Low levels of high-density lipoprotein cholesterol: an independent risk factor for late adverse cardiovascular events in renal transplant recipients

Barn, Kulpreet; Laftavi, M. R.; Pierce, Drew; Ying, Chin; Boden, William E.; Pankewycz, O.

doi:10.1111/j.1432-2277.2009.01021.x

Cited by 17 publications

(10 citation statements)

References 24 publications

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“…The results of the presented studies and those by of other laboratories have already shown that TG-rich apoB-containing apoCIII lipoproteins are linked to inflammation [1,2,[12][13][14], and that oxidation is not always proatherogenic [7,15]. Moderate oxidation that encompasses in vivo conditions destabilizes VLDL and promotes the fission of HDL-size particles.…”

Section: Discussionsupporting

confidence: 55%

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Moderate dyslipoproteinemia induced inflammation and remodeling HDL and VLDL particles in post-renal transplant patients

Kimak

Baranowicz-Gąszczyk

Białopiotrowicz

2017

Current Issues in Pharmacy and Medical Sciences

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oxidation of low density lipoprotein (LDL). These include apolipoprotein AI (apoAI), lecithin: cholesterol acyltransferase (LCAT), and paraoxonase-1 (PON1) [8,9]. However, the proteins interaction in the anti-oxidant activity of HDL is unknown. ApoAII has been shown to directly affect HDL modifications catalyzed by the plasma proteins. ApoAII is less efficient than apoAI at activating LCAT [10,20], and studies have shown that displacement of apoAI in HDL by apoAII inhibits cholesterol esterification. A possible mechanism of the pro-atherogenic action of human apoAII could be the inhibition of reverse cholesterol transport (RCT), depending, at least partly on a marked disease in endogenous The aim of this paper was to examine whether moderate dyslipoproteinemia can cause an increase of hsCRP and LPO levels in Tx patients who had received immunosuppressive therapy and were without acute inflammatory diseases. Herein, the lipid levels, hsCRP, LPO, apolipoprotein (apo)B, AI, AII, AIInonB, apoB-containing AII (apoB:AII), apoCIII, apoCIIInonB, apoB:CIII, LCAT level, as well as CETP and PON1 activity were determined. All examined Tx patients had moderate dyslipidemia and slightly increased hsCRP, LPO, apoB:AII and apoCIII levels, but decreased LCAT mass, PON1 activity and lipoprotein ratios. Tx patients with apoAI<150 mg/dl (n=28) had worse lipoprotein profiles than did Tx patients with apoAI>150mg/dl (n=39), but no difference in CETP activity was indicated. Multiple ridge forward regression and Spearman's correlation test were used. The results of the presented study, show for the first time that higher apoAI/apoB and apoAI/apoCIII ratios induced a decrease of the hsCRP concentration. Moreover, the composition of apoCIIInonB, LDL-C and apoAI brought about an increase of LCAT mass and PON1 activity. In Tx patients with lower concentration of apoAI, an increase of concentration of apoB:AII in VLDL generated a mild oxidation of lipoprotein and an elevated concentration of LPO. However, lower ApoAI/apoB ratio resulted in an increase of PON1 activity and apoB, as well as nonHDL-C levels, and in turn, PON1 activity increased LCAT mass. These disorders rearranged the HDL particle, and, simultaneously, remodeled the VLDL particle. This may prevent antioxidant activity, reverse cholesterol transport and accelerate the rejection of the transplant, as well as bringing about cardiovascular diseases in Tx patients with lower apoAI. Such metabolic pathways can be used as potentially novel targets for pharmacological intervention.

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Section: Discussionsupporting

confidence: 55%

“…Reverse kidney renal failure after renal transplantation is associated with various types of metabolic dysfunctions [2], and immunosuppressive therapy seems to be the main factor that influences the post-transplant lipidemic profile [19]. Our previously Table 2.…”

Section: Discussionmentioning

confidence: 99%

Moderate dyslipoproteinemia induced inflammation and remodeling HDL and VLDL particles in post-renal transplant patients

Kimak

Baranowicz-Gąszczyk

Białopiotrowicz

2017

Current Issues in Pharmacy and Medical Sciences

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“…Furthermore, it should be noted that levels of HDL-C is significantly negatively correlated with arterial stenosis whose occurrence is strongly associated with the phenomenon of plaque rupture [17]. Thus higher levels of HDL-C tend to have fewer problems with cardiovascular diseases such as MI, while those with low HDL-C cholesterol levels may easily suffer from MI [18], [19]. Variation in CETP activity could influence HDL-C levels and thus contribute to increased susceptibility to cardiovascular disease such as MI [20].…”

Section: Introductionmentioning

confidence: 99%

Seven Functional Polymorphisms in the CETP Gene and Myocardial Infarction Risk: A Meta-Analysis and Meta-Regression

et al. 2014

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ObjectiveThis meta-analysis aims to evaluate the relationships between seven functional polymorphisms in the CETP gene and myocardial infarction (MI) risk.MethodThe PubMed, CISCOM, CINAHL, Web of Science, Google Scholar, EBSCO, Cochrane Library, and CBM databases were searched for relevant articles published before March 1st, 2013 without any language restrictions. Meta-analysis was conducted using the STATA 12.0 software.ResultsNine case-control studies with a total 8,623 MI cases and 8,564 healthy subjects met the inclusion criteria. The results of our meta-analysis suggested that CETP rs708272 (C>T) polymorphism might be correlated with an increased risk of MI, especially among Caucasians. Furthermore, we observed that CETP rs1800775 (C>A) polymorphism might increase the risk of MI. Nevertheless, no similar findings were found for CETP rs5882 (A>G), rs2303790 (A>G), rs1800776 (C>A), rs12149545 (G>A), and rs4783961 (G>A) polymorphisms.ConclusionThe current meta-analysis suggests that CETP rs708272 (C>T) and rs1800775 (C>A) polymorphisms may contribute to MI susceptibility, especially among Caucasians. Thus, CETP rs708272 and rs1800775 polymorphisms may be promising and potential biomarkers for early diagnosis of MI.

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“…However, low HDL in kidney transplant recipients is an independent risk factor for CVD after transplant [89].…”

Section: Introductionmentioning

confidence: 98%

Diabetes and Cardiovascular Disease Following Kidney Transplantation

Boerner¹,

Shivaswamy²,

Desouza³

et al. 2011

CDR

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Kidney transplantation is being performed more frequently for individuals with end stage renal disease (ESRD) due to improved survival and quality of life compared to long-term dialysis. Though rates decrease after transplant, cardiovascular disease (CVD) remains the most common cause of death after kidney transplant. New-onset diabetes after transplant (NODAT), a common complication following kidney transplantation, and pre-transplant diabetes both significantly increase the risk for CVD. Several other risk factors for CVD in kidney transplant recipients have been identified; however, optimal therapy for controlling the risk factors of CVD after kidney transplantation, including NODAT and pretransplant diabetes, is not well defined. In the following review we will discuss the role of traditional and non-traditional risk factors in CVD after kidney transplant and the mechanisms involved therein. We will also examine the current literature regarding treatment of these risk factors for the prevention of CVD. Finally, we will review the current recommendations for pre-and post-transplant cardiovascular evaluation and management.

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Low levels of high-density lipoprotein cholesterol: an independent risk factor for late adverse cardiovascular events in renal transplant recipients

Cited by 17 publications

References 24 publications

Moderate dyslipoproteinemia induced inflammation and remodeling HDL and VLDL particles in post-renal transplant patients

Moderate dyslipoproteinemia induced inflammation and remodeling HDL and VLDL particles in post-renal transplant patients

Seven Functional Polymorphisms in the CETP Gene and Myocardial Infarction Risk: A Meta-Analysis and Meta-Regression

Diabetes and Cardiovascular Disease Following Kidney Transplantation

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