Moderate dyslipoproteinemia induced inflammation and remodeling HDL and VLDL particles in post-renal transplant patients
Curr Issues Pharm Med Sci., Vol. 30, No. 2, 75-80
Elzbieta Kimak1, Iwona Baranowicz-Gaszczyk2, Tomasz Bialopiotrowicz3
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.