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Renal Vein Levels of Endothelial Progenitor Cells (EPC) and Inflammatory Biomarkers in Renovascular (RVH) and Essential Hypertensive Patients (EH)
Author(s) -
Eirin Alfonso,
Gloviczki Monika L,
Gossl Mario,
Tang Hui,
Jordan Kyra L,
Lerman Amir,
Textor Stephen C,
Lerman Lilach O
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1030.2
Background Circulating inflammatory biomarkers are elevated in hypertensive patients and contribute to kidney and target organ injury, but their source remains unknown. EPC promote vascular repair and might attenuate target organ injury. We hypothesized that in renal artery stenosis (RAS) the injured kidney produces inflammatory mediators and retains EPC. Methods EH and RAS patients (n=19 each) were studied during chronic renin‐angiotensin system blockade. Single kidney renal blood flow (RBF) was measured by fast CT. Inferior vena cava (IVC) and RV levels of CD34+/KDR+ EPC, soluble E‐Selectin, vascular cell adhesion molecule (sVACM‐1), interleukin (IL‐6), monocyte chemoattractant protein (MCP‐1), and interferon (IF)‐γ were measured in EH and RAS, and their gradient (RV‐IVC) and net production (gradient x RBF) compared to systemic levels in control (n=7) subjects. Results Blood pressure and medications were similar in EH and RAS, but eGFR was lower in RAS. RV levels of sE‐selectin, sVCAM‐1, MCP‐1, IL‐6, IF‐γ were higher in the stenotic kidney vs. normal and EH (p<0.05), and their net production increased vs. EH (p<0.05). EPC showed a negative gradient across the RAS kidney, suggesting EPC retention (Figure). Conclusion The injured stenotic kidney contributes to increased inflammation in human RAS, and its reparative process may involve EPC recruitment. NIH grants: DK73608, DK77013, HL77131, HL085307.