Search Results

You are looking at 1 - 3 of 3 items for

  • Author: Elzbieta Kimak x
Clear All Modify Search
Open access

Elzbieta Kimak, Marcin Dziedzic, Aleksandra Kimak, Kamila Stachyra, Andrzej Prystupa and Janusz Solski


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, NT-proBNP 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 NT-proBNP concentration and creatinine levels, and a significant negative correlation between NT-proBNP 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 NT-proBNP, 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.

Open access

Elzbieta Kimak, Iwona Baranowicz-Gaszczyk and Tomasz Bialopiotrowicz


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.

Open access

Elzbieta Kimak, Grzegorz Dzida, Dariusz Duma, Andrzej Prystupa, Magdalena Halabis, Aleksandra Kimak, Bartosz Zieba, Iwona Kaznowska-Bystryk and Agnieszka Kowalska


The aim of the study was to examine concentrations and relationships between melatonin levels assessed at 0:200 hrs and 0:700 hrs, lipid hydroperoxide (LPO) assessed at 0:200 hrs and 0:700 hrs, and apolipoprotein (apo)AI, apoAII, apoB, high sensitivity C-reactive protein (hsCRP) and NT-proBNP, in 27 patients with chronic heart failure (CHF) (17 patients - with NYHA class II and 10 - with NYHA class III). In the study, Lipoproteins apoAI, apoAII, apoB, high sensitivity C-reactive protein (hsCRP) levels were determined by way of immunonephelometric methods, serum melatonin concentration was measured by using a competitive enzyme immunoassay technique, while serum LPO concentration was measured by using Cayman’s Lipid Hydroperoxide Assay Kit. In the study, CHF patients without acute inflammatory response demonstrated a decreased concentration of high density lipoprotein cholesterol (HDL-C), apoAI, apoAII levels, but an increased concentration of NT-proBNP, hsCRP and LPO at night, and LPO at daytime; however, the concentration of LPO at 0:700 was lower than at 0:200. Pearson’s correlation test and multiple ridge stepwise regression showed that melatonin administered at night exerts an effect on the composition of apoAI and apoAII of HDL particles, and induces decreased LPO at 0:700, but has no effect upon NT-proBNP levels in patients with NYHA class II. However, in patients with NYHA class III, melatonin administered at night induces an increase in the content of apoAII and apoAI, which further decreases hsCRP, and this, together with the administered melatonin, brings about daytime decreases in NT-proBNP and hsCRP levels. The results indicated that the content of apoAII and apoAI in HDL particles and melatonin demonstrate an anti-oxidative and anti-inflammatory effect, and together, have a cardio-protective effect on patients with advanced CHF. Hence, the results support melatonin being a cardio-protective agent. These relationships, however, need to be confirmed in further studies.