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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2012  |  Volume : 23  |  Issue : 6  |  Page : 1281-1284
Plasma lipoprotein abnormalities in hemodialysis patients

1 Department of Nephrology, Dialysis and Renal Transplantation, Military Hospital Mohammed V, Hay Riad, Rabat, Morocco
2 Department of Biochemistry, Military Hospital Mohammed V, Hay Riad, Rabat, Morocco

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Date of Web Publication17-Nov-2012

How to cite this article:
Aatif T, Asseraji M, Maoujoud O, Dami A, El Allam M, Oualim Z. Plasma lipoprotein abnormalities in hemodialysis patients. Saudi J Kidney Dis Transpl 2012;23:1281-4

How to cite this URL:
Aatif T, Asseraji M, Maoujoud O, Dami A, El Allam M, Oualim Z. Plasma lipoprotein abnormalities in hemodialysis patients. Saudi J Kidney Dis Transpl [serial online] 2012 [cited 2022 Jul 1];23:1281-4. Available from: https://www.sjkdt.org/text.asp?2012/23/6/1281/103577
To the Editor,

The disruptions of lipid metabolism seen in end-stage renal disease (ESRD) on dialysis are responsible for an atherogenic lipid profile and a high risk of cardiovascular morbidity and mortality. This lipid profile is typically characterized by lower high-density lipoprotein (HDL) cholesterol and elevated triglycerides (TG). [1],[2]

We undertook a monocentric cross-sectional comparative observational study with an aim to evaluate the qualitative and quantitative changes in lipid parameters and to determine the prevalence of dyslipidemia in patients on maintenance hemodialysis (MHD) in our center. A group of 30 patients with ESRD on MHD formed the study group (excluding those taking lipid-lowering agents, diuretics as well as those with acute or chronic infection), and 30 healthy people matched for age, sex and body mass index (BMI) served as the controls. Both MHD and the control group had 14 males (46%) and 16 females (54%) in each group. Age range among MHD and control groups was 45.8 ± 14.25 and 46.13 ± 16.42 years, respectively. The mean duration on HD among the MHD group was 47 ± 33 months. The aetiology of chronic kidney disease and other characteristics of the study population and control subjects are shown in [Table 1] and [Table 2], respectively.
Table 1: Characteristics of the hemodialysis group.

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Table 2: Characteristics of the control group.

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The parameters studied were TG, total cholesterol (TC), low-density lipoprotein (LDL) cholesterol, HDL cholesterol and atherogenic index (AI = TC/HDL-C). Dyslipidemia was defined as per the guidelines of the Adult Treatment Panel III (ATP III) of the National Cholesterol Education Program (NCEP) [3],[4] by the presence of at least one of the factors: LDL cholesterol >130 mg/dL, HDL cholesterol <40 mg/dL, TG >150 mg/dL or taking lipid-lowering treatment. Lipid risk was considered as high when the calculated AI was equal to or greater than 5. The results of lipid parameters of hemodialysis patients were compared with the controls. The data were analyzed using statistical program SPSS version 10.0. Quantitative variables were expressed as mean ± standard deviation. Qualitative variables were expressed as frequencies and percentages. Comparison of means was performed by Student's t test. A probability <0.05 was considered significant.

The prevalence of dyslipidemia in MHD patients was 80%. The most frequent abnormality was lower HDL cholesterol (<40 mg/dL) 70%, followed by hypertriglyceridemia (TG >150 mg/dL) 33.3% and hypercholesterolemia (LDL cholesterol >130 mg/dL) 23.3% of patients. We have noted the deterioration of two to three dyslipidemic parameters in half of the cases. The serum TG and AI were significantly higher in MHD patients than in the control group (P <0.001 and P <0.005, respectively), while HDL cholesterol was significantly lower in MHD patients compared with the control group (P <0.001) [Table 3].
Table 3: Lipid profile among study groups.

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The qualitative and quantitative disturbances in lipid profiles are common in ESRD. [5],[6] The prevalence of dyslipidemia in chronic hemodialysis patients vary between studies. It is 40% in the study reported by Fox et al, [7] 63% in the series of Cofan et al [8] and 67% in that of Kronenberg et al. [9] In our series, the prevalence was high in the order of 80%. Profile of dyslipidemia in chronic hemodialysis is characterized by hypertriglyceridemia and lower HDL cholesterol. Total cholesterol and LDL cholesterol are usually normal or slightly increased. [4],[10],[11] The hypertriglyceridemia, most commonly the lipid abnormality encountered in hemodialysis patients, [11] is seen in 20-70% of the cases. [11],[12] In our study, it was seen in 33.3% of the patients. The hypertriglyceridemia is related to reduced catabolism of triglyceriderich lipoproteins, resulting in its accumulation, mainly very low-density lipoproteins (VLDL) and intermediate density lipoproteins (IDL). This reduction appears to be due to a decrease in lipolytic activity of lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL). [11],[13] The cause of the reduced activity of LPL remains uncertain; several mechanisms have been proposed: the elevation of plasma apoC-III, [14] the presence in the circulation of LPL inhibitors that are not removed because of renal failure and the inability of conventional cellulose hemodialyzers to remove them, [15] the existence of secondary hyperparathyroidism, which causes an accumulation of calcium in the liver and adipose tissue, may interfere with the metabolism of lipoproteins [16] and repeated heparinization through depletion of tissue LPL resulting deficit. [2] Other authors, however, reported that the type of hemodialyser and the rate of parathyroid hormone has no effect on triglyceride levels. [17]

Concerning the metabolism of cholesterol and in accordance with the literature data, the abnormality most significant was the decline in HDL cholesterol in the hemodialysis group. This abnormality has affected 70% of the cases. This decline is typical in chronic uremics, and is particularly observed in the HDL2 fraction. [2] The hypertrigyceridemia, increased catabolism of ApoA-I and decreased plasma activity of LPL and HTGL of lecithin cholesterol acyltransferase (LCAT) are the factors responsible for disturbance in the metabolism of HDL cholesterol. [2],[12] In contrast, total cholesterol and LDL cholesterol showed no significant difference with the control group. [2],[12]

However, the absence of quantitative abnor malities cannot exclude the presence of qualitative disturbances of LDL particles that increase the atherogenicity. The increase in the oxidative susceptibility of LDL and accumulation of the small fraction in highly atherogenic dense LDL (LDL subclass-6) have been described. [10],[18] Moreover lipoprotein (a) [Lp (a)] is consistently high, with very high rates in peritoneal dialysis patients. [8] Many chronic hemodialysis patients have more than two parameters of dyslipidemia. [9],[19]

The levels of some lipid parameters have predictive powers in relation to cardiovascular events, but vary according to studies. [20] In our study, we used the AI (AI = TC/HDL-C). Chronic hemodialysis patients showed a significant increase of AI compared with the control group, which is explained by the significant decrease in HDL-C compared with controls. An AI greater than or equal to 5 is for a high risk of atherogenicity. In the hemodia-lysis group, AI was >5 in 33.3% of the cases. Dyslipidemia is a modifiable factor for morbidity and mortality in chronic hemodialysis patients, its control must be done strictly by use of lifestyle modifications and taking lipid-lowering drugs to establish a strategy for preventing cardiovascular risk.

   References Top

1.Liu J, Rosner MH. Lipid abnormalities associated with end-stage renal disease. Semin Dial 2006;19:32-40.  Back to cited text no. 1
2.Shoji T, Nishizawa Y. Plasma lipoprotein ab11n/ormalities in hemodialysis patients-clinical implications and therapeutic Guidelines. Ther Apher Dial 2006;10:305-15.  Back to cited text no. 2
3.National Cholesterol Education Program, Third repoprt of the expert panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adults Treatment panel III). NIH Publication No. 02-5215 September 2002.  Back to cited text no. 3
4.Cofan F, Vela E, Clèries ZM. Analysis of dyslipidemia in patients on chronic hemodialysis in Catalonia. Atherosclerosis 2006;184:94-102.  Back to cited text no. 4
5.Moulin B. Lipid abnormalities during renal failure: impact on the progression of renal failure and cardiovascular risk. Nephrologie 2000;21:339-41.  Back to cited text no. 5
6.Shoji T, Ishimura E, Inaba M, Tabata T, Nishizawa Y. Atherogenic lipoproteins in endstage renal disease. Am J Kidney Dis 2001;38 (4 suppl 1):S30-3.  Back to cited text no. 6
7.Fox CS, Longenecker JC, Powe NR, et al; CHOICE Study. Undertreatement of hyperlipidemia in a cohort of United States Kidney dialysis patients. Clin Nephrol 2004;61:299-307.  Back to cited text no. 7
8.Cofan F, Vela E, Cteries M. Collaborative Study Group for Dyslipidemia. Atherosclerosis 2006;184:94-102.  Back to cited text no. 8
9.Kronenberg F, Lingenhel A, Neyer U, et al. Prevalence of dyslipidemic risk factors in hemodialysis and CAPD patients. Kidney Int Suppl 2003;63:S113-6.  Back to cited text no. 9
10.Wanner C, Quaschning T. Dyslipidemia and renal disease: Pathogenesis and clinical consequences. Curr Opin Nephrol Hypertens 2001; 10:195-10.  Back to cited text no. 10
11.Verzola A, Perini L, Gatto S, Gilli P, Bedani PL. Causes and risks of hyperlipidemia during dialysis and after renal transplantation. Recenti Prog Med 1998;89:590-7.  Back to cited text no. 11
12.Lacour B, Massy ZA, Jungers P, Drucke T. Anomalies of lipoprotein metabolism in chronic renal insufficiency. Néphrologie 1993;14: 75-90.  Back to cited text no. 12
13.Lee DM, Knight-Gibson C, Samuelsson O, Attman PO, Wang CS, Alaupovic P. Lipoprotein particle abnormalities and the impaired lipolysis in renal insufficiency. Kidney Int 2002;61:209-18.  Back to cited text no. 13
14.Tornero F, García-Garzón A, Rincón B, Prieto S, Usón J, Lozano L. Apolipoprotein C-II and C-III anomalies in normolipemic and hyperlipemic patients with chronic kidney failure. Nefrologia 2000;20:47-53.  Back to cited text no. 14
15.Ingram AJ, Parbtani A, Churchill DN. Effects of two low-flux cellulose acetate dialysers on plasma lipids and lipoproteins -a cross-over trial. Nephrol Dial Transplant 1998;13:1452-7.  Back to cited text no. 15
16.Shoji T, Nishizawa Y, Kawagishi T, Emoto M, Morii H. Secondary hyperparathyroidism, decrease hepatic triglyceride lipase, elevated intermediate density lipoprotein and atherosclerosis in hemodialysis patients. Nephron 1998;78:121-2.  Back to cited text no. 16
17.Ottosson P, Attman PO, Knight C, Samuelsson O, Weiss L, Alaupovic P. Do high-flux dialysis membranes affect renal dyslipidemia? ASAIO J 2001;47:229-34.  Back to cited text no. 17
18.Rajman I, Harper L, McPake D, Kendall MJ, Wheeler DC. Low-density lipoprotein subfraction profiles in chronic renal failure. Nephrol Dial Transplant 1998;13:2281-7.  Back to cited text no. 18
19.Quaschning T, Krane V, Metzger T, Wanner C. Abnormalities in uremic lipoprotein metabolism and its impact on cardiovascular disease. Am J Kidney Dis 2001;38(Suppl 1): S14-9.  Back to cited text no. 19
20.Frey J, Couderc R. Semiologic value of LDL cholesterol and apolipoprotein B in risk of atherosclerosis. Ann Biol Clin 1998;56:517-20.  Back to cited text no. 20

Correspondence Address:
Taoufiq Aatif
Department of Nephrology, Dialysis and Renal Transplantation, Military Hospital Mohammed V, Hay Riad, Rabat
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1319-2442.103577

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  [Table 1], [Table 2], [Table 3]


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