The role of lipoprotein(a) in coronavirus disease 2019 (COVID-19) with relation to development of severe acute kidney injury

Lippi, Giuseppe; Szergyuk, Ivan; Oliveira, Maria Helena Santos de; Benoit, Stefanie; Benoit, Justin L.; Favaloro, Emmanuel J.; Henry, Brandon Michael

doi:10.1007/s11239-021-02597-y

Cited by 12 publications

(12 citation statements)

References 36 publications

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“…First, Lp(a) is an acute phase reactant, and its concentration can be consistently boosted during sustained inflammatory states, like that characterizing severe forms of COVID-19 and other acute conditions. This is in keeping with the findings of Nurmohamed et al [ 6 ], who reported a gradual increase of this lipoprotein during hospital stay, directly correlated with IL-6 variations, as well as with those of Lippi et al, who found similar concentrations between patients with COVID-19 and other acute diseased states [ 7 ]. Then, in all three studies that we could identified based on our digital search, Lp(a) values both at baseline (e.g., presumably genetically determined) or during illness progression (i.e., boosted by COVID-19 related inflammation) were found to have an impact on clinical outcome of SARS-CoV-2 infection.…”

supporting

confidence: 92%

“…In a subsequent study, Lippi et al measured Lp(a) in 50 patients with COVID-19 and 30 matched sick controls [ 7 ]. Interestingly, they first found that serum Lp(a) values in COVID-19 patients at hospital admission did not significantly differ from those of the control sick population (0.1 vs. 0.2 g/L; p = 0.098), though Lp(a) concentration was found to be a significant predictor of peak disease severity during hospital stay (r = 0.314; p = 0.03).…”

mentioning

confidence: 99%

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Lipoprotein(a) in COVID-19: Genetics and inflammation collide

Montagnana

Lippi

2022

Atherosclerosis

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supporting

confidence: 92%

mentioning

confidence: 99%

Lipoprotein(a) in COVID-19: Genetics and inflammation collide

Montagnana

Lippi

2022

Atherosclerosis

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“…Nonetheless, it has been suggested that screening for inherited thrombophilia may help identifying patients at higher risk of developing more severe forms of VTE and/or in situ pulmonary thrombosis. 48 Then, the contribution of additional prothrombotic risk factors such as lipoprotein(a), 49 lupus anticoagulant, 50 and antiphospholipid antibodies, 51 would need to be more extensively assessed, since their active participation to the pathogenesis of COVID-19-associated coagulopathy may require specific treatments for reducing the risk of unfavorable outcomes.…”

Section: Discussionmentioning

confidence: 99%

What We Know (and Do not Know) Regarding the Pathogenesis of Pulmonary Thrombosis in COVID-19

Lippi

Favaloro

2022

Semin Thromb Hemost

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The clinical course of coronavirus disease 2019 (COVID-19) is often complicated by the onset of venous thrombosis and thromboembolism (VTE), encompassing also pulmonary thrombosis. Recent statistics attests that the cumulative frequency of VTE can be as high as 30% in COVID-19 hospitalized patients, increasing to nearly 40 to 70% (depending on systematic screening) in those with severe illness, mechanical ventilation, or intensive care unit admission. The risk of venous thrombosis seems mostly limited to the active phase of disease, and is directly associated with some genetic (i.e., inherited prothrombotic predisposition) and demographical factors (male sex, overweight/obesity), disease severity (risk increasing progressively from hospitalization to development of severe illness, being the highest in patients needing mechanical ventilation and/or intensive care), presence and extent of pulmonary disease, coexistence of multiple risk factors (immobilization, mechanical ventilation, co- or superinfections), along with increased values of inflammatory and thrombotic biomarkers. At least three different phenotypes of pulmonary thrombosis may develop in COVID-19 patients, one caused by typical embolization from peripheral venous thrombosis (e.g., deep vein thrombosis), a second type triggered by local inflammation of nearby pulmonary tissue, and a third one mostly attributable to the prothrombotic state consequent to the pronounced systemic inflammatory response (i.e., the so-called cytokine storm) that is frequently observed in COVID-19. Although the pathogenesis of these three conditions has different features, their discrimination is essential for diagnostic and therapeutic purposes. The prognosis of COVID-19 patients who develop pulmonary thrombosis is also considerably worse than those who do not, thus probably needing frequent monitoring and more aggressive therapeutic management.

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“…On the other hand, Lippi et al [33] suggested that without correlation to IL-6, an inherited hyper-Lp(a) state, rather than an inflammation-driven increase, might contribute to the enhanced risk of micro-and macro-thrombosis in COVID-19 patients. Moriarty et al proposed that an elevated Lp(a) may also lead to acute destabilization of preexisting, but quiescent atherosclerotic plaques, which could induce acute myocardial infarction and stroke [36].…”

Section: Lipid Concentrations During Covid-19 Infectionmentioning

confidence: 99%

“…Serum lipoprotein(a) [Lp(a)] did not significantly differ between COVID-19 patients and disease controls, although its concentration was found to be significantly positively associated with severity of COVID-19 illness, including acute kidney failure stage, admission disease severity, and peak severity [33]. Serum Lp(a) concentrations were higher in patients with recurrent cerebral venous sinus thrombosis (CVST) compared to patients without; that is, 28 (19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36) mg/dl versus 14 (9-25) mg/dl [34]. The importance of elevated serum Lp(a) as a potential risk factor for CVST maybe even higher in patients with SARS-CoV-2 infection.…”

Section: Lipid Concentrations During Covid-19 Infectionmentioning

confidence: 99%

COVID-19 and Lipid Disorders

et al. 2022

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An elevated cholesterol concentration has been suspected to increase the susceptibility for SARS-COV-2 infection. Cholesterol plays a central role in the mechanisms of the SARS-COV-2 infection. In contrast, higher HDL-cholesterol levels seem to be protective. During COVID-19 disease, LDL-cholesterol and HDL-cholesterol appear to be decreased. On the other hand, triglycerides (also in different lipoprotein fractions) were elevated. Lipoprotein(a) may increase during this disease and is most probably responsible for thromboembolic events. This lipoprotein can induce a progression of atherosclerotic lesion formation. The same is suspected for the SARS-COV-2 infection itself. COVID-19 patients are at increased risk of incident cardiovascular diseases, including cerebrovascular disorders, dysrhythmias, ischemic and non-ischemic heart disease, pericarditis, myocarditis, heart failure, and thromboembolic disorders. An ongoing lipid-lowering therapy, including lipoprotein apheresis, is recommended to be continued during the COVID-19 disease, though the impact of lipid-lowering drugs or the extracorporeal therapy on prognosis should be studied in further investigations.

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The role of lipoprotein(a) in coronavirus disease 2019 (COVID-19) with relation to development of severe acute kidney injury

Cited by 12 publications

References 36 publications

Lipoprotein(a) in COVID-19: Genetics and inflammation collide

Lipoprotein(a) in COVID-19: Genetics and inflammation collide

What We Know (and Do not Know) Regarding the Pathogenesis of Pulmonary Thrombosis in COVID-19

COVID-19 and Lipid Disorders

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