Milana Bogorodskaya1, Kathleen V Fitch2, Tricia H Burdo3, Patrick Maehler2, Rebecca M Easly4, Gillian R Murray4, Meghan Feldpausch2, Gail K Adler4, Steven K Grinspoon2, Suman Srinivasa2. 1. Division of Infectious Disease, Beth Israel Deaconess Medical Center and Harvard Medical School, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, Pennsylvania. 2. Program in Nutritional Metabolism, Massachusetts General Hospital and Harvard Medical School, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, Pennsylvania. 3. Department of Neuroscience, Temple University School of Medicine, Philadelphia, Pennsylvania. 4. Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, Pennsylvania.
Abstract
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 α [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. CLINICAL TRIAL REGISTRATION: NCT01407237.
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 α [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. CLINICAL TRIAL REGISTRATION: NCT01407237.
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