Elevated lipoxygenase and cytochrome P450 products predict progression of chronic kidney disease.

Szczegóły
Abstrakt

Tytuł:: Elevated lipoxygenase and cytochrome P450 products predict progression of chronic kidney disease.
Autorzy:: Afshinnia F; Department of Internal Medicine-Nephrology, University of Michigan, Ann Arbor, MI, USA.
Zeng L; Department of Internal Medicine-Nephrology, University of Michigan, Ann Arbor, MI, USA.
Byun J; Department of Internal Medicine-Nephrology, University of Michigan, Ann Arbor, MI, USA.
Wernisch S; Department of Internal Medicine-Nephrology, University of Michigan, Ann Arbor, MI, USA.
Deo R; Division of Cardiovascular Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Chen J; Division of Nephrology and Hypertension, Tulane University, New Orleans, LA, USA.
Hamm L; Division of Nephrology and Hypertension, Tulane University, New Orleans, LA, USA.
Miller ER; Department of Internal Medicine, Jones Hopkins University, Baltimore, MD, USA.
Rhee EP; Department of Internal Medicine, Massachusetts General Hospital, Boston, MA, USA.
Fischer MJ; Department of Medicine, University of Illinois, Center of Innovation for Complex Chronic Healthcare, Jesse Brown VAMC, Chicago, IL, USA.
Sharma K; Department of Internal Medicine-Nephrology, University of Texas Health San Antonio, San Antonio, TX, USA.
Feldman HI; Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania, Philadelphia, PA, USA.
Michailidis G; Department of Statistics, University of Florida, Gainesville, FL, USA.
Pennathur S; Department of Internal Medicine-Nephrology, University of Michigan, Ann Arbor, MI, USA.; Michigan Regional Comprehensive Metabolomics Resource Core, University of Michigan, Ann Arbor, MI, USA.; Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA.
Corporate Authors:: CRIC Study Investigators
Źródło:: Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association [Nephrol Dial Transplant] 2020 Feb 01; Vol. 35 (2), pp. 303-312.
Typ publikacji:: Journal Article; Research Support, N.I.H., Extramural
Język:: English
Imprint Name(s):: Publication: Oxford : Oxford University Press
Original Publication: [Berlin ; New York, NY] : Springer International, [c1986-
MeSH Terms:: Cytochrome P-450 Enzyme System/*metabolism
Hydroxyeicosatetraenoic Acids/*metabolism
Kidney Failure, Chronic/*diagnosis
Lipoxygenase/*metabolism
Renal Insufficiency, Chronic/*complications
Case-Control Studies ; Cohort Studies ; Disease Progression ; Female ; Humans ; Kidney Failure, Chronic/etiology ; Kidney Failure, Chronic/metabolism ; Male ; Middle Aged
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Grant Information:: R01 DK072231 United States DK NIDDK NIH HHS; UL1 TR002548 United States TR NCATS NIH HHS; U01 DK060963 United States DK NIDDK NIH HHS; P30 DK089503 United States DK NIDDK NIH HHS; U01 DK061022 United States DK NIDDK NIH HHS; UL1 TR000003 United States TR NCATS NIH HHS; UL1 TR000439 United States TR NCATS NIH HHS; U01 DK060990 United States DK NIDDK NIH HHS; P30 DK020572 United States DK NIDDK NIH HHS; K08 DK106523 United States DK NIDDK NIH HHS; UL1 RR029879 United States RR NCRR NIH HHS; U01 DK061028 United States DK NIDDK NIH HHS; UL1 TR000433 United States TR NCATS NIH HHS; U01 DK060984 United States DK NIDDK NIH HHS; U01 DK061021 United States DK NIDDK NIH HHS; U24 DK060990 United States DK NIDDK NIH HHS; U01 DK060980 United States DK NIDDK NIH HHS; UL1 RR024131 United States RR NCRR NIH HHS; R24 DK082841 United States DK NIDDK NIH HHS; U54 GM104940 United States GM NIGMS NIH HHS; M01 RR013987 United States RR NCRR NIH HHS; UL1 TR000424 United States TR NCATS NIH HHS; M01 RR016500 United States RR NCRR NIH HHS; P20 GM109036 United States GM NIGMS NIH HHS; U01 DK060902 United States DK NIDDK NIH HHS; UL1 TR002003 United States TR NCATS NIH HHS; P30 DK081943 United States DK NIDDK NIH HHS; U24 DK097153 United States DK NIDDK NIH HHS
Contributed Indexing:: Investigator: LJ Appel; AS Go; J He; JW Kusek; JP Lash; PS Rao; M Rahman; RR Townsend
Keywords: CKD; cardiovascular; heart failure; progression; prostaglandins
Substance Nomenclature:: 0 (Hydroxyeicosatetraenoic Acids)
79551-86-3 (20-hydroxy-5,8,11,14-eicosatetraenoic acid)
9035-51-2 (Cytochrome P-450 Enzyme System)
EC 1.13.11.12 (Lipoxygenase)
Entry Date(s):: Date Created: 20180824 Date Completed: 20200910 Latest Revision: 20211009
Update Code:: 20240105
PubMed Central ID:: PMC7391277
DOI:: 10.1093/ndt/gfy232
PMID:: 30137494
: Czasopismo naukowe

Background: The clinical relevance of arachidonic acid (AA) metabolites in chronic kidney disease (CKD) progression is poorly understood. We aimed to compare the concentrations of 85 enzymatic pathway products of AA metabolism in patients with CKD who progressed to end-stage kidney disease (ESKD) versus patients who did not in a subcohort of Chronic Renal Insufficiency Cohort (CRIC) and to estimate the risk of CKD progression and major cardiovascular events by levels of AA metabolites and their link to enzymatic metabolic pathways.
Methods: A total 123 patients in the CRIC study who progressed to ESKD were frequency matched with 177 nonprogressors and serum eicosanoids were quantified by mass spectrometry. We applied serum collected at patients' Year 1 visit and outcome of progression to ESKD was ascertained over the next 10 years. We used logistic regression models for risk estimation.
Results: Baseline 15-hydroxyeicosatetraenoate (HETE) and 20-HETE levels were significantly elevated in progressors (false discovery rate Q ≤ 0.026). The median 20-HETE level was 7.6 pmol/mL [interquartile range (IQR) 4.2-14.5] in progressors and 5.4 pmol/mL (IQR 2.8-9.4) in nonprogressors (P < 0.001). In an adjusted model, only 20-HETE independently predicted CKD progression. Each 1 standard deviation increase in 20-HETE was independently associated with 1.45-fold higher odds of progression (95% confidence interval 1.07-1.95; P = 0.017). Principal components of lipoxygenase (LOX) and cytochrome P450 (CYP450) pathways were independently associated with CKD progression.
Conclusions: We found higher odds of CKD progression associated with higher 20-HETE, LOX and CYP450 metabolic pathways. These alterations precede CKD progression and may serve as targets for interventions aimed at halting progression.
(© The Author(s) 2018. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.)

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