Journal
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
Volume 312, Issue 3, Pages F375-F384Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajprenal.00266.2016
Keywords
surrogate marker; genomic; acute kidney injury; regenerative therapy
Categories
Funding
- National Institute of Diabetes and Digestive and Kidney Diseases [DK-56942]
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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-beta,oxidative stress, and inflammatory- and cell-based regenerative therapy may have add-on benefit.
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