Elevated plasma CL-K1 level is associated with a risk of developing disseminated intravascular coagulation (DIC)

K Takahashi, K Ohtani, M Larvie, P Moyo… - Journal of thrombosis …, 2014 - Springer
K Takahashi, K Ohtani, M Larvie, P Moyo, L Chigweshe, EM Van Cott, N Wakamiya
Journal of thrombosis and thrombolysis, 2014Springer
Abstract Collectin kidney 1 (CL-K1) is a recently identified collectin that is synthesized in
most organs and circulates in blood. CL-K1 is an innate immune molecule that may play a
significant role in host defense. As some collectins also play a role in coagulation, we
hypothesized that an effect of CL-K1 may be apparent in disseminated intravascular
coagulation (DIC), a gross derangement of the coagulation system that occurs in the setting
of profound activation of the innate immune system. DIC is a grave medical condition with a …
Abstract
Collectin kidney 1 (CL-K1) is a recently identified collectin that is synthesized in most organs and circulates in blood. CL-K1 is an innate immune molecule that may play a significant role in host defense. As some collectins also play a role in coagulation, we hypothesized that an effect of CL-K1 may be apparent in disseminated intravascular coagulation (DIC), a gross derangement of the coagulation system that occurs in the setting of profound activation of the innate immune system. DIC is a grave medical condition with a high incidence of multiple organ failure and high mortality and yet there are no reliable biomarkers or risk factors. In our present study, we measured plasma CL-K1 concentration in a total of 659 specimens, including 549 DIC patients, 82 non-DIC patients and 27 healthy volunteers. The median plasma CL-K1 levels in these cohorts were 424, 238 and 245 ng/ml, respectively, with no significant difference in the latter two groups. The incidence of elevated plasma CL-K1 was significantly higher in the DIC patients compared to the non-DIC patients, resulting in an odds ratio of 1.929 (confidence interval 1.041–3.866). Infection, renal diseases, respiratory diseases, and cardiac diseases were more frequently observed in the DIC group than in the non-DIC group. In the DIC group, vascular diseases were associated with elevated plasma CL-K1 levels while age and acute illness had little effect on plasma CL-K1 levels. Independent of DIC, elevated plasma CL-K1 levels were associated with respiratory disease and coagulation disorders. These results suggest that specific diseases may affect CL-K1 synthesis in an organ dependent manner and that elevated plasma CL-K1 levels are associated with the presence of DIC. Further investigations in cohorts of patients are warranted. We propose that elevated plasma CL-K1 may be a new useful risk factor and possibly biomarker for the prediction of developing DIC.
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