Abstract
The major clinical associations with the progression of diabetic kidney disease (DKD) are glycemic control and systemic hypertension. Recent studies have continued to emphasize vasoactive hormone pathways including aldosterone and endothelin which suggest a key role for vasoconstrictor pathways in promoting renal damage in diabetes. The role of glucose per se remains difficult to define in DKD but appears to involve key intermediates including reactive oxygen species (ROS) and dicarbonyls such as methylglyoxal which activate intracellular pathways to promote fibrosis and inflammation in the kidney. Recent studies have identified a novel molecular interaction between hemodynamic and metabolic pathways which could lead to new treatments for DKD. This should lead to a further improvement in the outlook of DKD building on positive results from RAAS blockade and more recently newer classes of glucose-lowering agents such as SGLT2 inhibitors and GLP1 receptor agonists.
Highlights
Diabetes mellitus, commonly referred to as diabetes, is clinically characterized by hyperglycemia due to insulin insufficiency arising from a lack of insulin production or insulin insensitivity [1]
Important biological roles have been discovered for other components of the Renin-Angiotensin-Aldosterone System (RAAS), including metabolites of Angiotensin II, Ang (1-7) and Ang (1-9) and enzymes involved in angiotensin II (Ang II) synthesis and degradation, ACE2 and neprilysin [15]
This hypothesis was supported by the study from Ye and colleagues, which showed that mice infused with an ACE2 antagonist developed albuminuria and glomerulosclerosis [44]
Summary
Commonly referred to as diabetes, is clinically characterized by hyperglycemia due to insulin insufficiency arising from a lack of insulin production or insulin insensitivity [1]. These complications are wide-ranging and are mainly caused because of chronic elevation of blood glucose levels. Underlying vascular injury causing organ and tissue damage results in diabetic complications. These complications include neuropathy (neural damage), retinopathy (eye disease) and nephropathy (kidney disease) [2]. More commonly known as diabetic kidney disease (DKD), remains a major cause of morbidity and mortality in both type 1 diabetes (T1D) and type 2 diabetes (T2D). It is evident that hemodynamic and metabolic pathways interact to promote the development of DKD [3], as reflected by the clinical associations of systemic blood pressure and glycemic control with DKD.
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