Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 220, Issue 9, Pages 1420-1424Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiz346
Keywords
HIV; renin-angiotensin-aldosterone system; lipocalin 2; inflammation; BNP
Categories
Funding
- National Institutes of Health [R01DK49302, K24 HL103845]
- Harvard KL2/Catalyst Medical Research Investigator Training (cMeRIT) award
- National Center for Research Resources and National Center for Advancing Translational Sciences [UL1 TR000170, UL1 RR025758, UL1 TR001102]
- [P30 DK040561]
- [K23 HL136262]
Ask authors/readers for more resources
Purpose: To evaluate the relationship of lipocalin 2 to inflammation and cardiac injury with increased aldosterone in human immunodeficiency virus (HIV). Methods: A standardized 6-day low-sodium diet was used to stimulate renin-angiotensin-aldosterone system (RAAS) activation, and serum lipocalin 2 and biomarkers of inflammation and cardiac stretch were assessed among persons with or without HIV. Results: Lipocalin 2 levels increased with RAAS activation compared with suppression in the HIV group (median level [interquartile range], 71.3 [59.2-99.7] vs 67.0 [51.8-86.3] ng/mL; P =.01). During RAAS activation, lipocalin 2 was related to biomarkers of inflammation (tumor necrosis factor a [P =.007]), monocyte/macrophage activation (soluble CD163 [P = .005] and chemokine [C-C motif] ligand 2 [P = .03]), and markers of cardiac stretch (brain natriuretic peptide [P <.001] and N-terminal fragment of the prohormone brain natriuretic peptide [P =.001]) in HIV. Conclusion: Lipocalin 2 may be important in modulating aldosterone-induced inflammation, monocyte activation, and cardiac stretch during RAAS activation in HIV.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available