Diabetic Nephropathies Clinical Trial
Official title:
Henagliflozin Delays the Progress of Diabetic Nephropathy Via Regulates Gut-Renal Axis
Diabetic kidney disease (DKD) is a serious complication of diabetes, and it is also the leading cause of end-stage renal disease (ESRD) in the world. The aggravation of progressive proteinuria and the decrease of glomerular filtration rate are the important reasons for the development of DKD into ESRD. It is an important task in the medical field to delay the development of DKD into ESRD. In recent years, gut microbiota disorder has been considered as an important influencing factor of DKD, and the concept of gut-renal axis has attracted more and more attention. The disorder of gut microbiota in DKD patients is mainly manifested by the decrease in the abundance of probiotics such as Lactobacillus, Bifidobacterium and Akkermansia, which produce short-chain fatty acids (SCFA), and the increase in the abundance of uremic toxin-producing bacteria such as Ruminococcus, Alistipes and Subdoligranulum. Improving gut microbiota disorder and increasing the concentration of beneficial metabolites such as SCFA in serum have positive effects on improving DKD. In recent years, with the application of sodium-glucose cotransporter 2 inhibitors (SGLT-2i), diabetes has been effectively treated. SGLT-2i can reduce blood glucose concentration by inhibiting renal tubular glucose reabsorption, and at the same time, it can play a renal protection role independent of blood glucose reduction by correcting the unbalanced tubuloglomerular feedback during diabetes and improving inflammation. However, the mechanism of its renal protection seems to be more than that. Studies have shown that SGLT-2i can reduce proteinuria in DKD mice by regulating the disordered gut microbiota during DKD, but not all SGLT-2i preparations have the effect of protecting target organs by regulating gut microbiota. Wang found that canagliflozin can regulate the gut microbiota of diabetes mice and improve cardiovascular complications; Lee reported that dapagliflozin could reduce the ratio of Firmicutes/Bacteroides in DKD mice and increase the abundance of Akkermansia. Yang found that dapagliflozin increased the abundance of Proteobacteria in diabetes rats, but it did not seem to affect the ratio of Firmicutes/Bacteroides. Van Bommel reported that dapagliflozin would not affect the gut microbiot of diabetes patients. Whether henagliflozin can improve DKD by regulating the gut-renal axis is worthy of further study.
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