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      Significant Elevations in Serum Mannose-Binding Lectin Levels in Patients with Chronic Renal Failure

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          Background/Aims: Mannose-binding lectin (MBL), a liver-derived C-type serum lectin, activates the complement cascade through the lectin pathway. Since the complement system contributes to the host defense against infections and mediates inflammatory processes including atherosclerosis, and since chronic renal failure (CRF) patients are prone to the development of infectious complications and cardiovascular disease, we focused on serum MBL levels in CRF patients who were either uremic, or who were receiving hemodialysis treatment. Methods: MBL levels were measured in the sera of subjects with CRF before they began dialysis treatment (pre-HD patients; n = 23) and in the sera of subjects who were receiving maintenance hemodialysis (HD patients; n = 178), by ELISA using polyclonal anti-rabbit IgG and a monoclonal antibody directed against MBL (3E7). Results: Mean levels (± SD) of serum MBL were significantly higher in pre-HD subjects (4.343 ± 2.533 µg/ml, p < 0.05) and in HD subjects (8.897 ± 4.920 µg/ml, p < 0.05), than in healthy controls (1.452 ± 0.692 µg/ml). Levels were also significantly higher in HD subjects than in pre-HD subjects (p < 0.05). Conclusions: Elevated serum MBL levels in patients with CRF might have significantly influence pathologic conditions such as alterations of the immune system and acceleration of atherogenesis.

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          Most cited references 2

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          Mannose-binding lectin: the pluripotent molecule of the innate immune system.

           M TURNER (1996)
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            Mannose-Binding Lectin Contributes to Glomerulonephritis Induced by Hepatitis C Virus Infection


              Author and article information

              S. Karger AG
              September 2002
              26 September 2002
              : 92
              : 3
              : 702-704
              aDivision of Nephrology, Internal Medicine II, Nihon University School of Medicine, Tokyo; bKasukabe-Kisen Hospital, Saitama; cDepartment of Biochemistry II, Fukushima Medical University, Fukushima, Japan
              64089 Nephron 2002;92:702–704
              © 2002 S. Karger AG, Basel

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