ApoA- and apoB-containing lipoproteins and Lp(a) concentration in non-dialyzed patients with chronic renal failure.
BACKGROUND
End-Stage renal disease is associated with accelerated atherosclerosis and a high incidence of cardiovascular disease.


METHODS
The serum levels of lipids and apolipoproteins and Lp(a) were determined in 51 patients with chronic renal failure (CRF) with various advancement, without interference of factors which might disturb Lp(a) metabolism and with proteinuria less than 0.5 g/24 h. The patients studied were divided into two groups: patients with moderate renal failure (CRF-M) and creatinine levels of 2-6mg/dL n = 27; and predialysis patients with end stage renal disease (ESRD) and creatinine levels higher than 8.5 mg/dL n=24.


RESULTS
In both studied groups serum concentrations of triglycerides (TG), total apoCIII, apoCIIInonB, apoB:CIII were statistically increased, (except total cholestrol (TC) and LDL-cholestrol (LDL-C), apoB, total apoE, apoEnonB, apoB:E), while the levels of HDL-cholestrol (HDL-C) and apoAl significantly decreased. Lipid and lipoprotein ratios as risk factors of atherosclerosis were similar in both groups. The TC/HDL-C ratio increased, while that of HDL-C/ apoAI and apoAI/apoCIII decreased. Serum Lp(a) concentrations were significantly increased in both studied groups. The medians and ranges of Lp(a) concentration were similar in both groups. Serum Lp(a) levels correlated with total cholesterol (r=0.295; p < 0.05), LDL-C (r = 0.312; p < 0.05) and apoB (r = 0.215; p < 0.05). In addition, no correlation was found between Lp(a) levels and albumin concentrations (r = 0.126; p = 0.421).


CONCLUSIONS
Our results may indicate that the reduced levels of apoA-containing lipoproteins and increased TG-rich apoB-containing lipoproteins and Lp(a) indicated a clear atherogenic pattern in early renal disease. Increased Lp(a) concentration may result in nonspecific synthesis or catabolism disturbances. Measurement and monitoring of lipoprotein family profiles offers a new means for selecting appropriate therapies targeted for normalizing dyslipidemia in non-dialyzed patients.
Kimak
Elibieta
E
Department of Clinical Laboratory Diagnostics, Medical University of Lublin, Poland. antuken@biotop.umcs.lublin.pl
Solski
Janusz
J
D000328:Adult; D001054:Apolipoproteins A / Q000097:blood*; D001055:Apolipoproteins B / Q000097:blood*; D001161:Arteriosclerosis / Q000097:blood / Q000209:etiology; D003404:Creatinine / Q000097:blood; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000150:complications; D017270:Lipoprotein(a) / Q000097:blood*; D008074:Lipoproteins / Q000097:blood*; D008297:Male
D001054:Apolipoproteins A; D001055:Apolipoproteins B; D017270:Lipoprotein(a); D008074:Lipoproteins; D003404:Creatinine