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Saudi Journal of Kidney Diseases and Transplantation
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RENAL DATA FROM THE ARAB WORLD  
Year : 2014  |  Volume : 25  |  Issue : 5  |  Page : 1098-1104
Frequency of abdominal aortic calcification in a group of Iraqi hemodialysis patients


1 Department of Nephrology, Faculty of Medicine, Al Kindy College of Medicine, Baghdad, Iraq
2 College of Basic Education, Al Mustansiriya, Baghdad, Iraq
3 Department of Physiology, Alkindi College of Medicine, Baghdad, Iraq

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Date of Web Publication2-Sep-2014
 

   Abstract 

Cardiovascular complications including abdominal aortic calcification significantly affect the mortality and morbidity in patients on a hemodialysis (HD) program. The objective of this study is to find the frequency of abdominal aortic calcification in patients on regular HD and to evaluate the effect of parameters on frequency and severity of abdominal aortic calcification. Fifty-four patients with end-stage renal disease on regular HD were studied from January 2011 to December 2011 to evaluate abdominal aortic calcification by plain abdominal X-ray. The study showed that 10 (18.5%) patients had abdominal aortic calcification. Only one (1.9%) had grade 3 calcification and among the remaining, five (9.3%) patients had grade 1 and four (7.4%), grade 2. There was a statistically significant difference (P <0.05) in the means of serum cholesterol among those with and without abdominal aortic calcification. Hypertension was noticed in most patients with abdominal aortic calcification. The frequency of abdominal aortic calcification is directly related to age and duration of dialysis. The only biochemical parameter with a statistically significant effect was serum cholesterol.

How to cite this article:
Hashim Al-Saedi AJ, Jameel NS, Qais A, Kareem AA, Mohssen TS. Frequency of abdominal aortic calcification in a group of Iraqi hemodialysis patients. Saudi J Kidney Dis Transpl 2014;25:1098-104

How to cite this URL:
Hashim Al-Saedi AJ, Jameel NS, Qais A, Kareem AA, Mohssen TS. Frequency of abdominal aortic calcification in a group of Iraqi hemodialysis patients. Saudi J Kidney Dis Transpl [serial online] 2014 [cited 2019 Nov 15];25:1098-104. Available from: http://www.sjkdt.org/text.asp?2014/25/5/1098/139964

   Introduction Top


Vascular calcification, specifically arterial, has been recognized for many years as a common complication of end-stage renal disease (ESRD). [1],[2],[3],[4] Patients on hemodialysis (HD) have an in­creased incidence of cardiovascular events 10 to 30-times greater than those of the general population. [5] This cannot simply be explained by the prevalence of atherosclerosis in those patients. It appears likely that metabolic para­meters such as hyperphosphatemia and elevated calcium-phosphorus products also play an im­portant role in the excess incidence of vascular calcification. [6]. This higher risk of vascular calci­fication in patients with ESRD, particularly abdominal aortic calcification (AAC), is much pronounced in patients on a dialysis regimen. [7]

Patients with ESRD are commonly treated with calcium-containing phosphate binders. Evi­dence from both animal and human studies indicate that this medication promotes aortic calcification. [6],[8] However, the currently availa­ble human studies investigating the relationship of renal failure to aortic calcification consist of small cohorts; thus, firm conclusions are diffi­cult to reach. Further studies with larger patient numbers are required to examine this issue more thoroughly. [9] The calcium content of athe­rosclerotic lesions is greater in patients under­going dialysis than in persons of the same age with normal renal function. [10]

Recent work has demonstrated that the extent of arterial calcification in patients with ESRD who are treated with dialysis far exceeds that of persons in the general population. [11],[12],[13] Such data using recently developed imaging methods thus confirm the results from earlier radiographic and pathological studies. [2],[14] For many years, vascular and soft-tissue calcification in ESRD was considered to occur predominantly by passive unregulated physicochemical mechanisms. [2],[14],[15]

However, vascular calcification is now consi­dered to be a regulated process that is influenced by tissue-specific cellular mechanisms and by selected components present in plasma. [16],[17],[18]


   Aim of the Study Top


This study was designed to determine the frequency of AAC in patients with ESRD on regular HD to evaluate the effect of different parameters like age, history of diabetes, ische-mic heart disease (IHD), duration of dialysis, different possible etiologies for ESRD and some biochemical variables like the assessment of renal function and lipid profile on the frequency of AAC and to assess the severity of AAC according to the AAC scoring system. The parathyroid hormone (PTH) results were not included as a parameter.


   Patients and Methods Top


This was a cross-sectional study that enrolled 54 patients with ESRD on regular HD during the period from January 2011 to December 2011 to evaluate AAC by plain abdominal X-ray. Patients were selected from those who were attending the dialysis unit in the Al-Kindi Teaching Hospital. A detailed history and tho­rough physical examination had been per­formed for each patient. Information obtained included age, gender, etiology of ESRD, dura­tion of HD, history of smoking, history of IHD, diabetes mellitus, hypertension, cerebrovascular accident and history of hepatitis.

Investigations included plain abdominal X-ray (lateral view), renal function tests, calcium and phosphorus, lipid profiles (cholesterol, high-density lipoprotein and serum triglyceride). Data obtained had been processed by using the software program SPSS (Statistical Package for the Social Sciences) version 18.


   Results Top


The study included 54 patients with ESRD on HD. Fifteen patients were male (27.8%) and 39 patients were female (72.2%). The mean age was 50.9 ± 14.5 years (52.6 ± 14.3 and 50.3 ± 14.8 years for the male and female patients, respectively). Ten of the 15 male patients were 50 year old or older.

Forty-seven patients (87%) were hypertensive, either alone or in association with other di­seases. Seven patients (13%) were hypertensive prior to the diagnosis of ESRD, while four patients (7.4%) were diabetic prior to the diag­nosis of renal failure. In contrast, 38 patients (70.4%) had no clear evidence of any possible etiology for their ESRD, i.e. they had a nega­tive past medical history. Thirty-nine patients (72.2%) had negative hepatitis serology results.

Ten patients (18.5%) had evidence of AAC on their abdominal X-ray finding. One patient had 2/3 rd area covered with calcification and five patients had only small scattered calcific de­posits filling less than 1/3 rd of the longitudinal wall [Table 1].
Table 1: Patients' distribution according to their grades of abdominal aortic calcification.

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Six patients with AAC (60% of those with AAC) were female, comprising 15.38% of the females enrolled in the sample, while four pa­tients with AAC were male (40% of those with AAC, 26.7% of the males enrolled in this study) [Table 2].
Table 2: Patients' distribution according to abdominal X-ray finding and gender.

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Eight patients with AAC were 50 years old or Older and four patients were 60 years old or older (40% of those with AAC). The mean age of those with AAC was 55.5 ± 13.15 years com­pared with the mean age of those without AAC, which was 49.86 ± 14.8 years [Table 3].
Table 3: Patients' distribution according to abdominal X-ray finding and age.

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One patient with AAC was on HD for two years and two patients with AAC were on HD for one year. The mean duration of HD for patients with and without AAC was 9.6 ± 7.02 and 13.3 ± 11.8 months, respectively [Table 4].
Table 4: Patients' distribution according to abdominal X-ray finding and duration of dialysis.

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Six patients with AAC had a blood urea level of less than 40 mmol/L at the time of study (60% of those with AAC). The mean blood urea level that had been observed in patients with and those without AAC was 37.8 ± 5.4 and 38.7 ± 7.7 mmol/L, respectively. Eight pa­tients with AAC had an albumin level of less than 40 g/L [Table 5].
Table 5: Patients' distribution according to the level of biochemical parameters.

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All patients included in the sample were on activated vitamin D3 therapy in a dose range of 0.25-1 μg, along with calcium supplements (4- 6 g/day orally).


   Discussion Top


The most common cause of death in dialysis patients is cardiovascular disease (CVD). The two most common forms of calcifications are coronary artery calcifications (CAC) and AAC. [19],[20],[21],[22],[23] Many studies indicated that the pres­ence of AAC is a marker of both subclinical atherosclerotic disease and atherosclerosis, and is also an independent predictor of cardiovas­cular morbidity and mortality. [24],[25] The impor­tance of screening for AAC using plain X-ray has been stressed by the 2005 K/DOQI clinical practice guidelines for CVD. The presence of calcification in one site predicts the presence of calcifications in other possible sites; hence, AAC can predict the cardiovascular risk in pa­tients with ESRD. [26] This study showed that ten patients (18.5%) had evidence of AAC on plain X-ray. This frequency of AAC is quite similar to what Milliner et al found in their study of 120 children who had died because of uremia. [27] They found that cardiac calcifications were observed in 29 patients (24.1%). In contrast, Goldsmith et al indicated that aorto-iliac calcifi­cation was seen in 39% of patients at the onset of dialysis. [28] These discrepancies in the results can be related to the fact that the Goldsmith study was a retrospective study and not a cross-sectional study. They studied the records of pa­tients admitted to one unit of dialysis during a period of 25 years (1970-1994) with a larger number of patients. Regarding the association between patients' age and frequency of AAC, this study found that there is a statistically significant association between the frequency of AAC and increasing age of the patients with ESRD (P <0.05). The mean age of patients with AAC was 55.5 ± 13.15 compared with the mean age of those without AAC, which was 49.86 ± 14.8 years. Furthermore, eight patients with AAC were 50 years old or older (80% of those with AAC), while only 24 patients with­out AAC were put in the same age group (54.6% of those without AAC). Several studies examined the relationship of AAC to age, and the finding across all the studies is that AAC is positively related to age. [29],[30],[31],[32],[33] Allison et al's study showed that at an age of <50 years, the prevalence of AAC is 16% and 20% in women and men, respectively, which increases to 93% and 98% by the age of more than 70 years in women and men, respectively. [30] In one compre­hensive systematic review of 30 studies over a period of 20 years, it was demonstrated that age and duration of HD were the main associations with vascular calcifications in patients with ESRD. [34] The effect of age is a bad prognostic parameter in assessing the risk of CVD events and mortality in dialysis patients with aortic stiffness and calcification. [35] According to the results of outcome of the calcification outcome in renal disease (CORD) study, it had been found that the mean age of those with cardiovascular events happening during the study period was 68.1 years compared with the mean age of 59.2 years observed in those with no events. [35] This study revealed a negative relation between the duration of dialysis and the frequency of AAC, i.e. AAC is more frequent among those with a short duration of dialysis. Seven patients with AAC (70%) were on dia­lysis for less than one year, and the mean dura­tion of dialysis among those with and without AAC was 9.6 ± 7.02 and 13.3 ± 11.8 months, respectively. These results can be related to the following factors: Most of the included patients were recently introduced into the dialysis pro­gram with a duration of less than one year (33 patients, 61.1% of the sample). Five of 10 patients with AAC were 50 years or older and, at the same time were on dialysis for less than one year. These five patients comprised 50% of those with AAC and 71.5% of those who were on dialysis for less than one year. The study revealed that those with AAC had a higher mean level of calcium in comparison with those without AAC (1.99 versus 1.92 mmol/L, res­pectively). This finding is not statistically sig­nificant. In addition, both means are within the normal range of serum calcium level. Much difference had been observed between the means of serum phosphorus in those with and those without AAC (2.12 versus 1.99 mmol/L, respectively), although this difference also is not statistically significant but the levels are absolutely in the hyperphosphatemic range. The exact biochemical mechanisms underlying vascular calcification in renal insufficiency are poorly understood. This is largely due to the difficulties posed in interpreting cross-sectional data because of a large number of confounding factors. [7] The progression of CKD to ESRD is associated with changes in mineral metabolism including disruption of the axis of vitamin D and PTH was not included in this study (for technical difficulties). Reductions in renal 1-alfa hydroxylase activity are linked with de­creased gastrointestinal calcium absorption lea­ding to secondary hyperparathyroidism, which, if unchecked, leads to accelerated bone loss in an attempt to maintain calcium hemostasis. When calcium is lost at an accelerated rate from the bone, it appears within the media of large vessels such as the aorta and smaller ones such as the coronary arteries. [36] Hyperphospatemia may contribute to phenotype change of vascular smooth muscle cells by up-regulating the sodium-dependent co-transporter, pituitary-spe­cific transcription factor (Pit1). Increased acti­vity of Pit1 leads to up-regulations of many genes associated with matrix mineralization as shown in animal models. It is known that, in humans preventing hyperphosphatemia can indirectly decrease vascular calcifications. [37],[38],[39] In comparison with the results of the CORD study, our patients with AAC had a lower calcium level (1.99 versus 2.4 mmol/L in the CORD study) and a higher serum phosphorus level (2.12 versus 1.7 in the CORD study). [7] However, the mean calcium phosphorus product that had been observed in our sample (4.07 mmol2/L2) is similar to what had been observed in the CORD study (4.0 mmol2 /L2). Statistical analysis of the CORD study data were similar to the statistical results of this study, although they excluded baseline serum calcium and calcium phosphorus product from the list of independent predictors of AAC. [7] This study indicated that there is a statistically signi­ficant difference in the means of serum cho­lesterol among those with and without AAC. This finding in our study is also similar to the results of the CORD study, although our values are slightly higher. The mean total serum cho­lesterol that had been observed in our sample was 4.76 mmol/L compared with the results of the CORD study (4.2 mmol/L). [7]

This study showed that only one patient had grade 3 AAC, i.e. 2/3 rd or more of the wall is calcified. Other patients with AAC had either grade 1 or grade 2. [7] When we re-evaluate the results, it had been found that this higher fre­quency of grade 1 and grade 2 in patients with AAC can be related to the effect of short duration of dialysis observed in this group of patients. It had been found that the patient with grade 3 was on the HD program for more than 1 year and the remaining were on HD for less than one year.


   Conclusions Top


The frequency of AAC is directly related to the age and the duration of dialysis. The only bio­chemical parameter with a statistically signifi­cant effect on the frequency of AAC in patients on HD was the total serum cholesterol. Hyper­tension was noticed in most patients with AAC.

 
   References Top

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33.Kiel DP, Kauppilla LI, Cupples LA, Hannan MT, O'Donnell CJ, Wilson PW. Bone loss and the progression of abdominal aortic calcification over a 25-year period: The Framingham Heart Study. Calcif Tissue Int 2001;68:271-6.  Back to cited text no. 33
    
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37.Huybers S, Bindels RJ. Vascular calcification in chronic kidney disease: New developments in drug therapy. Kidney Int 2007;72:663-5.  Back to cited text no. 37
    
38.Jono S, McKee MD, Murry CE, et al. Phosphate regulation of vascular smooth muscle cell calcification. Circ Res 2000;87:E10-7.  Back to cited text no. 38
    
39.Mathew S, Lund RJ, Strebeck F, Tustison KS, Geurs T, Hruska KA. Reversal of the a dynamic bone disorder and decreased vascular calci­fication in chronic kidney disease by sevelamer carbonate therapy. J Am Soc Nephrol 2007; 18:122-30.  Back to cited text no. 39
    

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Correspondence Address:
Dr. Ali J Hashim Al-Saedi
Department of Nephrology, Faculty of Medicine, Al Kindy College of Medicine, Baghdad
Iraq
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DOI: 10.4103/1319-2442.139964

PMID: 25193922

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