It is possible that novel markers portraying the pathophysiological underpinning processes may be useful.<b>Aim:</b> To investigate the associations between 80 circulating proteins, measured by a proximity extension assay, and prevalent DKD and major adverse cardiovascular events (MACE) in type 2 diabetes.<b>Methods:</b> We randomly divided individuals with type 2 diabetes from three cohorts into a two-thirds discovery and one-third replication set (total <i>n</i> = 813, of whom 231 had DKD defined by estimated glomerular filtration rate <60 mg/mL/1.73 m<sup>2</sup> and/or urinary albumin-creatinine ratio ≥3 g/mol).
Several Nrf2 activators are at various stages of clinical development and are being tested in clinical trials for chronic kidney disease (CKD) including diabetic kidney disease, Alport syndrome, autosomal dominant polycystic kidney disease and focal segmental glomerulosclerosis.
Patients with DN (urinary albumin [UA] >30 mg/g of creatinine) whose estimated glomerular filtration rate (eGFR) was more than 30 mL/min were selected and their plasma renin, parathyroid hormone, serum Vitamin D, serum calcium, serum creatinine, fasting blood sugar were done as baseline measurements.
Astragaloside IV inhibits excessive mesangial cell proliferation and renal fibrosis caused by diabetic nephropathy via modulation of the TGF-β1/Smad/miR-192 signaling pathway.
The six-week low-energy extracorporeal shock wave therapy regimen decreased urinary albumin excretion as well as reduced glomerular hypertrophy and renal fibrosis in the rat model of diabetic nephropathy.
The outcome of interest was DKD defined by estimated glomerular filtration rate (eGFR) values <60/mL/min/1.73 m<sup>2</sup> and/or 24-h albumin excretion >30 mg. Multivariable logistic regression models were employed to estimate odds ratios (ORs) for DKD with 95% confidence intervals (CIs).
These results suggest that H3K27me3 inhibition by TGF-β via dysregulation of related histone-modifying enzymes and miRNAs augments pathological genes mediating glomerular mesangial dysfunction and DN.
In addition, intravenous administration of KLPPR resulted in excellent kidney-targeted distribution and low urinary excretion in mice with streptozocin-induced diabetic nephropathy (DN), lowered the parameters of urea nitrogen, serum creatinine and kidney index, as well as facilitated the recovery of renal physiological function in improving the levels of urinary creatinine and the creatinine clearance rate by suppressing secretion and accumulation of fibronectin and TGF-β1.
To investigate the role of microRNA-130b in 1,25(OH)2D3 mediated improvement of renal fibrosis via transforming growth factor-beta 1 in a rat model of diabetic nephropathy (DN).
Treatment with Gandi capsule (GDC) not only decreased the levels of urinary albumin excretion, but also increased the levels of estimated glomerular filtration rate (eGFR), indicating that it produces a renal protective effect on diabetic nephropathy.
Recent evidence demonstrates that this anti-hyperglycaemic drug exerts renal protective effects, yet the mechanisms remain poorly understood. monocyte chemoattractant protein 1 (MCP-1) has been recognized as a key mediator of renal fibrosis in chronic kidney diseases, including diabetic nephropathy.
The anti-DN benefit of vitamin D can be enhanced when administrated in combination with angiotensin converting enzyme inhibitors or angiotensin II receptor blockers.
Away from conventional tactic, a recent report revealed the renoprotective potential of NEPi and angiotensin-converting enzyme (ACE2) activator combination therapy against diabetic nephropathy.
Sitagliptin may induce HO-1 expression via activation of PI3K and Nrf2 in rats with diabetic nephropathy; HO-1 can improve the oxidative stress of diabetic nephropathy, eventually protect from diabetic nephropathy.
The subjects were stratified into three groups according to classification of DN by urinary albumin to creatinine ratio (ACR) and four groups by estimated glomerular filtration rate (GFR), than analyzed.
Overall, this study showed that thiol-dependent changes in albumin's tertiary structure interfere with the lysosomal proteolysis of renal TBCs, inducing molecular changes associated with interstitial fibrosis and DN progression.
<b>Conclusion:</b> Non-DHP CCBs may be a reasonable therapeutic option for patients with diabetic kidney disease and persistent proteinuria despite maximum doses of ACE inhibitors or ARBs.
The aim of this study was to investigate the expression of MCP-1 under high glucose conditions, as well as the effects of microRNA-192 (miR-192) under these conditions, and to study the regulatory mechanism of MCP-1 in DKD.