A perspective on chronic kidney disease progression.
Jianyong ZhongHai-Chun YangAgnes B FogoPublished in: American journal of physiology. Renal physiology (2016)
Chronic kidney disease (CKD) will progress to end stage without treatment, but the decline of renal function may not be linear. Compared with glomerular filtration rate and proteinuria, new surrogate markers, such as kidney injury molecule-1, neutrophil gelatinase-associated protein, apolipoprotein A-IV, and soluble urokinase receptor, may allow potential intervention and treatment in the earlier stages of CKD, which could be useful for clinical trials. New omic-based technologies reveal potential new genomic and epigenomic mechanisms that appear different from those causing the initial disease. Various clinical studies also suggest that acute kidney injury is a major risk for progressive CKD. To ameliorate the progression of CKD, the first step is optimizing renin-angiotensin-aldosterone system blockade. New drugs targeting endothelin, transforming growth factor-β, oxidative stress, and inflammatory- and cell-based regenerative therapy may have add-on benefit.
Keyphrases
- chronic kidney disease
- end stage renal disease
- oxidative stress
- transforming growth factor
- acute kidney injury
- clinical trial
- randomized controlled trial
- stem cells
- cell therapy
- single cell
- dna damage
- angiotensin ii
- mesenchymal stem cells
- cardiac surgery
- cancer therapy
- signaling pathway
- drug delivery
- drug induced
- open label
- diabetic rats
- phase ii
- tissue engineering
- placebo controlled