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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2010  |  Volume : 21  |  Issue : 1  |  Page : 59-62
Cardiovascular risk factors in hemodialysis and peritoneal dialysis patients


Department of Internal Medicine A and Laboratory of Kidney Pathology 02 Charles Nicolle Hospital, Tunis, Tunisia

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Date of Web Publication8-Jan-2010
 

   Abstract 

Cardiovascular diseases are a major cause of morbidity and mortality in patients with end-stage renal disease (ESRD). The aim of our investigation was the evaluation of an extensive cardiovascular profile in hemodialysis (HD) and peritoneal dialysis (PD) patients. We studied 74 patients with ESRD (38 males, 36 females), maintained either on chronic HD (n= 50) or chronic PD (n= 24) and age and sex matched 20 healthy subjects as controls. The lipid profile, homo­cysteine (Hcy) and C reactive protein (CRP) were measured. When compared to a healthy popu­lation, HD patients displayed a marked atherogenic profile, as attested by increased levels of total cholesterol (TC), triglycerides (TG), low-density lipoprotein-cholesterol (LDL-C), apolipoprotein A (Apo A), CRP, Hcy and lower concentrations of high-density lipoprotein-cholesterol (HDL-C), Apo B, albumin (ALB). A significant difference was noted concerning the rates of Apo B, HDL­C, TC, ALB and Hcy. Same biological disorders that those found at HD patients were noted in these PD patients. One also noted lower concentration in Apo A. there were a significant diffe­rence with the reference group concerning the rates of albumin, Apo A, HDL-Cl and Hcy. When compared to PD patients, HD patients had significantly decreased concentration of LDL-C. The peculiar metabolic changes observed in the present study confirm the marked tendency of patients with impaired renal function for developing cardiovascular diseases, irrespectively of the type of dialysis. We suggest including uremia-related risk factors in the panel for evaluation of cardio­vascular risk in dialysis patients.

How to cite this article:
Helal I, Smaoui W, Hamida FB, Ouniss M, Aderrahim E, Hedri H, ELyounsi F, Maiz HB, abdallah TB, Kheder A. Cardiovascular risk factors in hemodialysis and peritoneal dialysis patients. Saudi J Kidney Dis Transpl 2010;21:59-62

How to cite this URL:
Helal I, Smaoui W, Hamida FB, Ouniss M, Aderrahim E, Hedri H, ELyounsi F, Maiz HB, abdallah TB, Kheder A. Cardiovascular risk factors in hemodialysis and peritoneal dialysis patients. Saudi J Kidney Dis Transpl [serial online] 2010 [cited 2017 Nov 24];21:59-62. Available from: http://www.sjkdt.org/text.asp?2010/21/1/59/58711

   Introduction Top


Cardiovascular diseases (CVD) are a major cause of morbidity and mortality in patients with end-stage renal disease (ESRD). Cardio­vascular mortality is 10 to 30 fold higher in ESRD patients than in general population after adjustment for age, gender, ethnic origin and diabetes. [1] The high prevalence of established traditional risk factors for atherosclerosis in these patients undoubtedly contributes to the accelerated rate of vascular disease. In addition, several hypotheses have emerged to explain the high prevalence of CVD in patients with ESRD. Growing evidence has been gathered over the last years regarding the role of ure­mia-related risk factors such as inflammation and oxidant stress in the pathogenesis of athe­rosclerosis in subjects with renal failure. [2]

Current data suggest that the addition of lipid screening to C reactive protein (CRP) can im­prove detection of absolute coronary risk. [3] Risk estimates using CRP in combination with lipid screening have been reported to be superior to assessments that evaluate just CRP, homocys­teine (Hcy), or lipoprotein A. [4] However, the cardiovascular risk assessment algorithm that uses CRP and lipid screening has not been tested in dialysis patients.

In this study, we determined CRP levels to demonstrate the inflammatory activity in addi­tion to other relatively new factors, such as apo A-l, apo B and Hcy levels in hemodialysis (HD) and peritoneal dialysis (PD) patients and com­pared the results with controls and between each other.

Treatment strategies like HD and PD have di­fferent effects on different parameters. We grouped the patients according to the treatment and aimed to examine the effect of treatment in ESRD patients. Each of the patients was examined about the traditional risk factors-age, diabetes mellitus, hypertension, smoking and dyslipidemia. We also investigated the relation­ship between traditional and non-traditional risk factors and CVD.


   Material and Methods Top


Patients and methods

We studied 74 patients with end-stage renal disease (38 males, 36 females), maintained either on chronic HD (n= 50) or chronic PD (n= 24). The control group consisted of 20 healthy sub­jects, matched for sex and age from the la­boratory staff. The clinical characteristics are shown in [Table 1]. The HD group comprised of 27 men and 23 women and the PD group com­prised 11 men and 13 women. The clinical pa­rameters are given in [Table 1].

Biochemical Analysis

Blood for biochemical analysis was collected after overnight fasting from PD patients and healthy controls and from the arterial needle from HD patients, prior to the first-of-the-week HD. The concentration of total proteins (TP), albumin (ALB), serum creatinine (Scr), total cholesterol (TC), high-density lipoprotein-cho­lesterol (HDL-C) and triglycerides (TG) were determined by enzymatic procedures. The con­centration of low-density lipoprotein-choleste­rol (LDL-C) was calculated using the formula of friede-wald. Apolipoprotein A (Apo A), apo­lipoprotein B (Apo B) and C reactive protein (CRP) were measured using commercial immu­nonephelometric assays. Total serum homocys­teine (Hcy) was measured by a commercial en­zyme immunoassay.


   Statistical Analysis Top


Values are presented as mean ± SD, with a P ­value < 0.05 indicating significance. Comparisons between groups were made using Chi­square test for qualitative parameters and non paired student's t test for continuous variable. All statistical calculations were done using the SPSS; for Windows 11.0 software program.


   Results Top


Main results of our investigations are shown in [Table 2]. When compared to a healthy po­pulation, HD patients displayed a marked athe­rogenic profile, as attested by 25% of patients were diabetic, 69.4% arterial hypertension, 15.4% dyslipimia, 2% cardiac ischemia, 12% cardiac insufficiency and 38.8% vascular throm­bosis. We found also increased levels of TC, TG, LDL-C, Apo A, CRP, Hcy and lower con­centrations of HDL-C, Apo B, TP. A significant difference was noted concerning the rates of Apo B, HDL-C, TC, ALB, CRP and Hcy.

The group of PD patients comprised of 12.5% diabetics, 79.2% with arterial hypertension, 4.2% cardiac ischemia and 4.2% vascular thrombo­sis. Same biological disorders that those found at HD patients were noted in this group. One also noted lower concentration in Apo A. there were a significant difference with the reference group concerning the rates of albumin, Apo A, HDL-C, CRP and Hcy.

When compared to PD patients, HD patients had significant decreased (P< 0.001) concen­tration of LDL-C.


   Discussion Top


In the present study, we evaluated cardiovas­cular disease risk in PD and HD patients. To that end, we measured serum lipid profiles and levels of CRP, albumin and Hcy.

Our study demonstrated that PD and HD pa­tients were associated with increased serum le­vels of Hcy and CRP. However, reduced levels of apo A/B and albumin were observed in se­rum from both patient groups than controls, in accord with previous reports. [5],[6],[7]

In past studies, CRP, a major systemic mar­ker of inflammation, was reported to induce adhesion molecule expression in human endo­thelial cells, supporting involvement of CRP in the atherosclerotic process. [8] Earlier laboratory assay methods were not sufficiently sensitive to measure blood levels of CRP within the nor­mal range (< 10 mg/L); however, the recent de­velopment of high-sensitivity assays for CRP has permitted mild elevation of CRP to be de­tected even within the normal range. Reliable and fully automated high-sensitivity assays for CRP are now widely available. Because a di­rect positive association between hs-CRP and future coronary events was previously repor­ted, [9],[10] the elevated CRP observed in our pa­tient groups might alone be a predictor of vas­cular risk.

The combination of TC:HDL-C ratio with CRP value has been suggested to be a signifi­cantly strong predictor of cardiovascular events.[3] Evaluating PD patients and HD patients with the cardiovascular risk assessment algorithm that uses CRP and TC:HDL-C ratio, the pa­tients were found to have an approximately three times greater risk than control subjects had.

We also found higher Hcy levels, another risk factor for cardiovascular disease in dialysis pa­tients than control subjects.

Many studies comparing Hcy levels in PD patients with those in HD patients have pro­duced conflicting results. [11],[12],[13] In our study, there was no significant difference in Hcy levels bet­ween HD and PD patients .

Possible causes of high serum Hcy levels in chronic renal failure may include reduced re­nal clearance, impaired degradation by the kid­ney, and deficiency of, or abnormally high re­quirement for, folic acid, vitamin B, and vita­min B12. [14]

Accordingly, we suggest that an intra-renal mechanism, such as a reduced ability of the kidney to metabolize Hcy, rather than an insu­fficiency of vitamin B12 and folic acid, may be the primary cause of hyperhomocysteine­mia in end-stage renal failure. We observed elevated Hcy levels in our patient groups, but the mechanism of the relationship between ele­vated Hcy and cardiovascular disease remains to be established.

In conclusion, the peculiar metabolic changes observed in the present study confirm the marked tendency of patients with impaired renal function for developing cardiovascular diseases, irrespective of the type of dialysis. We suggest including uremia-related risk fac­tors in the panel for evaluation of cardiovas­cular risk in dialysis patients.

 
   References Top

1.Foly RN, Parfrey PS, Sarnak MJ. Clinical epi­demiology of cardiovascular disease in chronic renal disease. Am J Kidney Dis 1998;32:S112-­9.  Back to cited text no. 1      
2.Cases A, Vera M, Lopez GJ. Cardiovascular risk in patients with chronic renal failure. Nefrologia 2002;22:68-74.  Back to cited text no. 2      
3.Braunwad E. Shattuck Lecture-Cardiovascular medicine at the turn of the millennium: triumphs concerns, and opportunities. N Engl J Med 1997;337:1360-9.  Back to cited text no. 3      
4.Rifai N, Ridker PM. Proposed cardiovascular risk assessment algorithm using high-sensi­tivity C-reactive protein and lipid screening. Clin Chem 2001;47:28-30.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]  
5.Samuelsson O, Mulec H, Knight-Gibson C, et al. Lipoprotein abnormalities are associated with increased rate of progression of human chronic renal insufficiency. Nephrol Dial Transplant 1997;12:1908-15.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]  
6.Lippi G, Tessitore N, Gammaro L, Rugiu C, Maschio G, Guidi G. Cardiovascular risk fac­tors in patients with chronic renal failure maintained on hemodialysis or continuous am­bulatory peritoneal dialysis. Thromb Res 2001; 101:517-9.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]  
7.Yilmaz FM, Yilmaz G, Duranay M, et al. Car­diovascular risk factors in haemodialysis and peritoneal dialysis patients. Scand J Clin Lab Invest 2005;65(8):739-45  Back to cited text no. 7      
8.Pasceri V, Willerson JT, Yeh ET. Direct pro­inflammatory effect of C-reactive protein on human endothelial cells. Circulation 2000;102: 2165-8.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]  
9.Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997;336:973-9.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]  
10.Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Plasma concentration of C-reactive protein and risk of developing peripheral vascular disease. Circulation 1998; 97:425-8.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]  
11.Moustapha A, Gupa A, Robinson K, et al. Pre­valence and determinants of hyperhomocystei­nemia in hemodialysis and peritoneal dialysis. Kidney Int 1999;55:1470-5.  Back to cited text no. 11      
12.Kim SS, Hirose S, Tamura H, et al. Hyper­homocysteinemia as a possible role for athe­rosclerosis in CAPD patients. Adv Perit Dial 1994;10:282-5  Back to cited text no. 12  [PUBMED]  [FULLTEXT]  
13.Suliman ME, Anderstam B, Lindholm B, Bergstrom J. Total, free, and protein-bound sulphur amino acids in uremic patients. Nephrol Dial Transplant 1997;12:2332-8.  Back to cited text no. 13      
14.Refsum H, Helland S, Ueland PM. Radio­enzymatic determination of homocysteine in plasma and urine. Clin Chem 1985;31:424-8.  Back to cited text no. 14      

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Correspondence Address:
Imed Helal
Department of Internal Medicine A and Laboratory of Kidney Pathology 02, Charles Nicolle Hospital, Boulevard 9 Avril, 1006 Tunis
Tunisia
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PMID: 20061694

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    Tables

  [Table 1], [Table 2]

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    Abstract
    Introduction
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    Statistical Analysis
    Results
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