Mobilization of endothelial progenitor cells (EPCs) independently of renal impairment in type 2 diabetic patients

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SUN 758-779-Cardiometabolic Risk & Vascular Biology
Sunday, June 16, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SUN-771
Aoki Atsushi*1, Yamada Hodaka2, Murata Miho2 and Ishikawa San-e2
1Jichi Medical University Saitama Medical Center, Saitama, Japan, 2Jichi Medical University Saitama Medical Center
Bone marrow-derived endothelial progenitor cells (EPCs) can have beneficial effects on angiogenesis and vascular repair. The present study was undertaken to determine whether EPCs are involved in mechanism for modulating the progression of diabetic nephropathy. Fifty-five type 2 diabetic patients were enrolled. The number of EPCs were defined as CD34+/133+ cells by flow cytometry. There was no difference in the numbers of EPCs among the stages of 1-4 of diabetic nephropathy(stage1:86.9±14.8 ; stage2:40.3±6.9 ; stage3:82.6±26.0 ; and stage 4F72.1±13.7  cells/100μl, n.s). EPCs were measured under an acute exercise load that obligated to stimulate a maximal oxygen uptake. The exercise load significantly increased the number of EPCs from 70.2 to 88.3 cells/100μl in the patients with eGFR of > 60 ml/min/1.73 m2 (P=0.0001), but did not alter EPCs in those with eGFR of < 60 ml/min/1.73m2. Lastly we divided the patients into two groups by the mean value (50.7 cells/100μl) of EPCs, and determined a reduction in eGFR during the 5 years observation period. There was no difference in the reduction of eGFRs between the two groups of patients. For 5 years observation, eGFR was decreased by 13.2 ml/min/1.73m   in the high EPCs group (n=18), and by 13.2 ml/min/1.73m2 in the low EPCs group (n=18). These findings indicate that the numbers of EPCs are not associated with progression or protection of nephropathy in the type 2 diabetic subjects. Rather, impaired response of EPCs to acute exercise load may be related to vascular impairment concomitantly developed with diabetic microangiopathy.

Nothing to Disclose: AA, YH, MM, IS

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