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The Effect of Chronic Kidney Disease on Endothelial‐Dependent Dilation and Progenitor Cells
Author(s) -
Kuczmarski James Matthew,
Darocki Mark,
Sikes Robert A.,
Cooper Carlton R.,
Farquhar William B.,
Edwards David G.
Publication year - 2010
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.24.1_supplement.lb547
Subject(s) - cd34 , medicine , progenitor cell , kidney disease , peripheral blood mononuclear cell , myeloid , haematopoiesis , bone marrow , endothelial progenitor cell , endothelial dysfunction , flow cytometry , brachial artery , endocrinology , immunology , stem cell , biology , blood pressure , biochemistry , genetics , in vitro
The purpose of this study was to determine if circulating hematopoietic and myeloid progenitor cell subpopulations are reduced, colony forming ability (CFA) of peripheral blood mononuclear cells (PBMNC) is impaired, and endothelial‐dependent dilation (EDD) is attenuated in chronic kidney disease (CKD) patients as compared to healthy controls. Ten patients with stage 3–5 CKD and ten healthy controls were studied. Brachial artery flow‐mediated dilation was used to assess EDD. Circulating progenitor cells (CPC) were quantified in venous blood samples via flow cytometry and PBMNC were cultured to assess CFA. EDD was reduced in CKD (5.39 ± 1 vs. 10.12 ± 1.4; p = 0.007) as were hematopoietic CPC subpopulations CD34+/KDR+ (276.9 ± 65.9 vs. 475.2 ± 93.2, p = 0.046), CD34+/CD45‐ (131.8 ± 30.4 vs. 428.4 ± 100.7, p = 0.004), and CD34+/KDR+/CD45‐ (107 ± 2.8 vs. 298.5 ± 41.2, p < 0.001). Furthermore, myeloid CPCs CD45+ (9.9 × 10 4 ± 1.3 × 10 4 vs. 1.32 × 10 5 ± 1.6 × 10 4 , p = 0.07) and CD45+/KDR+ (1.1 × 10 4 ± 5.9 × 10 3 vs. 4.1 × 10 4 ± 1.8 × 10 4 , p = 0.07) were lower and CFA (2.64± .502 vs. 4.3 ± .953, p = 0.065) was impaired, approaching significance. Reductions in CPC populations may be a potential mechanism by which vascular integrity is compromised, leading to endothelial dysfunction, ultimately increasing the risk of cardiovascular disease and contributing to renal disease progression in CKD patients. Supported by Grants DK077306 and P20 RR016472‐09 .