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Publication Information
Affiliation
Division of Nephrology, University of California San Francisco, San Francisco, California.; Division of Biostatistics, University of Pennsylvania, Philadelphia, Pennsylvania.; Division of Renal Medicine, Brigham and women's Hospital and Harvard Medical School, Boston, Massachusetts.; Division of Nephrology, Johns Hopkins University, Baltimore, Maryland.; Division of Research, Kaiser Permanente Northern California, Oakland, California.; Division of Nephrology, University of California San Francisco, San Francisco, California.; Division of Nephrology, University of Illinois, Chicago, Illinois.; Division of Nephrology, Northwestern University, Chicago, Illinois.; Division of Nephrology and Hypertension, Center for Translational Metabolism and Health, Institute for Public Health and Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois.; Department of Epidemiology, Tulane University, New Orleans, Louisiana.; Department of Epidemiology, Tulane University, New Orleans, Louisiana.; Division of Nephrology, University of Michigan, Ann Arbor, Michigan.; Division of Nephrology, University of California San Francisco, San Francisco, California.
Authors
McCoy Ian E., Hsu Jesse Y., Bonventre Joseph V., Parikh Chirag R., Go Alan S., Liu Kathleen D., Ricardo Ana C., Srivastava Anand, Cohen Debbie L., He Jiang, Chen Jing, Rao Panduranga S., Hsu Chi-yuan, Appel Lawrence J., Feldman Harold J., Lash James P., Nelson Robert G., Rahman Mahboob, Shah Vallabh O., Unruh Mark L.
Studies
Abstract
Levels of TNF receptors 1 and 2 (TNFR1 and TNFR2) and kidney injury molecule 1 (KIM-1) vary considerably among patients with CKD; those with higher levels have faster subsequent disease progression. The reasons why some individuals have higher levels of biomarkers of inflammation and injury are unknown. In this observational cohort study, the authors investigated whether these higher biomarker levels reflect effects of prior episodes of AKI. They found that levels of TNFR1, TNFR2, and KIM-1 in banked plasma samples increased after AKI, and these elevations persist for months, a longer timeframe than examined in prior studies. These findings may provide insight into the pathophysiology of kidney disease progression and the potential role of AKI episodes punctuating the course of CKD.