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| http://dx.doi.org/10.1093/ndt/gfad004 | DOI Listing |
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Lymphocyte-C-reactive protein ratio upon admission to predict disease progression and ICU admission in adult patients with diabetic ketoacidosis.
Sci Rep
January 2025
Department of Critical Care Medicine, The Sixth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, People's Republic of China.
This study aimed to investigate whether lymphocyte-C-reactive protein ratio (LCR) upon admission can predict disease progression and intensive care unit (ICU) admission in adult patients with diabetic ketoacidosis (DKA). A single-center retrospective study was conducted, including adult DKA patients admitted to the First Affiliated Hospital of Harbin Medical University between March 2018 and March 2023. Multiple demographic and clinical data were collected from the medical records upon admission and during hospitalization.
View Article and Find Full Text PDFThe Case | A rare cause of acute kidney injury and proteinuria.
Kidney Int
February 2025
Department of Pathology and Cell Biology, Columbia University Medical Center, New York, New York, USA.
When two signals cross paths: cGAS-STING and ER stress in kidney disease progression.
Kidney Int
February 2025
Department of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Institute for the Advanced Study of Human Biology, Kyoto University, Kyoto, Japan. Electronic address:
Previous reports have suggested that both the endoplasmic reticulum (ER) stress and cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes pathways contribute to the progression of chronic kidney disease; however, the relationship between these 2 pathways in kidney injury has not been fully elucidated. Andrade-Silva et al. revealed that the cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes pathway can enhance ER stress through the protein kinase R-like ER kinase (PERK)-mediated signaling cascade in kidney tubular epithelial cells and sequentially augment fibrosis during kidney injury.
View Article and Find Full Text PDFHMGB1 encapsulated in podocyte-derived exosomes plays a central role in glomerular endothelial cell injury in lupus nephritis by regulating TRIM27 expression.
Lab Invest
January 2025
Department of Pathology; Center of Metabolic Diseases and Cancer Research, Institute of Medical and Health Science, Hebei Medical University; Key Laboratory of Kidney Diseases of Hebei Province; Shijiazhuang 050017, China. Electronic address:
Exosomes play a role in cell communication by transporting content between cells. Here, we tested whether renal podocyte-derived exosomes affect the injury of glomerular endothelial cells in lupus nephritis (LN). We found that exosomes containing high levels of high mobility group box 1 (HMGB1) were released from podocytes in patients with LN, BALB/c mice injected with pristane (which induces lupus-like disease in mice), and cultured human renal glomerular endothelial cells (HRGECs) treated with LN plasma.
View Article and Find Full Text PDFMetabolic Dysfunction-Associated Steatotic Liver Disease and the Cardiovascular System.
Trends Cardiovasc Med
January 2025
Department of Cardiology, Euroclinic Hospital, Athens, Greece; First Department of Cardiology, Athens University School of Medicine, Athens, Greece. Electronic address:
Metabolic dysfunction-associated steatotic liver disease (MASLD), previously termed nonalcoholic fatty-liver disease, is an important and rising health issue with a link with atherosclerotic cardiovascular (CV) disease (CVD), affecting ∼25-30% of the adults in the general population; in patients with diabetes, its prevalence culminates to ∼70%; its evolutive form, nonalcoholic steatohepatitis, is estimated to be the main cause of liver transplantation in the future. MASLD is a multisystem disease that affects, besides the liver, extra-hepatic organs and regulatory pathways; it raises the risk of type 2 diabetes mellitus (T2D), CVD, and chronic kidney disease; the disease may also progress to hepatocellular carcinoma. Its diagnosis requires hepatic steatosis and at least one cardiometabolic risk factor and the exclusion of both significant alcohol consumption and other competing causes of chronic liver disease.
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