The role of lipoprotein(a) in coronavirus disease 2019 (COVID-19) with relation to development of severe acute kidney injury.
Autor: | Lippi G; Section of Clinical Biochemistry, University of Verona, Verona, Italy., Szergyuk I; Faculty of Medicine, Jagiellonian University Medical College, Kraków, Poland., de Oliveira MHS; Department of Statistics, Federal University of Parana, Curitiba, Brazil., Benoit SW; Division of Nephrology and Hypertension, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.; Department of Pediatrics, College of Medicine, University of Cincinnati, Cincinnati, OH, USA., Benoit JL; Department of Emergency Medicine, University of Cincinnati, Cincinnati, OH, USA., Favaloro EJ; Haematology, Sydney Centres for Thrombosis and Haemostasis, Institute of Clinical Pathology and Medical Research (ICPMR), NSW Health Pathology, Westmead Hospital, Westmead, NSW, Australia., Henry BM; Cardiac Intensive Care Unit, The Heart Institute, Cincinnati Children's Hospital Medical Center, 3333 Burnet Ave., Cincinnati, OH, 45229, USA. bhenry@txbiomed.org.; Host-Pathogens Interactions and Population Health Programs, Texas Biomedical Research Institute, San Antonio, TX, USA. bhenry@txbiomed.org. |
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Jazyk: | angličtina |
Zdroj: | Journal of thrombosis and thrombolysis [J Thromb Thrombolysis] 2022 Apr; Vol. 53 (3), pp. 581-585. Date of Electronic Publication: 2021 Oct 28. |
DOI: | 10.1007/s11239-021-02597-y |
Abstrakt: | Lipoprotein(a) (Lp(a)) is a prothrombotic and anti-fibrinolytic lipoprotein, whose role has not been clearly defined in the pathogenesis of coronavirus disease 2019 (COVID-19). In this prospective observational study, serum Lp(a) as well as outcomes were measured in 50 COVID-19 patients and 30 matched sick controls. Lp(a) was also assessed for correlation with a wide panel of biomarkers. Serum Lp(a) did not significantly differ between COVID-19 patients and sick controls, though its concentration was found to be significantly associated with severity of COVID-19 illness, including acute kidney failure stage (r = 0.380, p = 0.007), admission disease severity (r = 0.355, p = 0.013), and peak severity (r = 0.314; p = 0.03). Lp(a) was also positively correlated with interleukin (IL)-8 (r = 0.308; p = 0.037), fibrinogen (r = 0.344; p = 0.032) and creatinine (r = 0.327; p = 0.027), and negatively correlated with ADAMTS13 activity/VWF:Ag (r = - 0.335; p = 0.021); but not with IL-6 (r = 0.241; p = 0.106). These results would hence suggest that adverse outcomes in patients with COVID-19 may be aggravated by a genetically determined hyper-Lp(a) state rather than any inflammation induced elevations. (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.) |
Databáze: | MEDLINE |
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