Association Between Lipids, Lipoproteins Composition of HDL Particles and Triglyceride-Rich Lipoproteins, and LCAT and CETP Activity in Post-renal Transplant Patients

Kimak, Elżbieta; Bylina, Jerzy; Solski, Janusz; Hałabiś, Magdalena; Baranowicz-Gąszczyk, Iwona; Książek, Andrzej

doi:10.1007/s12013-013-9559-y

Cited by 11 publications

(17 citation statements)

References 25 publications

(27 reference statements)

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“…TC, LDL-C, and HDL-C levels of the HD group were significantly lower than those of the all study groups. In line with our finding, Kimak et al 59 found increased TG levels in KT patients than those of the controls. However, Tsai et al 47 reported increased TC levels and C¸olak et al 60 did not find any significant differences between the KTR, HD, and the control groups.…”

Section: Discussionsupporting

confidence: 93%

Adiponectin, leptin, nitric oxide, and C-reactive protein levels in kidney transplant recipients: comparison with the hemodialysis and chronic renal failure

2016

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Background: Cardiovascular disease (CVD) is the leading cause of mortality and morbidity in patients with chronic kidney disease (CKD) including kidney transplant recipients (KTR). Secondary lipid metabolism disorders, endothelial dysfunction, and inflammation enhance the risk of CVD development in these patients. The aim of the present study was to investigate the lipid profile, adiponectin, leptin, nitric oxide (NO), and high sensitivity C-reactive protein (hs-CRP) levels in KTR and to compare these parameters with those of the patients with chronic renal failure (CRF), hemodialysis (HD) patients, and healthy controls. Methods: Serum adiponectin and leptin levels were measured by radioimmunoassay; hs-CRP was determined immunoturbidimetrically. Determination of NO was based on the Griess reaction. Results: Compared with the control group, serum NO and adiponectin levels were significantly higher in the KTR, CRF, and HD groups; hs-CRP levels were significantly higher in the KTR and HD groups; leptin levels were significantly higher in the KTR. In addition, serum NO level was significantly higher in the KTR compared to CRF cases. Adiponectin correlated positively with high density lipoprotein-cholesterol in the control and patient groups. A positive correlation was observed between hs-CRP and NO in the KTR and the patients with CRF. Serum adiponectin levels were inversely correlated with hs-CRP and leptin in the HD group. Conclusion: KTR suffer from inflammation and accompanying changes in levels of adipocytokines and NO which contribute to the increased risk of CVD in these patients.

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Section: Discussionsupporting

confidence: 93%

Adiponectin, leptin, nitric oxide, and C-reactive protein levels in kidney transplant recipients: comparison with the hemodialysis and chronic renal failure

2016

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“…Oxidative stress and inflammation have recently gained a considerable support as factors relevant in CVD in the setting of CKD. These disturbances result from overproduction, as well as impairment in the clearance of apolipoproteinB (apoB)-containing lipoproteins that reflects abnormalities in lipid substrates, enzymes, lipid transfer proteins and lipoprotein receptor activity [9][10][11][12][13][14][15][16]. Decreased HDL cholesterol has been long recognized to be a powerful negative-risk factor for CVD, and has emerged as a new target for intervention in the progression and even the regression of atherosclerosis [2].…”

Section: Discussionmentioning

confidence: 99%

“…Decreased HDL cholesterol has been long recognized to be a powerful negative-risk factor for CVD, and has emerged as a new target for intervention in the progression and even the regression of atherosclerosis [2]. It should be noted that low HDL-C is a consistent finding at all stages of CKD [7,16,17].…”

Section: Discussionmentioning

confidence: 99%

Can chronic heart failure induce kidney function damage?

Kimak

Dziedzic

Kimak

et al. 2016

Current Issues in Pharmacy and Medical Sciences

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events, hospitalisation, and more cardiovascular complications following a myocardial infarct [4,5]. Even microalbuminuria, in the absence of an apparent decrease in renal function or diabetes, predicts more cardiovascular disease (CVD) and death [6]. The impact of CVD in CKD is illustrated by reports on the natural history of patients with early CKD. These indicate that the risk of premature CVD death is much higher than the risk of dialysis/transplantation progress [7,8]. Such observations are significant not only because of a high incidence and prevalence of end stage CKD, but because the number of patients with early CKD far exceeds those with end stage CKD. This trend is continuing to rise [9].Patients with CKD, have the highest risk for atherosclerotic CVD. Current interventions have been insufficiently Accelerated atherosclerosis and increased cardiovascular events have been extensively documented in patients with end stage chronic kidney disease. The aim of our work was to find evidence supporting the theory that chronic heart failure (CHF) induces renal function damage. In our work, lipids, apolipoprotein (apo)AI, NTproBNP, hsCRP, lipid hydroperoxide (LPO) and creatinine levels were determined in patients with CHF. A total of 37 patients who were diagnosed with CHF, as well as 15 healthy persons, were recruited for the study. The patients were placed into 2 groups: patients with NYHA class 2 and NYHA class 3. Using routine laboratory methods, NTproBNP level, and lipids were measured by way of employing a Cobas Integra analyser, while the concentration of hs-CRP was measured by immunonephelometric methods. Moreover, serum LPO concentration was measured using Cayman's Assay Kit (LPO). The statistical analysis of the obtained results was performed using the nonparametric Kruskal-Wallis test and Spearman's correlation analysis. Our work demonstrated that the CHF patients had significantly decrease concentration of HDL cholesterol and apoAI, but increased NT-pro-BNP, hsCRP and LPO levels. In all CHF patients, a significant positive correlation between NTproBNP concentration and creatinine levels, and a significant negative correlation between NTproBNP concentration and apoAI levels, as well as between concentration of creatinine and apoAI levels, was shown. The study results suggest that variation in the concentration of NTproBNP, LPO, hsCRP, apoAI, creatinine, in addition to chronic heart failure progression, gradually accompany the progress of chronic renal failure. What is more, the disorders may lead to the occurrence of cardiovascular events, consequently, to patient death.

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“…Non-HDL-C was calculated as total cholesterol (TC) minus HDL-C. Lipoproteins apoAI, total apoAII, apoAIInonB, apoB, hsCRP were determined with immunonephelometric methods, using the Health Care Diagnostic Product (Siemens GmbH, Germany) on a Dade Behring nephelometer BNII System (Germany). Total apoCIII and apoCIIInonB were measured by electroimmunodiffusion, according to Laurell, using a commercial kit (Sebia, USA), TRLs (apoB:CIII and apoB:AII) were separated as non-HDL lipoproteins by using anti-apoB antibodies [12][13][14].…”

Section: Detection Of Lipids Lipoproteins Hscrp and Routine Laboratmentioning

confidence: 99%

“…of the samples to the standard curve. The PON-1 activity was measured by the modified Fourlong's method as described previously [12], from the initial velocity of p-nitrophenol production at 37°C, and its increased absorbance at 405 nm. This was recorded by an autoanalyzer (Cobas-Mira Plus, Roche Diagnostica, Switzerland).…”

Section: Determination Of a Concentration Of Lpo Lcat And Pon1 And Cmentioning

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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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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Association Between Lipids, Lipoproteins Composition of HDL Particles and Triglyceride-Rich Lipoproteins, and LCAT and CETP Activity in Post-renal Transplant Patients

Cited by 11 publications

References 25 publications

Adiponectin, leptin, nitric oxide, and C-reactive protein levels in kidney transplant recipients: comparison with the hemodialysis and chronic renal failure

Adiponectin, leptin, nitric oxide, and C-reactive protein levels in kidney transplant recipients: comparison with the hemodialysis and chronic renal failure

Can chronic heart failure induce kidney function damage?

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

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