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Article type: Research Article
Authors: Hammes, Mary S. | Watson, Sydeaka | Coe, Frederic L. | Ahmed, Faris | Beltran, Emily | Dhar, Promila
Affiliations: Department of Medicine, Nephrology Section, The University of Chicago, Chicago, IL, USA | Department of Health Studies, Biostatistics Laboratory, The University of Chicago, Chicago, IL, USA | Department of Biomedical Engineering, Illinois Institute of Technology, Chicago, IL, USA
Note: [] Corresponding author: Mary S. Hammes, DO, Associate Professor of Medicine, University of Chicago, 5841S Maryland MC 5100, Chicago, IL 60637, USA. Tel.: +1 773 702 9892; Fax: +1 773 702 5818; E-mail: [email protected]
Abstract: BACKGROUND: Renal failure is a disease with accelerated atherosclerosis beginning with endothelial cell dysfunction. Factors affecting endothelial cell dysfunction include whole blood viscosity (WBV) and asymmetric dimethylarginine (ADMA). The relationship in controls and renal failure was determined. METHODS: 51 subjects, 20 controls, 11 renal transplant recipients, 10 chronic kidney disease and 10 end-stage renal disease patients had blood samples drawn for WBV, Hematocrit, and ADMA. WBV was measured at various shear rates from 10 s−1 to 780 s−1 at 37°C. Hematocrit using CritSpin, and ADMA was assayed using an ELISA method. The significance between groups was compared by boxplots and analysis of variance. Linear relationships were shown by regression lines and correlation coefficients. RESULTS: ADMA was elevated in all groups with renal failure when compared to controls (p < 0.05). Control subjects showed a positive correlation between ADMA and WBV, while those who received a renal transplant had a negative correlation (p < 0.05). The difference in ADMA comparing pre-dialysis to post-dialysis conditions was positive (p < 0.05). CONCLUSIONS: The positive relationship between WBV and ADMA in controls is a novel finding and allows for comparison with other groups. This relationship is dramatically altered in renal failure.
Keywords: Asymmetric dimethylarginine, endothelial cell, nitric oxide, renal failure, viscosity
DOI: 10.3233/CH-141843
Journal: Clinical Hemorheology and Microcirculation, vol. 59, no. 3, pp. 245-255, 2015
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