Diabetic kidney disease (DKD) is the most common cause of end-stage kidney disease (ESKD) worldwide.
There are multiple pathophysiologic mechanisms responsible for the progression of kidney disease in diabetic patients. These include hyperfiltration theory, renin-angiotensin-aldosterone system (RAAS), advanced glycation end products (AGE), polyol pathway, epithelial-mesenchymal transition, thrombomodulin receptors and metabolic memory due to epigenetic changes. These multiple pathways pave the way to various potential pharmacotherapies. However, until recently RAAS inhibitors were the only group of agents found to be effective in DKD.
In 2019, a new group of oral hypoglycemic agents namely sodium-glucose cotransporter 2 (SGLT2) inhibitors, were found to have both reno and cardio-protective action. In addition, incretin-related drugs like liraglutide and semaglutide showed reno-protective ability.
In 2020, there was a resurgence of aldosterone receptor blockers in DKD with the FIDELIO-DKD trial showing the cardiorenal efficacy of finrenone.
The other potential targets of pharmacotherapy are AGE inhibitors, histone modification inhibitors, prolyl hydroxylase inhibitors and role of combination therapies.
This research topic aims to better understand the complex patho-mechanisms of DKD, novel pharmacotherapies, drug metabolism and transport (in vitro and in vivo) and clinical outcomes of DKD.
This Research Topic welcomes manuscripts of original research, systematic review, review, mini review, hypothesis, clinical trials, theory and perspective that will cover the following topics (but are not limited to):
(1) Novel pathogenic mechanisms in DKD involving animal as well human studies.
(2) Non-diabetic kidney disease in diabetic patients-diagnostic implications and long-term outcomes.
(3) Oral hypoglycemic agents in DKD: pharmacokinetic studies, safety and efficacy.
(4) Novel reno-protective therapies in DKD.
Diabetic kidney disease (DKD) is the most common cause of end-stage kidney disease (ESKD) worldwide.
There are multiple pathophysiologic mechanisms responsible for the progression of kidney disease in diabetic patients. These include hyperfiltration theory, renin-angiotensin-aldosterone system (RAAS), advanced glycation end products (AGE), polyol pathway, epithelial-mesenchymal transition, thrombomodulin receptors and metabolic memory due to epigenetic changes. These multiple pathways pave the way to various potential pharmacotherapies. However, until recently RAAS inhibitors were the only group of agents found to be effective in DKD.
In 2019, a new group of oral hypoglycemic agents namely sodium-glucose cotransporter 2 (SGLT2) inhibitors, were found to have both reno and cardio-protective action. In addition, incretin-related drugs like liraglutide and semaglutide showed reno-protective ability.
In 2020, there was a resurgence of aldosterone receptor blockers in DKD with the FIDELIO-DKD trial showing the cardiorenal efficacy of finrenone.
The other potential targets of pharmacotherapy are AGE inhibitors, histone modification inhibitors, prolyl hydroxylase inhibitors and role of combination therapies.
This research topic aims to better understand the complex patho-mechanisms of DKD, novel pharmacotherapies, drug metabolism and transport (in vitro and in vivo) and clinical outcomes of DKD.
This Research Topic welcomes manuscripts of original research, systematic review, review, mini review, hypothesis, clinical trials, theory and perspective that will cover the following topics (but are not limited to):
(1) Novel pathogenic mechanisms in DKD involving animal as well human studies.
(2) Non-diabetic kidney disease in diabetic patients-diagnostic implications and long-term outcomes.
(3) Oral hypoglycemic agents in DKD: pharmacokinetic studies, safety and efficacy.
(4) Novel reno-protective therapies in DKD.
