American Journal of Epidemiology and Infectious Disease
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American Journal of Epidemiology and Infectious Disease. 2014, 2(1), 33-40
DOI: 10.12691/ajeid-2-1-7
Open AccessArticle

High-Density Lipoproteins and Inflammation in Patients on Renal Replacement Therapies

Despina Kyriaki1, Panagiotis N. Kanellopoulos1 and Vaia D. Raikou1,

1Department of Medicine - Propaedaetic, National & Kapodistrian University of Athens, School of Medicine. General Hospital “LAΪKO”, ΑΤΗΕΝS, GREECE

Pub. Date: January 21, 2014

Cite this paper:
Despina Kyriaki, Panagiotis N. Kanellopoulos and Vaia D. Raikou. High-Density Lipoproteins and Inflammation in Patients on Renal Replacement Therapies. American Journal of Epidemiology and Infectious Disease. 2014; 2(1):33-40. doi: 10.12691/ajeid-2-1-7


Background/aim: High-density lipoprotein (HDL) protects against atherosclerotic plaque formation. The present study examined the relationship between HDL serum concentrations and markers of inflammation in patients on renal replacement therapies. Methods: We studied 96 dialyzed patients, 62 males and 34 females, on mean age 62.1 ± 14.27 years old and 24 healthy controls. The treatment modalities which were applied were: regular hemodialysis (HD, n = 34), predilution hemodiafiltration (HDF, n = 42) and peritoneal dialysis (PD, n = 20). Dialysis adequacy was defined by Kt/V for urea and serum bicarbonate levels were measured in gas machine. Cholesterol, triglycerides, HDL and LDL concentrations were biochemically measured. Oxidized LDL (ox-LDL) and hsCRP serum concentrations were measured by ELISA. Beta2-microglobulin (beta2M) and leptin serum concentrations were measured by radioimmunoassays. Results: The patients presented increased beta2M, hsCRP, leptin and triglycerides than control group, but HDL exhibited significant reduction (p < 0.05). The patients on PD had significantly higher serum bicarbonate levels and lower oxLDL than other groups of patient (p < 0.05). HDL positively associated with Kt/V, presented negative correlation with both, ox-LDL and beta2M (r = -0.237, p = 0.02 and r = -0.291, p = 0.004 respectively). Beta2M was positively associated with hsCRP (r = 0.257, p = 0.01). Serum bicarbonate levels were inversely associated with hsCRP and oxLDL (r = -0.232, p = 0.05 and r = -0.289, p = 0.01 respectively). Conclusions: The low HDL was associated with increased beta2M concentrations in patients on renal replacement therapies. The HDL reduction was combined with an elevation of oxLDL, which was lower in PD patients compared to hemodialysis modalities patients. The acidosis state influenced both, the inflammatory environment and the increase of oxidized lipids. Dialysis adequacy was positively correlated to HDL serum concentrations.

hemodialysis HDL lipoprotein beta2-microglobulin inflammation hsCRP acidosis

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[1]  Vaziri ND. Dyslipidemia of chronic renal failure: The nature, mechanisms and potential consequences. Am J Physiol, Renal Physiol. 2006; 290: 262-272.
[2]  Vaziri ND. Oxidative stress in chronic renal failure: The nature, mechanism and consequences. Semin Nephrol. 2004; 24: 469-473.
[3]  Gleissner CA, Leitinger N, Ley K. Effects of native and modified low-density lipoproteins on monocyte recruitment in atherosclerosis. Hypertension. 2007; 50: 276-283.
[4]  Hansson GK, Robertson AK, Söderberg-Nauclér C. Inflammation and atherosclerosis. Annu Rev Pathol. 2006; 1: 297-329.
[5]  Davidson MH, Toth PP. High-density lipoprotein metabolism: potential therapeutic targets. Am J Cardio. 2007; 100: n32-n40.
[6]  Feig JE, Shamir R, Fisher EA. Atheroprotective effects of HDL: beyond reverse cholesterol transport. Curr Drug Targets. 2008; 9: 196-203.
[7]  Vaziri ND, Navab M, Fogelman AM. HDL metabolism and activity in chronic kidney disease. Nat Rev Nephrol. 2010; 6: 287-296.
[8]  Kalantar-Zadeh K, Kopple JD, Kamranpour N, et al. HDL-inflammatory index correlates with poor outcome in hemodialysis patients. Kidney Int. 2007; 72: 1149-1156.
[9]  Chauveau P, Nguyen H, Combe C, Chêne G, Azar R, Cano N, Canaud B, Fouque D, Laville M, Leverve X, Roth H, Aparicio M; French Study Group for Nutrition in Dialysis.Dialyzer membrane permeability and survival in hemodialysis patients. Am J Kidney Dis. 2005; 45 (3): 565-71.
[10]  Daugirdas JT. Second generation logarithmic estimates of single-pool variable volume Kt/V: an analysis of error. J Am Soc Nephrol 1993; 4: 1205-1213.
[11]  Dugirdas JT: Simplified equations for monitoring Kt/V, PCRn, eKt/V, and ePCRn. Adv Ren Replace Ther 1995; 2: 295-304.
[12]  Moradi H, Yuan J, Ni Z, et al. Reverse cholesterol pathway in experimental chronic kidney disease. Am J Nephrol. 2009; 30: 147-154.
[13]  Kim C, Vaziri ND. Downregulation of hepatic LDL receptor-related protein (LRP) in chronic renal failure. Kidney Int. 2005; 67: 1028-1032.
[14]  Vaziri ND, Liang K. Down regulation of VLDL receptor expression in chronic experimental renal failure. Kidney Int. 1997; 51: 913-919.
[15]  Moradi H, Pahl MV, Elahimehr R, et al. Impaired Antioxidant Activity of HDL in Chronic Kidney Disease. Transl Res. 2009; 153: 77-85.
[16]  Vaziri ND, Liang K. ACAT inhibition reverses LCAT deficiency and improves plasma HDL in chronic renal failure. Am J Physiol, Renal Physiol. 2004; 287: F1038-F1043.
[17]  Price SR, Du JD, Bailey JL, Mitch WE: Molecular mechanisms regulating protein turnover in muscle. Am J Kidney Dis 2001; 37: S112-S114.
[18]  London GM, Drueke TB. Atherosclerosis and arteriosclerosis in chronic renal failure Kidney Int. 1997; 51 (6): 1678-95.
[19]  Okuno S, Ishimura E, Kohno K, Fujino-Katoh Y, Maeno Y, Yamakawa T, Inaba M, Nishizawa Y. Serum beta2-microglobulin level is a significant predictor of mortality in maintenance haemodialysis patients. Nephrol Dial Transplant 2009; 24 (2): 571-7.
[20]  Wilson AM, Kimura E, Harada RK, Nair N, Narasimhan B, Meng XY, Zhang F, Beck KR, Olin JW, Fung ET, Cooke JP. Beta2-microglobulin as a biomarker in peripheral arterial disease: proteomic profiling and clinical studies. Circulation 2007; 116: 1396-1403.
[21]  R.Barazzoni, G.Biolo, M.Zanetti, A.Bernardi, G.Guarnieri. Inflammation and Adipose Tissue in Uremia. J of Renal Nutrition 2006; 16 (3): 204-207.
[22]  Burl R Don, Laura M Rosales, Nathan W Levine, William Mitch and George A Kaysen. Leptin is a negative acute phase protein in chronic hemodialysis patients. Kidney Intl 2001; 59: 1114-1120.
[23]  Vaziri ND, Moradi H, Pahl MV, et al. In vitro stimulation of HDL anti-inflammatory activity and inhibition of LDL pro-inflammatory activity in the plasma of patients with end-stage renal disease by an apoA-1 mimetic peptide. Kidney Int. 2009; 76: 437-44.
[24]  Van Lenten BJ, Reddy ST, Navab M, et al. Understanding changes in high density lipoproteins during the acute phase response. Arterioscler Thromb Vasc Biol. 2006; 26: 1687-1688.
[25]  Sonikian M, Gogusev J, Zingraff J, et al: Potential effect of metabolic acidosis on beta2-microglobulin generation: in vivo and in vitro studies. J Am Soc Nephrol 1996; 7: 350-356.
[26]  Gugliucci A, Mehlhaff K, Kinugasa E, et al. Paraoxonase-1 concentrations in end-stage renal disease patients increase after hemodialysis: correlations with low molecular AGE adduct clearance. Clin Chim Acta. 2007; 377: 213-220.
[27]  Albertini R, Rindi S, Passi A, et al. The effect of heparin on Cu (2+)-mediated oxidation of human low-density lipoproteins. FEBS Lett. 1995; 377 (2): 240-242.
[28]  Sandström J, Carlsson L, Marklund SL, et al. The heparin-binding domain of extracellular superoxide dismutase C and formation of variants with reduced heparin affinity. J Biol Chem. 1992; 267: 8205-18209.