Non-linear association of triglyceride-glucose index with cardiovascular and all-cause mortality in T2DM patients with diabetic kidney disease: NHANES 2001-2018 retrospective cohort study.

Background: The triglyceride glucose (TyG) index is a cutting-edge and highly effective marker of insulin resistance, a crucial factor in the development and exacerbation of diabetic kidney disease (DKD). To date, there has been limited research on how the triglyceride-glucose (TyG) index affects the outlook for patients suffering from DKD.

Methods: In this multicenter retrospective cohort study, the analysis recruited 2,203 DKD patients from the National Health and Nutrition Examination Survey (NHANES) dataset, which covers the US from 2001 to 2018.

Separating the effects of life course adiposity on diabetic nephropathy: a comprehensive multivariable Mendelian randomization study.

Aims: Previous Mendelian randomization (MR) of obesity and diabetic nephropathy (DN) risk used small sample sizes or focused on a single adiposity metric. We explored the independent causal connection between obesity-related factors and DN risk using the most extensive GWAS summary data available, considering the distribution of adiposity across childhood and adulthood.

Methods: To evaluate the overall effect of each obesity-related exposure on DN (Ncase = 3,676, Ncontrol = 283,456), a two-sample univariate MR (UVMR) analysis was performed.

Preliminary study on 24p3 / neutrophil gelatinase-associated lipocalin (NGAL) ferroptosis inhibition in renal tubular epithelial cells.

The 24p3/neutrophil gelatinase-associated lipocalin (NGAL) protein plays an important protective role in acute kidney injury (AKI), but the exact mechanism remains unclear. Therefore, we have made a preliminary exploration of its mechanism. The experimental group was formed by constructing and transfecting 24P3 overexpressed plasmid into renal tubular epithelial cells.

A case report of mitochondrial myopathy with membranous nephropathy.

Background: MtDNA 3243 A > G mutation leads to mitochondrial myopathies with predominant hyperlactatemia. Given the ubiquitous nature of mitochondria, cellular dysfunction can also appear in tissues with high metabolic turnover; thus, there can be cardiac, digestive, ophthalmologic, and kidney complications. MtDNA 3243 A > G mutation has been shown to be with renal involvement in the previous cases of which are FSGS and tubularinterstitial nephritis.

NLRP3 associated with chronic kidney disease progression after ischemia/reperfusion-induced acute kidney injury.

Nod-like receptor protein 3 (NLRP3), as an inflammatory regulator, has been implicated in acute kidney injury (AKI). Failed recovery after AKI can lead to chronic kidney disease (CKD). However, the role of NLRP3 in the AKI-CKD transition is still unknown.

[Effect of Jiedu Limai decoction in septic patients with syndrome of heat-toxin exuberance].

Objective: To investigate the clinical effect of Jiedu Limai decoction in septic patients with syndrome of heat-toxin exuberance.

Methods: A prospective randomized controlled trial was conducted. From March 2019 to April 2020, septic patients with syndrome of heat-toxin exuberance admitted to intensive care unit (ICU) of Shanghai General Hospital and Songjiang Branch of Shanghai General Hospital were enrolled as the research objects, and they were divided into routine treatment group and Jiedu Limai decoction group by the random number table method.

Protective effect of taraxasterol on ischemia/reperfusion-induced acute kidney injury via inhibition of oxidative stress, inflammation, and apoptosis.

Ischemia/reperfusion injury (IRI), the most common cause of acute kidney injury (AKI), is correlated with oxidative stress and subsequent inflammation. Taraxasterol, a natural product, has been shown to exert anti-oxidative and anti-inflammatory effects. However, the role of taraxasterol in renal IRI remains unknown.

Pharmacological inhibition of autophagy by 3-MA attenuates hyperuricemic nephropathy.

Autophagy has been identified as a cellular process of bulk degradation of cytoplasmic components and its persistent activation is critically involved in the renal damage induced by ureteral obstruction. However, the role and underlying mechanisms of autophagy in hyperuricemic nephropathy (HN) remain unknown. In the present study, we observed that inhibition of autophagy by 3-methyladenine (3-MA) abolished uric acid-induced differentiation of renal fibroblasts to myofibroblasts and activation of transforming growth factor-β1 (TGF-β1), epidermal growth factor receptor (EGFR), and Wnt signaling pathways in cultured renal interstitial fibroblasts.

Phosphate stimulates myotube atrophy through autophagy activation: evidence of hyperphosphatemia contributing to skeletal muscle wasting in chronic kidney disease.

Background: Accelerated muscle atrophy is associated with a three-fold increase in mortality in chronic kidney disease (CKD) patients. It is suggested that hyperphosphatemia might contribute to muscle wasting, but the underlying mechanisms remain unclear. Although evidence indicates that autophagy is involved in the maintenance of muscle homeostasis, it is not known if high phosphate levels can result in activation of autophagy, leading to muscle protein loss.

Methylglyoxal and advanced glycation end-products promote cytokines expression in peritoneal mesothelial cells via MAPK signaling.

Background: Peritoneal dialysis fluid degrades glucose into glucose degradation products that impair peritoneal mesothelial cell functions. These compounds are known to interfere with many cellular functions and to promote the formation of advanced glycation end products (AGEs). This study aimed to investigate the biological effects and the underlying mechanism of glucose degradation products and AGEs on mesothelial cells.

HSP70 inhibits high glucose-induced Smad3 activation and attenuates epithelial-to-mesenchymal transition of peritoneal mesothelial cells.

Heat shock proteins (HSPs) are molecular chaperones that were initially identified as proteins expressed following exposure of cells to environmental stress. However, the function of HSPs in epithelial‑to‑mesenchymal transition (EMT) of peritoneal mesothelial cells remains unknown. In the present study, the regulation of HSPs and their function in cell EMT, particularly in rat peritoneal mesothelial cells (RPMCs), and the surrounding glucose concentrations and the molecular mechanism involved were investigated.

[Infection in lupus nephritis: risk factors and significance of immune cell functional assay].

Objective: To explore the risk factors for infection in lupus nephritis (LN) and identify the correlation of ImmuKnow adenosine triphosphate (ATP) value with the development of infections.

Methods: We respectively followed up 96 patients from January 2006 to December 2012 and all infectious episodes were recorded. The amount of ATP produced by CD4(+)T cells was measured by ImmuKnow assay and compared with the results of 27 healthy controls.

[Autophagy-lysosome pathway in skeletal muscle of diabetic nephropathy rats and the effect of low-protein diet plus α-keto acids on it].

Objective: To explore the regulation of autophagy-lysosome pathway (ALP) in skeletal muscle of diabetic nephropathy and examine the effect of low protein diet plus α-keto acid on ALP.

Methods: A total of 45 24-week-old Goto-Kakizaki rats were randomized to receive normal protein (22%) diet (NPD), low-protein (6%) diet (LPD) or low-protein (5%) plus α-keto acids (1%) diet (Keto) (n = 15 each). Wistar control rats had a normal protein diet.

Effect of a low-protein diet supplemented with ketoacids on skeletal muscle atrophy and autophagy in rats with type 2 diabetic nephropathy.

A low-protein diet supplemented with ketoacids maintains nutritional status in patients with diabetic nephropathy. The activation of autophagy has been shown in the skeletal muscle of diabetic and uremic rats. This study aimed to determine whether a low-protein diet supplemented with ketoacids improves muscle atrophy and decreases the increased autophagy observed in rats with type 2 diabetic nephropathy.

[Effect of Notch1 signal on hepatitis B virus X-mediated abnormal immune activity in renal tubular epithelial cells].

Objective: To explore the expression of Notch1 receptor in renal tubular epithelial cells transfected with hepatitis B virus X(HBx) gene and its role in immunologic activity.

Methods: The eukaryotic vector pcDNA3.1/myc-HBx containing HBx gene or vector pcDNA3.

High mobility group box protein-1 correlates with microinflammatory state and nutritional status in continuous ambulatory peritoneal dialysis patients.

High mobility group box protein-1 (HMGB-1) was recently identified as a new type of inflammatory cytokine. Inflammation can lead to malnutrition to some extent. Our study was aimed to clarify the relationship between serum HMGB-1 level with microinflammatory state and nutritional status in continuous ambulatory peritoneal dialysis (CAPD) patients.