian randomization study.

Background: Obesity is reported as closely correlated with the development of chronic kidney disease (CKD); however, whether causation exists is unknown, and controversy remains about whether the role of obesity is protective or destructive in CKD. In this study, we attempted to infer the causal relationship between life course adiposity and CKD, to provide a rationale for obesity management in CKD patients.

Methods: A 2-sample Mendelian randomization (MR) analysis was conducted to explore the causal relationship of life course adiposity traits including body mass index (BMI), childhood BMI, body fat percentage (BF%), birth weight (BW), waist circumference, hip circumference, and waist-to-hip ratio (WHR) to CKD.

Predictive markers for severe hypocalcemia in dialysis patients with secondary hyperparathyroidism after near-total parathyroidectomy.

Background: Secondary hyperparathyroidism (SHPT) is common in dialysis patients with end-stage renal disease (ESRD). Parathyroidectomy (PTX) is an effective treatment for SHPT. Postoperative severe hypocalcemia (SH) is a common and severe complication after PTX.

Systems analysis of plasma IgG intact -glycopeptides from patients with chronic kidney diseases EThcD-sceHCD-MS/MS.

Immunoglobulin G (IgG) molecules modulate an immune response. However, site-specific -glycosylation signatures of plasma IgG in patients with chronic kidney disease (CKD) remain unclear. This study aimed to propose a novel method to explore the -glycosylation pattern of IgG and to compare it with reported methods.

Loss of phosphatidylserine flippase β-subunit Tmem30a in podocytes leads to albuminuria and glomerulosclerosis.

The asymmetric distribution of phosphatidylserine (PS) in the cytoplasmic leaflet of eukaryotic cell plasma membranes is regulated by a group of P4-ATPases (named PS flippases) and the β-subunit TMEM30A. Podocytes in the glomerulus form a filtration barrier to prevent the traversing of large cellular elements and macromolecules from the blood into the urinary space. Damage to podocytes can disrupt the filtration barrier and lead to proteinuria and podocytopathy.