Abstract
Diabetic kidney disease (DKD) is the leading cause of chronic kidney disease and end-stage renal disease. The natural history of DKD includes glomerular hyperfiltration, progressive albuminuria, declining estimated glomerular filtration rate, and, ultimately, kidney failure. It is known that DKD is associated with metabolic changes caused by hyperglycemia, resulting in glomerular hypertrophy, glomerulosclerosis, and tubulointerstitial inflammation and fibrosis. Hyperglycemia is also known to cause programmed epigenetic modification. However, the detailed mechanisms involved in the onset and progression of DKD remain elusive. In this review, we discuss recent advances regarding the pathogenic mechanisms involved in DKD.
Highlights
Diabetes Mellitus and Diabetic Kidney DiseaseMore than 400 million people live with diabetes mellitus (DM) globally
Kidney and Diabetic Complications Research Team (KDCRT), Chang Gung Memorial Hospital, School of Traditional Chinese Medicine, College of Medicine, Chang Gung University, Kidney Research Center, Chang Gung Memorial Hospital, Taoyuan 333423, Taiwan
Such excess reactive oxygen species (ROS) production is known to cause DNA damage [21], and this in turn induces poly-ADP ribose polymerase-1 (PARP-1) activation to inhibit glyceraldehyde 3-phosphate dehydrogenase (G3PDH) function [22,23], which results in the accumulation of glycolytic metabolites
Summary
More than 400 million people live with diabetes mellitus (DM) globally. This number is expected to increase to 600 million by 2035 [1]. Among DM patients, 20% may progress to diabetic kidney disease (DKD) [3], which is known to be influenced by both genetic and environmental factors and induced by microvascular and macrovascular changes, including accumulation of extracellular matrix and hypertrophy and fibrosis of the kidney glomeruli and interstitium [4,5]. DKD patients typically show microalbuminuria symptoms, with 30 to 300 mg of albumin excreted per day; this gradually develops into macroalbuminuria, with more than 300 mg of albumin excreted per day at later disease stages [6]. Endothelin-1 (ET-1) has been associated with vasoconstriction, kidney injury, mesangial hyperplasia, glomerulosclerosis, fibrosis, and inflammation, and endothelin receptor antagonists have been proposed as potential treatments for DKD [10]
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