Strong predictive value of mannose-binding lectin levels for cardiovascular risk of hemodialysis patients.
Strong predictive value of mannose-binding lectin levels for cardiovascular risk of hemodialysis patients.
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DOI:
10.1186/s12967-016-0995-5
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发表时间:
2016-08-05
影响因子:
7.4
通讯作者:
Seelen MA
中科院分区:
文献类型:
--
作者:
Poppelaars F;Gaya da Costa M;Berger SP;Assa S;Meter-Arkema AH;Daha MR;van Son WJ;Franssen CF;Seelen MA
Hemodialysis patients have higher rates of cardiovascular morbidity and mortality compared to the general population. Mannose-binding lectin (MBL) plays an important role in the development of cardiovascular disease. In addition, hemodialysis alters MBL concentration and functional activity. The present study determines the predictive value of MBL levels for future cardiac events (C-event), cardiovascular events (CV-event) and all-cause mortality in HD patients. We conducted a prospective study of 107 patients on maintenance hemodialysis. Plasma MBL, properdin, C3d and sC5b-9 was measured before and after one dialysis session. The association with future C-events, CV-events, and all-cause mortality was evaluated using Cox regression models. During median follow-up of 27 months, 36 participants developed 21 C-events and 36 CV-events, whereas 37 patients died. The incidence of C-events and CV-events was significantly higher in patients with low MBL levels (<319 ng/mL, lower quartile). In fully adjusted models, low MBL level was independently associated with increased CV-events (hazard ratio 3.98; 95 % CI 1.88–8.24; P < 0.001) and C-events (hazard ratio 3.96; 95 % CI 1.49–10.54; P = 0.006). No association was found between low MBL levels and all-cause mortality. Furthermore, MBL substantially improved risk prediction for CV-events beyond currently used clinical markers. Low MBL levels are associated with a higher risk for future C-events and CV-events. Therefore, MBL levels may help to identify hemodialysis patients who are at risk to develop cardiovascular disease. The online version of this article (doi:10.1186/s12967-016-0995-5) contains supplementary material, which is available to authorized users.