title: A perspective on chronic kidney disease progression.
abstract: 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.
authors.affiliation: Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee.|Division of Pediatric Nephrology, Vanderbilt University Medical Center, Nashville, Tennessee; and.
authors.forename: Jianyong
authors.initials: J
authors.lastname: Zhong
authors.affiliation: Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee.|Division of Pediatric Nephrology, Vanderbilt University Medical Center, Nashville, Tennessee; and.
authors.forename: Hai-Chun
authors.identifier: 0000-0003-4265-7492
authors.initials: HC
authors.lastname: Yang
authors.affiliation: Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee; agnes.fogo@vanderbilt.edu.|Division of Pediatric Nephrology, Vanderbilt University Medical Center, Nashville, Tennessee; and.|Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
authors.forename: Agnes B
authors.initials: AB
authors.lastname: Fogo
mesh_terms: D058186:Acute Kidney Injury / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control; D000818:Animals; D018450:Disease Progression; D044127:Epigenesis, Genetic; D005819:Genetic Markers; D020022:Genetic Predisposition to Disease; D005919:Glomerular Filtration Rate; D006801:Humans; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D010641:Phenotype; D011507:Proteinuria / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control; D051436:Renal Insufficiency, Chronic / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D012084:Renin-Angiotensin System; D012307:Risk Factors; D064804:Urological Agents / Q000009:adverse effects / Q000627:therapeutic use*
chemical_list: D005819:Genetic Markers; D064804:Urological Agents
keywords: acute kidney injury; genomic; regenerative therapy; surrogate marker