Hyperlipoproteinaemia(a) – apheresis and emerging therapies

Vogt, Anja

doi:10.1007/s11789-017-0083-2

Cited by 6 publications

(4 citation statements)

References 54 publications

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“…is the most effective, well-tolerated, and approved treatment for lowering Lp(a) levels [237,238]. is process removes all apoB-containing lipoproteins (specifically LDL-C and Lp(a)) from the blood using antibody-coupled columns, precipitation, and complex creation at low pH.…”

Section: Apheresis Extracorporeal Elimination With Apheresismentioning

confidence: 99%

Lipoprotein(a) the Insurgent: A New Insight into the Structure, Function, Metabolism, Pathogenicity, and Medications Affecting Lipoprotein(a) Molecule

2020

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Lipoprotein(a) [Lp(a)], aka “Lp little a”, was discovered in the 1960s in the lab of the Norwegian physician Kåre Berg. Since then, we have greatly improved our knowledge of lipids and cardiovascular disease (CVD). Lp(a) is an enigmatic class of lipoprotein that is exclusively formed in the liver and comprises two main components, a single copy of apolipoprotein (apo) B-100 (apo-B100) tethered to a single copy of a protein denoted as apolipoprotein(a) apo(a). Plasma levels of Lp(a) increase soon after birth to a steady concentration within a few months of life. In adults, Lp(a) levels range widely from <2 to 2500 mg/L. Evidence that elevated Lp(a) levels >300 mg/L contribute to CVD is significant. The improvement of isoform-independent assays, together with the insight from epidemiologic studies, meta-analyses, genome-wide association studies, and Mendelian randomization studies, has established Lp(a) as the single most common independent genetically inherited causal risk factor for CVD. This breakthrough elevated Lp(a) from a biomarker of atherosclerotic risk to a target of therapy. With the emergence of promising second-generation antisense therapy, we hope that we can answer the question of whether Lp(a) is ready for prime-time clinic use. In this review, we present an update on the metabolism, pathophysiology, and current/future medical interventions for high levels of Lp(a).

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Section: Apheresis Extracorporeal Elimination With Apheresismentioning

confidence: 99%

Lipoprotein(a) the Insurgent: A New Insight into the Structure, Function, Metabolism, Pathogenicity, and Medications Affecting Lipoprotein(a) Molecule

2020

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“…A recent study reported that low-density lipoprotein apheresis (LDL-A) decreased the risk of maintenance dialysis in 49 CCE patients with renal dysfunction after 24 weeks [ 58 ]. Lipoprotein apheresis (LA) can significantly lower lipoprotein cholesterol levels, and is recommended in some countries in very high-risk patients with early or progressive cardiovascular disease (CVD) [ 59 ]. LDL-A may have beneficial effect on renal outcome of CCE.…”

Section: Treatmentsmentioning

confidence: 99%

Cholesterol Crystal Embolism and Chronic Kidney Disease

Bayliss

Zhuang

2017

IJMS

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Renal disease caused by cholesterol crystal embolism (CCE) occurs when cholesterol crystals become lodged in small renal arteries after small pieces of atheromatous plaques break off from the aorta or renal arteries and shower the downstream vascular bed. CCE is a multisystemic disease but kidneys are particularly vulnerable to atheroembolic disease, which can cause an acute, subacute, or chronic decline in renal function. This life-threatening disease may be underdiagnosed and overlooked as a cause of chronic kidney disease (CKD) among patients with advanced atherosclerosis. CCE can result from vascular surgery, angiography, or administration of anticoagulants. Atheroembolic renal disease has various clinical features that resemble those found in other kidney disorders and systemic diseases. It is commonly misdiagnosed in clinic, but confirmed by characteristic renal biopsy findings. Therapeutic options are limited, and prognosis is considered to be poor. Expanding knowledge of atheroembolic renal disease due to CCE opens perspectives for recognition, diagnosis, and treatment of this cause of progressive renal insufficiency.

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“…We speculated that the decrease of the expression of EGR1 might be due to the change of the patient's condition, which inhibited the binding of zinc finger structure coding region of EGR1 to downstream related genes, leading to the difference of expression of many biochemical factors, so as to result in the occurrence of CHD in patients. As a cholesterol macromolecule lipoprotein, [Lp(a)] plays an important role in the occurrence of CHD and it has been shown to be an independent risk factor for CHD (24). hs-CRP is a new independent prognostic indicator for the diagnosis of CHD in recent years, and its expression level is positively correlated with the pathological changes of CHD (25).…”

Section: Discussionmentioning

confidence: 99%

Value analysis of CD69 combined with EGR1 in the diagnosis of coronary heart disease

Peng

Xiang

2019

Exp Ther Med

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Expression and clinical significance of CD69 and early growth response (EGR1) in plasma of patients with coronary heart disease (CHD) were investigated. A total of 194 patients with CHD and 130 healthy subjects, respectively, were selected as CHD and control group, clinical data were collected and coronary angiography was performed. RT-qPCR was used to detect the expression of EGR1. Flow cytometry was used to detect the expression level of CD69 and the receiver operating characteristic curve was used to analyze the values of relative expression of CD69 and EGR1. The relative expression of CD69 in plasma of patients with CHD was higher than that in control group, while the relative expression of EGR1 was lower than that in control group. The relative expression of EGR1 in plasma of patients with CHD was negatively correlated with lipoprotein a [Lp(a)] and high sensitive C-reactive protein (hs-CRP) (r=−0.394 and −0.524, P<0.05), and the relative expression of CD69 in peripheral blood was positively correlated with [Lp(a)] and hs-CRP (r=0.352 and 0.402, P<0.05). The area under curve (AUC) of the relative expression of CD69 in peripheral blood of patients with CHD in evaluating the course of the disease of patients was 0.889 (95% CI: 0.822–0.958). The AUC of the relative expression of EGR1 in plasma in evaluating the course of the disease of patients was 0.933 (95% CI: 0.867–0.978). By the combined detection of CD69 and EGR1, it was found that the AUC was 0.954 (95% CI: 0.887–0.982). The expression level of EGR1 in plasma of patients with CHD decreased, while the expression level of CD69 increased, and both of them were related to the severity of the disease of patients, which could be used as an indicator to evaluate the progression of the patients' conditions.

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Hyperlipoproteinaemia(a) – apheresis and emerging therapies

Cited by 6 publications

References 54 publications

Lipoprotein(a) the Insurgent: A New Insight into the Structure, Function, Metabolism, Pathogenicity, and Medications Affecting Lipoprotein(a) Molecule

Lipoprotein(a) the Insurgent: A New Insight into the Structure, Function, Metabolism, Pathogenicity, and Medications Affecting Lipoprotein(a) Molecule

Cholesterol Crystal Embolism and Chronic Kidney Disease

Value analysis of CD69 combined with EGR1 in the diagnosis of coronary heart disease

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