Relationships between serum lipid, lipoprotein, triglyceride-rich lipoprotein, and high-density lipoprotein particle concentrations in post-renal transplant patients

Abstract

Abstract:Objective: Disturbances in lipid and lipoprotein profiles in patients after kidney transplantation (Tx) are still not understood. Methods: Serum levels of lipids, lipoprotein, triglyceride-rich lipoproteins (TRLs), and high-density lipoprotein (HDL) particles were determined, lipid and lipoprotein ratios were calculated, and their relationships in Tx patients with hypertriglyceridemia (HTG) and lower apolipoprotein AI (apoAI) concentration were examined. Serum lipid and lipoprotein levels were measured in 109 Tx patients and 89 healthy subjects. HDL particle levels were determined by enzyme-linked immunosorbent assay (ELISA). Results: Tx patients had disturbed concentration, composition, and metabolism of TRLs and HDL particles. Multivariance analysis showed significant and positive correlation between HDL cholesterol/apoAI (HDL-C/apoAI) and HDL-C/HDL ratios, which indicates that both ratios could sensitively reflect changes in the HDL subclasses and their distribution into smaller size particles. In Tx patients, the decreased HDL-C/apoAI ratio indicates that, along with the decreased apoAI concentration, the HDL-C level is decreased. However, a low HDL-C/HDL ratio indicates that HDL particles in Tx patients transport lesser content of HDL-C but more triglyceride (TG) (high TG/HDL ratio), and thus are hypercatabolized and removed; therefore, concentration of HDL particles in serum was decreased. Conclusion: The decrease of HDL-C/apoAI ratio seems to be a good marker of HDL subclass distribution into smaller size particles.

Lipid abnormalities in kidney disease and management strategies

“…Studies have shown a role of parathyroidectomy in reducing triglyceride levels in CKD patients [26,27] . Among renal transplant recipients, it has been seen that lipids and lipoprotein profile ratios were more beneficial when the TG levels were less than 150 mg/dL and apoA1 was greater than 150 mg/dL when compared to the opposite [28] . They are also on immunosuppressive medications, many of which affect the lipid profile adversely.…”

Association between moderately oxidized low-density lipoprotein and high-density lipoprotein particle subclass distribution in hemodialyzed and post-renal transplant patients

“…No cardiac incidence occurred in Tx patients. The control group consisted of 89 subjects chosen from among apparently normolipidemic people as described previously (Kimak et al, 2010). The study was carried out in accordance with the guidelines of the Ethics Committee of the Medical University of Lublin, Poland.…”

“…Serum was immediately separated and stored in aliquots at −80 °C until use. Routine laboratory parameters (the levels of urea, uric acid, creatinine, total protein, and albumin) and lipids and lipoproteins (apoA, apoB) were determined by use of the Hitachi 902 analyzer, and hemoglobin was determined by using ADVIA analyzer, as described previously (Kimak et al, 2010). ApoA-I and apoB were measured using the turbidimetric methods (Roche kits).…”

“…The studies suggest that paraoxonase (PON) prevents low-density lipoprotein (LDL) oxidation by hydrolyzing lipid peroxides (Draganov et al, 2005). Oxidized LDL (ox-LDL), together with risk factors, damages the endothelium of the arterial wall and impairs lipoprotein metabolism in hemodialyzed (HD) and post-renal transplant (Tx) patients, as well as characteristic abnormalities such as hypertriglyceridemia and decreased high-density lipoprotein (HDL) cholesterol (Chen et al, 2005;Kimak et al, 2010). HDL possesses antioxidant, anti-inflammatory, antithrombotic and endovascular properties.…”

Can chronic heart failure induce kidney function damage?

“…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].…”