Use of SGLT2i in Non-Diabetic Kidney Transplant Recipients.

Background: The potential anti-proteinuric effect of sodium-glucose cotransporter-2 inhibitors (SGLT2i) is of special interest in kidney transplantation. Its benefits have been demonstrated in diabetic kidney transplant recipients (KTRs). We analyzed the efficacy and safety of SGLT2i in non-diabetic KTRs collecting clinical and analytical data at baseline and 6 months after the introduction of the drug.

Predictors of anterior chamber angle status at the time of neovascular glaucoma diagnosis.

Purpose: To identify clinical features which may predict the angle status of a large cohort of NVG eyes at the time of diagnosis.

Observations: Chart review was performed for all NVG eyes from 2010 to 2022. Complete angle closure was defined as having >75 % PAS, partial angle closure as having 1-75 % PAS, and open angles as having 0 % PAS.

Unraveling Diabetic Kidney Disease: The Roles of Mitochondrial Dysfunction and Immunometabolism.

Mitochondria are essential for cellular energy production and are implicated in numerous diseases, including diabetic kidney disease (DKD). Current evidence indicates that mitochondrial dysfunction results in alterations in several metabolic pathways within kidney cells, thereby contributing to the progression of DKD. Furthermore, mitochondrial dysfunction can engender an inflammatory milieu, leading to the activation and recruitment of immune cells to the kidney tissue, potentially perturbing intrarenal metabolism.

Type I IFN induces long-chain acyl-CoA synthetase 1 to generate a phosphatidic acid reservoir for lipotoxic saturated fatty acids.

Long-chain acyl-CoA synthetase 1 (ACSL1) catalyzes the conversion of long-chain fatty acids to acyl-CoAs. ACSL1 is required for β-oxidation in tissues that rely on fatty acids as fuel, but no consensus exists on why ACSL1 is induced by inflammatory mediators in immune cells. We used a comprehensive and unbiased approach to investigate the role of ACSL1 induction by interferon type I (IFN-I) in myeloid cells in vitro and in a mouse model of IFN-I overproduction.

Hyperchylomicronemia causes endothelial cell inflammation and increases atherosclerosis.

The effect of increased triglycerides (TGs) as an independent factor in atherosclerosis development has been contentious, in part, because severe hypertriglyceridemia associates with low levels of low-density lipoprotein cholesterol (LDL-C). To test whether hyperchylomicronemia, in the absence of markedly reduced LDL-C levels, contributes to atherosclerosis, we created mice with induced whole-body lipoprotein lipase (LpL) deficiency combined with LDL receptor (LDLR) deficiency. On an atherogenic Western-type diet (WD), male and female mice with induced global LpL deficiency (i ) and LDLR knockdown ( ) developed hypertriglyceridemia and elevated cholesterol levels; all the increased cholesterol was in chylomicrons or large VLDL.