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Saudi Journal of Kidney Diseases and Transplantation
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BRIEF COMMUNICATION  
Year : 2011  |  Volume : 22  |  Issue : 6  |  Page : 1193-1198
Obesity and metabolic syndrome in hemodialysis patients: Single center experience


1 Prince Salman Center for Kidney Diseases, Riyadh, Saudi Arabia
2 Mansoura Urology and Nephrology Center, Mansoura University, Egypt

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Date of Web Publication8-Nov-2011
 

   Abstract 

Recent evidence highlights the relationship between metabolic syndrome (MS) and increased risk of cardiovascular (CV) diseases. The overall prevalence of the MS is increased in hemodialysis population. To evaluate the prevalence of the MS and obesity in our hemodialysis (HD) patients, we studied 234 HD patients and 34 patients were excluded from the study due to incomplete data at the time of analysis. For the remaining 200 patients, 92% were below the age of 70 years old, 162 (81%) were hypertensive, 90(45%) were diabetic, 54 (27%) had ischemic heart diseases, and 116 (58%) had MS. The incidence of MS in the male and female patients was 50% and 67%, respectively, with a mean abdominal girth more than 94 cm in males and only 14% of the patients revealed abdominal girth measurement below 80 cm in females. We conclude that there is a high prevalence of obesity and MS in our HD patients. Such patients may be at risk of developing morbidities and may benefit from therapy such as lifestyle changes including weight reduction and increased physical activity.

How to cite this article:
Al Saran K, Elsayed S, Sabry A, Hamada M. Obesity and metabolic syndrome in hemodialysis patients: Single center experience. Saudi J Kidney Dis Transpl 2011;22:1193-8

How to cite this URL:
Al Saran K, Elsayed S, Sabry A, Hamada M. Obesity and metabolic syndrome in hemodialysis patients: Single center experience. Saudi J Kidney Dis Transpl [serial online] 2011 [cited 2019 Nov 14];22:1193-8. Available from: http://www.sjkdt.org/text.asp?2011/22/6/1193/87231

   Introduction Top


The World Health Organization (WHO) estimates that over a billion of adults are overweight and over 300 million are obese, worldwide. Overweight and obesity have increased rapidly in an epidemic proportion as two-thirds of adults are obese or overweight and the rate is increasing among children and adolescents. Obesity should be controlled in order to prevent its morbidities especially cardiovascular diseases (CVD). [1] Recent evidence highlights the relationship between the metabolic syndrome (MS) and increased risk of CVD. [2] The overall prevalence of the MS may reach 70% in the hemodialysis (HD) population and is especially prevalent among diabetics, females, and Caucasian patients with end-stage renal disease (ESRD). [3]

The aim of our study is to examine the prevalence of MS and obesity in our HD patients and to identify the most common element of the MS in them.[Table 1]
Table 1: Ethnic group waist circumference (abdominal girth).

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   Patients and Methods Top


We obtained a complete medical history, and physical examination included recording of data, smoking status, birth date (age), current medication for diabetes, hypertension and hyperlipidemia, history of original kidney disease, and associated co-morbid diseases. Abdominal circumference was measured at the level of the umbilicus with the participant in the supine position.

The following laboratory investigations were obtained after an overnight fasting blood sample: cholesterol, triglycerides, low density lipoprotein (LDL)-cholesterol, high density lipoprotein (HDL)-cholesterol, and fasting glucose.

MS was defined using the International Diabetes Federation (IDF) proposal for diagnosis of MS criteria in 2004. [4] Central obesity is an essential element in this definition, with increased waist circumference in addition to any two of the following: Triglycerides >150 mg/ dL (1.7 mmol/L) or treatment for elevated triglycerides, HDL cholesterol <40 mg/dL (1.03 mmol/L) in men or <50 mg/dL (1.29 mmol/L) in women, or treatment for low HDL, systolic blood pressure >130 mmHg, diastolic blood pressure >85 mmHg, or treatment for hypertension, and fasting plasma glucose >100 mg/dL (5.6 mmol/L), or previously diagnosed as type II diabetes. An oral glucose tolerance test was done for patients with elevated fasting plasma glucose.

Individuals who received antihypertensive medications were considered to have the "hypertension" factor and individuals who received anti-diabetic medications were considered to have the "fasting glucose" factor.

Dialysis patients were classified according to their body mass index (BMI) into underweight (<18.5 kg/m 2 ), normal (18.5 to ≤25 kg/m 2 ), overweight (25 to ≤30 kg/m 2 ), obese (30 to <35 kg/m 2 ), or morbidly obese (BMI ≥35 kg/m 2 ) using the patient's height and dry body weight.


   Statistical Analysis Top


Analysis was performed using SPSS software (Statistical Package for Social Science, version 14, SPSS Inc, and Chicago, IL, USA). All values are expressed as mean ± SD, and P value <0.05 was considered statistically significant.


   Results Top


Out of the 200 HD patients included in this study, the mean age was 50.1 ± 15.9 years old (92% were below the age of 70 years); 110 (55%) were males and 90 (45%) were females. Chronic renal failure was due to diabetic nephropathy in (41%) 82 patients, hypertension in 40 (20%), chronic glomerulo-nephritis in 12 (6%), hypoplastic kidney in 4%, lupus nephritis in 3%, and other causes in 4% while 22% were of unknown etiology.

[Table 2] and [Table 3] show the demographic data of the studied population including age, BMI, triglyceride, HDL-cholesterol, dialysis duration, and Kt/V, and [Table 3], shows the abdominal circumference measured in the study population.
Table 2: Demographic data of the study patients.

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Table 3: Abdominal girth in according to gender of the study patients.

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Of the study patients, 162 (81.5%) patients were hypertensive (80.9% in males and 90% in females), 90 (45%) patients were diabetic (41.8% in males and 51.1% in females), 54 (27%) had ischemic heart diseases, and 116 (58%) had MS (52.7% in males and 74.4% in females). In males, 50% revealed an abdominal girth more than 94 cm, while in females, only 14% had abdominal girth below 80 cm. Furthermore, 12% of the female patients had morbid obesity.

[Figure 1] shows the distribution of MS, while [Figure 2] shows the distribution of body mass index in men and women of the study population.
Figure 1: Metabolic syndrome distribution in the study patients.

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Figure 2: Distribution of body mass index.

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   Discussion Top


The MS has main features consisting of abdominal obesity, hyper-triglyceridemia, low HDL-cholesterol levels, high blood pressure, and high fasting blood glucose levels. [5] The MS was stressed on during the 2 nd report of the Adult Treatment Panel (ATP-II) in 1993 and to be controlled from the perspective of prevention of cardiovascular (CV) disease (ATP-II, 1994). [1]

Increased body weight plays the most important role in the development of MS. The observed prevalence of the MS in the National Health and Nutrition Examination Survey (NHANES)-III study was 5% in the subjects of normal weight, 22% in the overweight, and 60% in the obese. [6]

Also, a number of findings indicate that obesity (the cardinal feature of the MS) is an independent factor for causing renal dysfunction. The multivariate analysis performed by Chen et al showed that the risk for being affected by chronic kidney disease (CKD) was more than twice as high in patients with an increased waist circumference. [7]

It should be realized that as many as 80% of obese children become obese adults. [8] The greater threat from obesity is acquired at young age than that acquired during adulthood, which can be perceived easily from studies on life-expectancy. Once people have reached the age of 70, there is no noticeable effect of obesity on life-expectancy. [9] In 92% of patients in our study, the mean age was below 70 years; most of the population study was under the maximum effect of obesity regarding life expectancy.

The complications of obesity are multiple, and include type 2 diabetes, hypertension, coronary heart disease, stroke, heart failure, venous thrombo-embolism, atrial fibrillation, osteoarthritis, cancer (breast, endometrial, colon, kidney), cholelithiasis, infertility, polycystic ovary syndrome, and sleep apnea. [10],[11],[12]

Obesity is increasingly recognized as a cause of CKD. Specific pathological features have been identified and termed obesity-related glomerulopathy (ORG). The primary features are glomerulomegaly, focal and segmental glomerulosclerosis, and increased mesangial matrix and cellularity. [13],[14] These features bear a striking resemblance to glomerulopathy induced by diabetes and/or hypertension. Similarly, the clinical course of obesity-related glomerulopathy appears to be progressive. [13] Renal involvement in MS can be anticipated as obesity is associated with an excess excretory load as progressive weight gain is followed by sustained period of hyperinsulinemia without hyperglycemia. This is followed by overt hyperglycemia and subsequently by declining insulin levels. The first clinical evi-dence of renal disease in obesity is protei-nuria. [15] Weisinger et al first reported massive proteinuria associated with obesity in 1974 and subsequent reports have consistently confirmed the presence of proteinuria and glomerulomegaly in obesity, often with focal segmental glomerulosclerosis. [8],[16]

Evidence is accumulating that adipose tissue releases a number of active metabolic compounds, including pro-inflammatory cytokines. These compounds include leptin, adipsin, resistin, angiotensinogen, tumor necrosis factor-α (TNF-α), plasminogen activator inhibitor type-1, and interleukin (IL)-6. Therefore, obese patients or whose clearance of cytokines is impaired, as in advanced CKD, may be prone to insulin resistance and accelerated atherosclerosis. [17],[18]

Recent data indicate that fat itself, particularly in the abdomen, is the source of cytokines secretion which produce endothelial damage, which is the hallmark of vascular injury associated with atherosclerosis. In addition, adiponectin, an adipocyte-derived hormone that has anti-atherogenic and anti-inflammatory properties, is reduced in those patients with MS and increased intra-abdominal fat. [19]

Previously, it was thought that there is no direct correlation between obesity and ESRD, Rebecca A et al, in 2006, reported an association between family history of ESRD and obesity among incident dialysis patients. The association was strong, increased in strength with more severe degrees of obesity, and persisted after adjustment for other patient characteristics, including history of DM and HTN and primary cause of ESRD. In addition, we noted that younger age, increasing number of first-degree relatives, female sex, black race, and history of HTN were associated with a family history of ESRD in the adjusted analysis. [20]

In a recent study conducted in Saudi Arabia, by Alfadda et al, in 2008, using the same definition for MS, (IDF proposal), MS prevalence was 57.2% in Saudi normal population. [21] In our study, the prevalence of MS in HD patients was 62% and it was more common in females than males, which could be explained by its high prevalence in the normal Saudi population.

Our results are comparable to those found by Hsu et al, Williams et al and Stephan et al. [22],[23],[24] The most common element of the MS was hypertension as it affected up to 85%, while DM affected 46% of patients.

The MS has been exposed to a vigorous critique as the medical value of diagnosing since there is no single treatment for the syndrome, and instead treatment of each component was independent till the recent discovery of the endocannabinoid system and its role in the metabolic homeostasis. [25] The endogenous cannabinoid system is a novel, physiological signaling system comprising the recently identified ligands with corresponding selective receptors and the machinery of proteins and enzymes involved in their biosynthesis, release, transport, and degradation. [26],[27]

Patients with ESRD are more physically inactive compared with apparently healthy population. This reduction of physical activity may result in deterioration of muscle function and exercise tolerance, progressive disability, and various other unwanted events. However, there is still yet no study that demonstrates the proper amount and the duration of exercise. [28] Nevertheless, physical exercise is considered to be safer than the actual dialysis treatment itself as no unwanted events have been reported on exercise and ESRD. [29]

Due to high prevalence of obesity and MS in Saudi HD patients, obese and overweight persons would then deserve a priority in the clinical efforts to prevent the development of co-morbidities through lifestyle changes, particularly weight reduction and increased physical activity.

 
   References Top

1.National Cholesterol Education Program. Second Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II). Circulation 1994;89:1333-45.  Back to cited text no. 1
    
2.Segura J, Campo C, Roldán C, et al. Hypertensive renal damage in metabolic syndrome is associated with glucose metabolism disturbances. J Am Soc Nephrol 2004;15:S37-42.  Back to cited text no. 2
    
3.Young DO, Lund RJ, Haynatzki G, Dunlay RW.. Prevalence of the metabolic syndrome in an incident dialysis population. Hemodial Int 2007;11(1): 86-95.  Back to cited text no. 3
    
4.Alberti KG, Zimmet P, Shaw J. The metabolic syndrome. A new worldwide definition. Lancet 2005;366:1059.  Back to cited text no. 4
    
5.Reaven GM. The metabolic syndrome: requiescat in pace. Clin Chem 2005;51:931-8.  Back to cited text no. 5
    
6.Locatelli F, Pozzoni P, Del Vecchio L, Renal manifestations in the metabolic syndrome. J Am Soc Nephrol 2006;17:81-5.  Back to cited text no. 6
    
7.Chen J, Muntner P, Hamm LL, et al. The metabolic syndrome and chronic kidney disease in US adults. Ann Intern Med 2004;140:167 -74.  Back to cited text no. 7
    
8.Wyllie R. Obesity in childhood: an overview. Curr Opin Pediatr 2005;17:632-5.  Back to cited text no. 8
    
9.Reynolds SL, Saito Y, Crimmins EM. The impact of obesity on active life expectancy in older American men and women. Gerontologist 2005;45:438-44.  Back to cited text no. 9
    
10.Willett WC, Dietz WH, Colditz GA. Guidelines for healthy weight. N Engl J Med 1999;341:427-34.  Back to cited text no. 10
    
11.Murphy NF, MacIntyre K, Stewart S, et al. Long Long-term cardiovascular consequences of obesity: 20-year follow-up of more than 15 000 middle-aged men and women (the Renfrew-Paisley study). Eur Heart J 2006;27:96-106 .  Back to cited text no. 11
    
12.Arias MA, Alonso-Fernandez A, Garcia-Rio F, Pagola C. Association between obesity and obstructive sleep apnoea. Eur Heart J 2005;26: 2744-5.  Back to cited text no. 12
    
13.Kambham N, Markowitz GS, Valeri AM, et al. Obesity-related glomerulopathy: an emerging epidemic. Kidney Int 2001;59:1498-509.  Back to cited text no. 13
    
14.Katherine RT. Renal manifestations of the metabolic syndrome. Nephrol Dial Transpl 2005;20(5):861-4 .  Back to cited text no. 14
    
15.Susan PB. Obesity-initiated metabolic syndrome and the kidney: A recipe for chronic kidney disease? J Am Soc Nephrol 2004;15: 2775-91.  Back to cited text no. 15
    
16.Praga M, Hernandez E, Morales E, et al. Clinical features and long-term outcome of obesity-associated focal segmental glomerulo sclerosis. Nephrol Dial Transplant 2001;16: 1790-8.  Back to cited text no. 16
    
17.Juhan V I, Roul C, Alessi MC, et al. Increased plasminogen activator inhibitor activity in non insulin-dependent diabetic patients: relationship with plasma insulin. Throm Haemost 1989; 61:370-3.  Back to cited text no. 17
    
18.Hotamisligil GS, Arner P, Caro JF, et al. Increased adipose tissue expression of tumor necrosis factor-á in human obesity and insulin resistance. J Clin Invest 1995;95:2409-15.  Back to cited text no. 18
    
19.Salmennienmi U, Ruotsalainen E, Pihlajamäki J, et al. Multiple abnormalities in glucose and energy metabolism and coordinated changes in levels of adiponectin, cytokines, and adhesion molecules in subjects with metabolic syndrome. Circulation 2004 ; 110:3842-8.  Back to cited text no. 19
    
20.Rebecca AS, William MM, Nataliya VV et al. Obesity is associated with family history of ESRD in incident dialysis patients. Am J Kid Dis 2006;48:1.  Back to cited text no. 20
    
21.Alfadda AA, Al-Daghri NM, Malabu U. Apolipoprotein B/apolipoprotein A-I ratio in relation to various definitions of metabolic syndrome among Saudi patients with type 2 diabetes mellitus. Saudi Med J 2008;29(6):821-5.  Back to cited text no. 21
    
22.Hsu CY, McCulloch CE, Iribarren C, et al. Body mass index and risk for end-stage renal disease. Ann Intern Med 2006;144:21-8.  Back to cited text no. 22
    
23.Williams JD, Woods FH. Insulin resistance, the metabolic syndrome and renal failure - Is there a special problem for patients treated with peritoneal dialysis? Eur Endocr Rev 2006. 29:351-66.  Back to cited text no. 23
    
24.Bakker SJ, Ron T. Gansevoort and Dick de Zeeuw, Metabolic syndrome: a fata morgana? Nephro Dial Transpl 2007;22(1):15-20.  Back to cited text no. 24
    
25.Kyrou I, Valsamakis G, Tsigos G. The Endocannabnoid system as a target for the treatment of visceral obesity and metabolic syndrome. stress, obesity, and metabolic syndrome. Ann NY Acad Sci 2006;1083:270-305 .  Back to cited text no. 25
    
26.Li, A, Maglione M, Tu W, et al. Meta-analysis: Pharmacologic treatment of obesity. Ann Intern Med 2005;142:532-46.  Back to cited text no. 26
    
27.Kyrou J, Valsamakis G, Tsigos C. The endocannabinoid system as a target for the treatment of visceral obesity and metabolic syndrome. Ann NY Acad Sci 2006;1083:270-305.  Back to cited text no. 27
    
28.Brunier GM, Graydon J. The influence of physical activity on fatigue in patients with ESRD on hemodialysis. ANNA Journal 1993; 20(4):7-61 .  Back to cited text no. 28
    
29.Mirmiran P, Mirbolooki M, Azizi F. Familial clustering of obesity and the role of nutrition: Tehran lipid and glucose study. Int J Obes Relat Metab Disord 2002;26:1617-22.  Back to cited text no. 29
    

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Correspondence Address:
Khalid Al Saran
Prince Salman Center for Kidney Diseases, P.O. Box 52948, Riyadh 11573
Saudi Arabia
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PMID: 22089780

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