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Endotoxins and inflammation in hemodialysis patients
Author(s) -
ElKoraie Ahmed F.,
Naga Yasmine S.,
Saaran Amina M.,
Farahat Nahla G.,
Hazzah Walaa A.
Publication year - 2013
Publication title -
hemodialysis international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.658
H-Index - 47
eISSN - 1542-4758
pISSN - 1492-7535
DOI - 10.1111/hdi.12007
Subject(s) - medicine , hemodialysis , limulus amebocyte lysate , dialysis , inflammation , hemoglobin , gastroenterology , c reactive protein , albumin , immunology , lipopolysaccharide
Long‐term endotoxin challenge may promote frequent complications in dialysis patients, namely malnutrition, chronic inflammation, and atherosclerosis, which are recognized as the so‐called MIA syndrome. Circulating soluble vascular cell adhesion molecule‐1 ( sVCAM ‐1) levels may be used to determine the stage of atherosclerosis. This study aimed to assess endotoxin level in hemodialysis ( HD ) patients and its role in inducing inflammation. The study was conducted on 50 HD patients, chosen from four dialysis centers in A lexandria. Serum blood samples were collected for the determination of albumin and C ‐reactive protein ( CRP ), and whole blood samples were used for the measurement of hemoglobin level. A heparinized whole blood sample was taken postdialysis for endotoxin assay by limulus amebocyte lysate test, and in addition to sVCAM ‐1 was estimated using enzyme‐linked immunosorbent assay. The mean endotoxin level was 76.30 pg/ mL ;80% exhibited values higher than 60 pg/ mL . Half the studied patients had CRP values that exceeded the upper limit of the laboratory reference range (<6.0 mg/ L ). A statistically significant correlation was found between endotoxin and CRP levels (r = 0.47, P = 0.001). The mean pre‐ HD level of VCAM was 1851.00 ng/ mL , while the mean post‐ HD level was 2829.00 ng/ mL with statistically significant correlation (r = 0.354, P = 0.012) and it also correlated significantly with endotoxin as well as CRP levels. Endotoxemia may play an important role in the aggravation of endothelial dysfunction in HD patients as indicated by the post‐ HD rise in sVCAM ‐1.