Viewing Study NCT06031389



Ignite Creation Date: 2024-05-06 @ 7:30 PM
Last Modification Date: 2024-10-26 @ 3:08 PM
Study NCT ID: NCT06031389
Status: NOT_YET_RECRUITING
Last Update Posted: 2023-09-11
First Post: 2023-07-29

Brief Title: Henagliflozin Delays the Progress of Diabetic Nephropathy Via Regulates Gut-Renal Axis
Sponsor: Qianfoshan Hospital
Organization: Qianfoshan Hospital

Study Overview

Official Title: Henagliflozin Delays the Progress of Diabetic Nephropathy Via Regulates Gut-Renal Axis
Status: NOT_YET_RECRUITING
Status Verified Date: 2023-09
Last Known Status: None
Delayed Posting: No
If Stopped, Why?: Not Stopped
Has Expanded Access: False
If Expanded Access, NCT#: N/A
Has Expanded Access, NCT# Status: N/A
Acronym: None
Brief Summary: 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 FirmicutesBacteroides 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 FirmicutesBacteroides 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
Detailed Description: None

Study Oversight

Has Oversight DMC: None
Is a FDA Regulated Drug?: False
Is a FDA Regulated Device?: False
Is an Unapproved Device?: None
Is a PPSD?: None
Is a US Export?: False
Is an FDA AA801 Violation?: None