Albuminuria is both a characteristic hallmark and a known risk factor for progressive glomerular disease. Although the molecular basis for a potential causative role for albuminuria in progressive chronic kidney disease remains poorly understood, there have been several recent advances in our understanding of the role of albumin, and its molecular modifications, in the development and progression of glomerular disease. This review discusses recent findings related to the ability of albumin and its associated factors to directly induce podocyte and glomerular injury. Additional recent studies confirming the ability and mechanisms by which podocytes endocytose albumin are also discussed. Lastly, we present several known molecular modifications in the albumin molecule itself, as well as substances bound to it, which may be important and potentially clinically relevant mediators of albumin-induced glomerular injury. These recent findings may create entirely new opportunities to develop novel future therapies directed at albumin that could potentially help reduce podocyte and renal tubular injury and slow the progression of chronic glomerular disease.
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http://dx.doi.org/10.1007/s00424-017-2029-4 | DOI Listing |
Ren Fail
December 2025
Center for Cardiac Intensive Care, Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, China.
Background: The incidence of acute kidney injury (AKI) increases after surgical aortic valve replacement (SAVR). This study aimed to characterize the risk factors of AKI after SAVR.
Methods And Results: We conducted a retrospective registry study based on data from 299 consecutive patients undergoing SAVR.
Ren Fail
December 2025
Department of Nephrology, Xiamen Key Laboratory of Precision Diagnosis and Treatment of Chronic Kidney Disease, The Fifth Hospital of Xiamen, Xiamen, Fujian, China.
Adult nephrotic syndrome is primarily caused by membranous nephropathy (MN), with idiopathic membranous nephropathy (IMN) being a prominent subtype. The onset of phospholipase A2 receptor (PLA2R1)-associated IMN is critically linked to M-type PLA2R1 exposure, yet the mechanism underlying glomerular injury remains unclear. In this study, membranous nephropathy datasets (GSE115857, GSE200828) were retrieved from GEO.
View Article and Find Full Text PDFThe maintenance of a healthy epithelial-endothelial juxtaposition requires cross-talk within glomerular cellular niches. We sought to understand the spatially-anchored regulation and transition of endothelial and mesangial cells from health to injury in DKD. From 74 human kidney samples, an integrated multi-omics approach was leveraged to identify cellular niches, cell-cell communication, cell injury trajectories, and regulatory transcription factor (TF) networks in glomerular capillary endothelial (EC-GC) and mesangial cells.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Pediatrics, Faculty of Medicine, Kagawa University, 1750-1 Ikenobe Mikicho, Kidagun, 761-0793, Kagawa, Japan.
Acute kidney injury (AKI) has been reported to occur in 30-70% of asphyxiated neonates. Hydrogen (H) gas became a major research focus in neonatal medicine after the identification of its robust antioxidative properties. However, the ability of H gas to ameliorate AKI is unknown.
View Article and Find Full Text PDFClin Respir J
January 2025
Division of Nephrology, Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Pok Fu Lam, Hong Kong SAR, China.
Introduction: Bronchiectasis exacerbation (BE) is associated with unfavorable sequelae in other organs such as the cardiovascular system; data regarding its impact on adverse term renal outcomes, however, is lacking.
Methods: A territory-wide retrospective cohort study was conducted in Hong Kong between 1/1/1993 and 31/12/2017. All patients with bronchiectasis followed in the public healthcare system in 2017 were classified as "Exacerbators" or "Non-Exacerbators," and their adverse renal outcomes (renal progression [decrease in eGFR by 30 mL/min lasted for more than 12 months during follow up], acute kidney injury [AKI], and annual rate of eGFR decline) in the ensuing 7 years were compared.
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