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 Table of Contents  
ORIGINAL ARTICLE
Year : 2016  |  Volume : 3  |  Issue : 1  |  Page : 28-30

Study of dyslipidemia and antioxidant status in chronic kidney disease patients at a hospital in South East Asia


1 Department of Biochemistry, Sri Aurobindo Institute of Medical Sciences, Indore, Madhya Pradesh, India
2 Department of Biochemistry, Saraswati Institute of Medical Sciences, Hapur, Uttar Pradesh, India
3 Department of Anatomy, MIMS, Bhopal, Madhya Pradesh, India
4 Department of Pharmacology, IMS and SUM Hospital, SOA University, Bhubaneswar, Odisha, India

Date of Web Publication25-Feb-2016

Correspondence Address:
Kamal Kachhawa
Department of Biochemistry, Sri Aurobindo Institute of Medical Sciences, Indore, Madhya Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2394-2010.177494

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  Abstract 

Introduction: The prevalence of hyperlipidemia is a most common problem in developed and developing society. Abnormal increase level of total cholesterol, triglyceride (TG), very low-density lipoprotein (VLDL), and LDL caused cardiovascular disease (CVD) in chronic kidney disease (CKD). Dyslipidemia is a known marker for CVD in the common population. Significant abnormal total cholesterol, LDL, TG, VLDL, and high-density lipoprotein (HDL) are present in CKD patients. Materials and Methods: In this study, we tried to find out the levels of lipid profile and antioxidant levels in CKD patients and its correlation with CVD. This study included 159 human subjects of age group between 40 and 65 years, out of which 78 patients were CKD and rest 81 patients are matched healthy subjects (control group). Results and Discussion: Our study showed a significant increase in Blood Pressure compared to control subjects. Lipid profile (total cholesterol, VLDL, TG, and LDL) was found significantly deranged (P < 0.001) and there was a decrease in the levels of HDL-cholesterol compared to control subjects. Conclusion: Enzyme level (superoxide dismutase) was significantly decreased, and malondialdehyde level was significantly increased compared to control subjects which show the effect of dyslipidemia and oxidative stress associated with the chronic kidney disorder.

Keywords: Antioxidant, cardiovascular disease, chronic kidney disease, lipid profile


How to cite this article:
Kachhawa K, Varma M, Kachhawa P, Agrawal D, Shaikh M, Kumar S. Study of dyslipidemia and antioxidant status in chronic kidney disease patients at a hospital in South East Asia. J Health Res Rev 2016;3:28-30

How to cite this URL:
Kachhawa K, Varma M, Kachhawa P, Agrawal D, Shaikh M, Kumar S. Study of dyslipidemia and antioxidant status in chronic kidney disease patients at a hospital in South East Asia. J Health Res Rev [serial online] 2016 [cited 2019 Oct 14];3:28-30. Available from: http://www.jhrr.org/text.asp?2016/3/1/28/177494


  Inroduction Top


Chronic kidney disease (CKD) is a worldwide health problem. In developing nation, CKD has severe implication on health and economic output. The rapid increase of common risk factors such as hypertension, obesity, and diabetes will result in greater and more burdens to developing country are not easy to handle. Definition of CKD as persistent kidney damage accompanied by a reduction in the glomerular filtration rate and the presence of albuminuria.[1] Specific metabolic abnormalities of plasma lipoprotein are characterized by CKD.[1] Many studies have shown that total cholesterol and LDL-cholesterol values are important markers of cardiovascular mortality.[2] In patients with CKD, hypertriglyceridemia is a common quantitative lipid abnormalities.[3],[4] It is known that in CKD patients, cardiovascular disease (CVD) is a known cause of death and motility.[5],[6] Most of the time, CKD patients die because of CVD before dialysis becomes necessary. The oxidative stress generated in CKD patients caused increases reactive oxygen species (ROS), which leads to the activation of various redox-sensitive cell signaling molecules and the production of cytotoxic materials. This is followed by cellular dysfunction and damage and ultimately results in microvascular complications.[7]


  Materials and Methods Top


The study was conducted in the Department of Biochemistry at SAIMS Medical College and Hospital, Indore, Madhya Pradesh, India. Approval for this study was obtained by the ethical committee of the institute. Informed consent was obtained from all patients. The study population comprised 81 control and 78 CKD patients who were consecutively recruited from the nephrology clinic of the hospital between September 2014 and May 2015.

The study was conducted in 159 human subjects. The CKD patients diagnosed by Department of Nephrology in SAIMS hospitals were included in this research work by their consent. A structured questionnaire regarding the demographic data, such as age, sex, height, and body weight, was measured while wearing lightweight clothing, but not shoes. Blood pressure, smoking habit, family history of diabetes, renal disease, and hypertension were recorded for each patient. CKD patients with advance stage (IV and V) and from different medical conditions (cardiac disease) were not included.

5 ml of blood sample was withdrawn from the antecubital vein following overnight fasting. The blood sample was collected in plain, fluoride, and ethylenediaminetetraacetic acid vacutainers. The blood sample was centrifuged for 15 min. At 3000 rpm at room temperature. The serum was stored at 4°C for biochemical investigations. Urea, creatinine, uric acid, and lipid profile were estimated by enzymatic method. All biochemical investigation done by fully automated analyzer Hitachi 902.

By using the method of Marklund and Marklund (1974), serum superoxide dismutase (SOD) activity was estimated.[8] Plasma malondialdehyde (MDA) was estimated by Jean et al.[9]

Statistical analysis

Statistical analysis was done using SPSS version 16 (SPSS Inc., Chicago, IL). Results were expressed as mean ± standard deviation and were analyzed by unpaired Student's t-test. The value of P < 0.01 was considered significantly.


  Results Top


Demographic data and clinical characteristics of the study of control subjects and CKD patients are shown in [Table 1]. The mean age of the 78 diabetic nephropathy patients was 40 ± 10 with 53.84% of the patients being male. There is no difference in age, sex, and body mass index in both groups. Blood pressure (systolic blood pressure and diastolic blood pressure) was significantly increased in the Group II compare to control subjects. Serum urea levels, serum creatinine levels, and serum uric acid level significantly increased (P < 0.001) as compared to control. The data which are provided indicates the high risk of CVD in patients suffering from CKD.
Table 1: Demographic, clinical, and biochemical characteristics of control subjects and diabetic nephropathy patients (mean±SD)

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Serum lipid profile (total cholesterol, triglyceride [TG], LDL, and very low-density lipoprotein [VLDL]) except high-density lipoprotein-cholesterol (HDL-C) was showed significantly increased compared to control subjects. Some other studies also shown similar results.[1],[10],[11] Antioxidant level (SOD and uric acid) showed significantly decreased (P < 0.001) and MDA was found significantly high (P< 0.001) in comparison to control subjects as shown in [Table 1]. Various other studies also consistency with our results.[12],[13]


  Discussion Top


Oxidative stress and lipid profile were studied by assessing renal function, and the results suggested that lipid profile and stress marker were profoundly deranged in CVD patients of CKD.

In our result increased the level of lipid profile (total cholesterol, VLDL, TG, and LDL) found a possible explanation of abnormal lipid metabolism to accelerate the progression of CVD in CKD patients through various paths. First, reabsorption of fatty acids, phospholipids, and cholesterol contained in the filtered proteins by tubular epithelial cells can stimulate tubulointerstitial inflammation, foam cell formation, and tissue injury.[14] Second, accumulation of lipoproteins in glomerular mesangium can promote matrix production and glomerulosclerosis.[15] For CKD patients, some of the studies have shown a good association between risk for cardiovascular events and total cholesterol values,[16] whereas other studies did not show any significant correlation.[10] Several other studies have demonstrated that HDL-C is a negative risk factor for atherosclerosis.[17] In our CKD patients have reduced plasma HDL-C levels, many other study consistency with us [1],[11] possible explanation of decrease level of HDL is decrease level of apolipoproteins AI and AII, abnormal activity of lecithin: Cholesterol, cholesteryl ester transfer protein shows increased activity which facilitates the transfer of cholesterol esters from HDL to TG-rich lipoproteins, and so there is reduction in the serum concentrations of HDL-C.[18],[19]

Oxidative stress status of the CKD patients was obtained by measuring plasma lipid peroxidation end product MDA, whereas antioxidant enzyme (SOD) and uric acid measured the antioxidant status. The cascade of hypoxic-ischemic injury, inflammation, apoptosis, and cell death result in compromised antioxidant functions.[20] ROS increases peroxidation of cellular membrane lipids as well as increasing the oxidation of proteins that yield protein carbonyl derivatives, producing a high level of MDA in the CKD patients which is a suggestive feature of oxidative stress in long-standing chronic disease. Our results are also consistent with the study reported by Hong and Chia [12] and Rutkowski et al.[13] In this study too, a noticeable reduction in serum SOD and uric acid were seen in CKD patients with respective renal dysfunction. Uric acid is a powerful antioxidant and is a scavenger of singlet oxygen and other radicals.[21] In this study, the significantly higher plasma uric acid concentration that was found compared is probably a consequence of the failure of the excretory function of the kidneys as well as increased protein catabolism as part of the hypercatabolic state in CKD.[22]


  Conclusion Top


The results obtained from this study only shows of very little population who are suffering from CKD; therefore, much more data are required for exactly evaluating the role of oxidative stress in diagnosis and management of CVD disorder. A follow-up study which would be aim for investigating the lipid profile levels and oxidative stress levels in a healthy population would be of great help for CKD patients.

Acknowledgments

Authors are thankful to colleague, staff of the laboratory, Department of Biochemistry, and the patients for their cooperation.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Kaysen GA. Lipid and lipoprotein metabolism in chronic kidney disease. J Ren Nutr 2009;19:73-7.  Back to cited text no. 1
    
2.
Prospective Studies Collaboration, Lewington S, Whitlock G, Clarke R, Sherliker P, Emberson J, et al. Blood cholesterol and vascular mortality by age, sex, and blood pressure: A meta-analysis of individual data from 61 prospective studies with 55,000 vascular deaths. Lancet 2007;370:1829-39.  Back to cited text no. 2
    
3.
Attman PO, Samuelsson O. Dyslipidemia of kidney disease. Curr Opin Lipidol 2009;20:293-9.  Back to cited text no. 3
    
4.
Kwan BC, Kronenberg F, Beddhu S, Cheung AK. Lipoprotein metabolism and lipid management in chronic kidney disease. J Am Soc Nephrol 2007;18:1246-61.  Back to cited text no. 4
    
5.
Yamamoto S, Kon V. Mechanisms for increased cardiovascular disease in chronic kidney dysfunction. Curr Opin Nephrol Hypertens 2009;18:181-8.  Back to cited text no. 5
    
6.
Van Biesen W, De Bacquer D, Verbeke F, Delanghe J, Lameire N, Vanholder R. The glomerular filtration rate in an apparently healthy population and its relation with cardiovascular mortality during 10 years. Eur Heart J 2007;28:478-83.  Back to cited text no. 6
    
7.
Evans JL, Goldfine ID, Maddux BA, Grodsky GM. Oxidative stress and stress-activated signaling pathways: A unifying hypothesis of type 2 diabetes. Endocr Rev 2002;23:599-622.  Back to cited text no. 7
    
8.
Marklund S, Marklund G. Involvement of the superoxide anion radical in the autoxidation of pyrogallol and a convenient assay for superoxide dismutase. Eur J Biochem 1974;47:469-74.  Back to cited text no. 8
    
9.
Jean CD, Maryse T, Marie JF. Plasma malondialdehyde levels during myocardial infarction. Clin Chim Acta 1983;129:319-22.  Back to cited text no. 9
    
10.
Shlipak MG, Fried LF, Cushman M, Manolio TA, Peterson D, Stehman-Breen C, et al. Cardiovascular mortality risk in chronic kidney disease: Comparison of traditional and novel risk factors. JAMA 2005;293:1737-45.  Back to cited text no. 10
    
11.
Vaziri ND, Deng G, Liang K. Hepatic HDL receptor, SR-B1 and Apo A-I expression in chronic renal failure. Nephrol Dial Transplant 1999;14:1462-6.  Back to cited text no. 11
    
12.
Hong CY, Chia KS. Markers of diabetic nephropathy. J Diabetes Complications 1998;12:43-60.  Back to cited text no. 12
    
13.
Rutkowski P, Malgorzewicz S, Slominska E, Renke M, Lysiak-Szydlowska W, Swierczynski J, et al. Interrelationship between uremic toxicity and oxidative stress. J Ren Nutr 2006;16:190-3.  Back to cited text no. 13
    
14.
Magil AB. Interstitial foam cells and oxidized lipoprotein in human glomerular disease. Mod Pathol 1999;12:33-40.  Back to cited text no. 14
    
15.
Li W, Wang G, Lu X, Jiang Y, Xu L, Zhao X. Lycopene ameliorates renal function in rats with streptozotocin-induced diabetes. Int J Clin Exp Pathol 2014;7:5008-15.  Back to cited text no. 15
    
16.
Koch M, Kutkuhn B, Trenkwalder E, Bach D, Grabensee B, Dieplinger H, et al. Apolipoprotein B, fibrinogen, HDL cholesterol, and apolipoprotein (a) phenotypes predict coronary artery disease in hemodialysis patients. J Am Soc Nephrol 1997;8:1889-98.  Back to cited text no. 16
    
17.
Després JP, Lemieux I, Dagenais GR, Cantin B, Lamarche B. HDL-cholesterol as a marker of coronary heart disease risk: The Québec cardiovascular study. Atherosclerosis 2000;153:263-72.  Back to cited text no. 17
    
18.
Kimura H, Miyazaki R, Imura T, Masunaga S, Suzuki S, Gejyo F, et al. Hepatic lipase mutation may reduce vascular disease prevalence in hemodialysis patients with high CETP levels. Kidney Int 2003;64:1829-37.  Back to cited text no. 18
    
19.
Tsimihodimos V, Mitrogianni Z, Elisaf M. Dyslipidemia associated with chronic kidney disease. Open Cardiovasc Med J 2011;5:41-8.  Back to cited text no. 19
    
20.
Griendling KK, Minieri CA, Ollerenshaw JD, Alexander RW. Angiotensin II stimulates NADH and NADPH oxidase activity in cultured vascular smooth muscle cells. Circ Res 1994;74:1141-8.  Back to cited text no. 20
    
21.
Tolun AA, Zhang H, Il'yasova D, Sztáray J, Young SP, Millington DS. Allantoin in human urine quantified by ultra-performance liquid chromatography-tandem mass spectrometry. Anal Biochem 2010;402:191-3.  Back to cited text no. 21
    
22.
Davison AM, Clumming AD, Swainson CP, Turner N. Diseases of the kidney and urinary system: CRF. In: Haslett C, Chilvers ER, Hunter JA, Boon NA, editors. Davidson's Principles and Practice of Medicine. London, (UK): Churchil Livingstone; 1999. p. 433-9.  Back to cited text no. 22
    



 
 
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  [Table 1]


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