Recent Advances in Diabetic Kidney Diseases: From Kidney Injury to Kidney Fibrosis

• Published in: International journal of molecular sciences Vol. 22; no. 21; p. 11857
• Main Authors: Hung, Peir-Haur, Hsu, Yung-Chien, Chen, Tsung-Hsien, Lin, Chun-Liang
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 01.11.2021; MDPI
• Subjects: Angiogenesis; Apoptosis; Cytokines; Dehydrogenases; Diabetes; Diabetic Nephropathies - complications; Diabetic Nephropathies - genetics; Diabetic Nephropathies - physiopathology; Diabetic nephropathy; Extracellular matrix; Fibroblasts; Gene Regulatory Networks; Glomerular Filtration Rate; Glucose; Humans; Hyperglycemia; Hypertension; Inflammation; Kidney diseases; Kidney Failure, Chronic - etiology; Kidney Failure, Chronic - genetics; Kidney Failure, Chronic - physiopathology; Kinases; Metabolism; Metabolites; Nitric oxide; Oxidative stress; Proteins; Review; Signal transduction; Tumor necrosis factor-TNF; diabetic kidney disease; albuminuria; fibrosis; glomerulosclerosis; inflammation
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms222111857

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.