Association of triglyceride glucose-body mass index and left ventricular hypertrophy in patients with IgA nephropathy: a retrospective study.

Introduction: IgA nephropathy (IgAN) is one of the most prevalent forms of glomerulonephritis worldwide, particularly affecting 40-50% of the East Asian population. Cardiovascular mortality represents a leading cause of death in patients with IgAN. Left ventricular hypertrophy (LVH) serves as a predictor of heart failure and cardiovascular mortality.

Analysis of Risk Factors for Otitis Media with Effusion in Children with Adenoid Hypertrophy.

Objective: This study aimed to explore whether children with AH have a higher obesity prevalence and analyze the risk factors for otitis media with effusion(OME) in AH children.

Methods: AH patients aged 3-12 years old that were hospitalized in our hospital for adenoidectomy from June 2020 to September 2022 were included in this study. Height and weight were measured to calculate the body mass index, weight for height and weight z-score to evaluate the development of AH children.

HDAC6-mediated α-tubulin deacetylation suppresses autophagy and enhances motility of podocytes in diabetic nephropathy.

Histone deacetylase 6 (HDAC6) is the specific subtype of HDACs which preferentially located in the cytoplasm, and is crucial in insulin signalling. However, the role of HDAC6 in type 2 diabetic nephropathy (DN) remains undefined. In current study, we observed that HDAC6 was markedly activated in the kidneys of type 2 diabetic patients and db/db mice with albuminuria, along with the advanced glycation end products (AGE)-treated podocytes.

Podocyte-specific knockin of PTEN protects kidney from hyperglycemia.

Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) has proven to be downregulated in podocytes challenged with high glucose (HG), and knockout of PTEN in podocytes aggravated the progression of diabetic kidney disease (DKD). However, whether podocyte-specific knockin of PTEN protects the kidney against hyperglycemia in vivo remains unknown. The inducible podocyte-specific PTEN knockin (PPKI) mice were generated by crossing newly created transgenic loxP-stop- loxP-PTEN mice with podocin-iCreER mice.