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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2019  |  Volume : 30  |  Issue : 4  |  Page : 819-824
Calcification of abdominal aorta in patients recently starting hemodialysis: A single-center experience from Egypt

Department of Internal Medicine, Nephrology Unit, School of Medicine, Cairo University, Cairo, Egypt

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Date of Submission09-May-2018
Date of Decision13-Jul-2018
Date of Acceptance16-Jul-2018
Date of Web Publication27-Aug-2019


Vascular calcification (VC) is a well-known complication in patients with chronic kidney disease (CKD). Keeping in mind, the end goal to assess the genuine effect of mineral bone disease in the pathogenesis of blood vessel calcification during the pre-dialysis course of CKD, we assessed the prevalence and extent of abdominal aortic calcification (AAC) in nondiabetic CKD patients recently starting hemodialysis (HD). Eighty-one patients with end-stage renal disease beginning HD over a one-month period were selected. They underwent a detailed clinical examination and laboratory evaluation, including serum calcium, phosphorus, parathyroid hormone, fibroblast growth factor (FGF-23), and alkaline phosphatase were measured, and spiral computed tomography was performed to evaluate AAC score. AAC was present in 64 patients (79%). There was a significant correlation between the AAC score and age (r = 0.609, P <0.001) and FGF-23 (r = 0.800, P <0.001). This study suggests that the prevalence and extent of AAC are critical in incident HD patients. Serum FGF-23 level is the sole statistically significant correlate of AAC in these patients.

How to cite this article:
Fayed A, Elnokeety MM, Attia K, Sharaf El Din UA. Calcification of abdominal aorta in patients recently starting hemodialysis: A single-center experience from Egypt. Saudi J Kidney Dis Transpl 2019;30:819-24

How to cite this URL:
Fayed A, Elnokeety MM, Attia K, Sharaf El Din UA. Calcification of abdominal aorta in patients recently starting hemodialysis: A single-center experience from Egypt. Saudi J Kidney Dis Transpl [serial online] 2019 [cited 2020 Nov 26];30:819-24. Available from: https://www.sjkdt.org/text.asp?2019/30/4/819/265457

   Introduction Top

Cardiovascular disease (CVD) is a significant cause of mortality among chronic kidney disease (CKD) patients.[1] Forty percent of mortality among CKD patients in the initial three years of dialysis is because of CVD.[2] Vascular calcification (VC) has drawn much consideration as an index of CVD and as a pre-dictor of mortality in hemodialysis (HD) patients. In addition to conventional hazard factors for CVD, mineral bone disease related to CKD has been distinguished as illness particular hazard factors for CVD in HD patients.[3] In clinical perceptions, a solid connection between coronary calcification and cardiovascular mortality has been accounted for in HD patients.[4]

Electron-beam computed tomography (CT) and multidetector CT remain the highest quality level imaging methods for the determination of VC since they give a quantitative calcification score. Calcification scores emphatically predict cardiovascular events in the whole community and in the dialysis population.[5] The Kidney Disease Improving Global Outcomes advocates performing lateral abdominal X-ray and echocardiography as other options to cardiovascular CT to identify VC.[6] While plain X-ray might be a good first option, it is less sensitive and does not take into account a quantitative evaluation of calcification load. Thus, electron-beam CT or multidetector spiral CT ought to be utilized to measure and evaluate time-related changes in VC score.[7]

In order to assess the genuine weight of mineral bone issue as significant hazard factor for blood vessel calcification in the pre-dialysis course of CKD, we conducted this cross-sectional investigation to search for the predo-minance and extent of abdominal aortic calcification (AAC) in CKD patients that do not have diabetes mellitus and are recently started on HD.

   Patient and Methods Top

The Cairo University Hospital is a major hospital and a tertiary referral center serving patients from Cairo and also patients referred from all other governorates of Egypt. This cross-sectional cohort study included 81 CKD stage 5D patients who were initiated on HD on a regular basis 30 days or less before, between June 2016 and January 2018. Patients with diabetes, on oral anticoagulation or with a history of parathyroidectomy were not included in our study.

Informed consent was obtained from all patients. All our patients were subjected to full history, thorough clinical examination and full drug history. Laboratory assessment was made to evaluate pre-dialysis serum calcium, albumin, phosphorus, alkaline phosphatase, intact parathormone hormone (PTH), and fibroblast growth factor (FGF-23).

Enzyme-linked immunosorbent assay technique was used to determine FGF-23 levels. Venous blood samples were collected in serum separator tubes and allowed to clot for 2 h at room temperature before centrifugation for 15 min at 10,000 rpm. Serum was aliquoted and stored at -20°C. The assay employs quantitative enzyme immunoassay technique.

Radiological examination in the form of non-contrast abdominal CT scans were performed utilizing GE medical systems light speed 16 multi-slice spiral CT scanner (120 kVp, 75 mAs, 1.375 pitch and 10-mm slice thickness). Images were procured in a spiral mode in the supine position with free breathing. The scanning range was from T12 to L4 vertebral levels.[8]

Calcification score was calculated. The last 10 cuts of the abdominal aorta before its division into the two common iliac arteries were taken. Each cut was separated by 1 cm and divided into four quarters and the dots of calcification were counted giving a calcification score out of 40.[8]

   Statistical Analysis Top

Data were coded and entered using the Statistical Package for the Social Sciences) version 23 (IBM Corp., Armonk, NY, USA). Data were summarized using mean, standard deviation, median, minimum, and maximum in quantitative data and using frequency (count) and relative frequency (percentage) for categorical data. For comparing categorical data, Chi square test was performed. Exact test was used instead when the expected frequency was <5. P <0.05 were considered as statistically significant.

   Results Top

The study included 81 CKD stage 5D patients who were on regular HD for 30 days or less. There were 47 males (58%) and 34 females (42%). The mean age was 43.68 ± 13.66 years (19–71 years). The average duration on HD was 16.37 ± 7.04 (3–30 days). Eighteen patients (22.2%) had history of coronary disease, four (5%) had peripheral vascular disease and 28 (34.6%) were smokers.

The cause of end-stage renal disease (ESRD) in our patients was systemic hypertension in 54 (66.7%), glomerulonephritis in three (3.7%), two (2.5%) had autosomal dominant poly-cystic kidney disease, and the remaining 27.1% of patients had CKD of indistinct etiology. [Table 1] demonstrates a summary of various laboratory data.
Table 1: Laboratory characteristics among the studied group.

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There was no calcification seen in the abdominal aorta in 17 patients (21%), while the remaining patients had variable calcification scores [Figure 1]. There was a positive and significant correlation between calcification score and age (P <0.001). There was a positive and significant correlation between calcification score and FGF-23 (P <0.001) and PO4 levels (P = 0.004) [Table 2]. There was a positive and significant correlation between calcification score and hypertension as a cause of renal failure (P <0.001) and the presence of ischemic heart disease (IHD) (P <0.001). There was a noteworthy positive correlation between FGF-23 and both intact PTH (P = 0.004) and PO4 levels (P 0.009) [Table 3].
Table 2: Correlation between calcification score and chemical parameters.

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Figure 1: Percentage of calcification score.

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Table 3: Correlation between FGF-23 and chemical parameters.

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Logistic regression analysis revealed that the aortic calcification score in the study group showed positive correlation with FGF-23, age, blood pressure, IHD and significant negative correlation with gender, peripheral ischemia, PO4 and ALP levels [Table 4].
Table 4: Multiple regression analysis for detection of calcification score using variable methods. FGF-23 adjusted for age, gender, hypertension, ischemic heart disease, peripheral ischemia, phosphorus, and alkaline phosphatase.

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   Discussion Top

Cardiovascular calcifications influence the vast majority of CKD patients with most astounding death rate contrasted with other co-morbidities.[9] The vast majority of this calcification is related to inappropriate renal phosphate handling. In a previous pilot study performed by our group, VC was seen in 100% of the modest number of patients beginning dialysis.[8] This disturbing finding prompted the investigation group to recruit more incident HD patients for appropriate assessment. In this new study, the prevalence of AAC in incident HD patients was 79%. This predominance concurs with that of a three year line up study of 742 patients with non-dialysis CKD stages 3–5 from 39 centers in Spain.[10] On the literature review, we did not encounter studies performing CT scan in incident HD patients. Goldsmith et al showed that aortoiliac calcification as identified by plain radiography, was seen in 39% of patients at the beginning of dialysis. These inconsistencies in the outcomes can be identified with the strategy utilized for discovery.[11] Another study was performed to distinguish recurrence of AAC in 45 Iraqi patients undergoing HD regularly for one year or less by lateral abdominal radiography. The predominance of AAC in this cohort study was 18.5%.[12] A lateral lumbar radiography to evaluate extent of AAC is not as sensitive as other modalities such as CT.[13]

Despite the rejection of CKD patients who are at higher risk for VC, particularly, diabetic patients, patients with a history of intake of oral anticoagulants and those with history of hyperparathyroidism, the prevalence of AAC is still high. Being a solid indicator of major cardiovascular incidents in the dialysis popu- lation,[14] this disturbing finding ought to stimulate the medical group for energetic approach toward early detection and/or reduce the progression of this overwhelming pathology starting early in the course of CKD.

It is obvious that customary hazard factors for atherosclerosis, for example, dyslipidemia, diabetes, hypertension, smoking, gender and age, just partly clarify the calcification that seems more connected to the uremic milieu and abnormalities of mineral metabolism.[2] Abnormalities in bone and mineral disease were presumed to cause VCs.[3]

The present study affirmed the noteworthy correlation between AAC and age. In a comprehensive systemic review of 30 studies conducted over 20 years, it was shown that age was one of the fundamental correlates with VCs in patients with ESRD.[15] Another study performed on 140 prevalent HD patients with a mean age of 55 years and dialysis duration of 2.7 years, AAC was fundamentally related to age.[16]

FGF-23 correlated to VC independently in patients on dialysis and in pre-dialysis patients.[8],[17]In that study, FGF-23 level was elevated in incident HD patients and positively correlated to AAC, independent of other risk factors. Different studies have affirmed that FGF-23 was elevated in incident HD patients.[18] The outcomes uncovered a positive relationship between FGF-23 and PTH, which was also shown by Krajisnik et al.[19] This is presumed to be a compensatory mechanism to maintain phosphate balance by preventing elevation of serum phosphate from the early stages of CKD together with PTH, up to stage five CKD.[19] However, there is recent evidence of a paradoxical action of FGF-23 in the pathogenesis and progression of VC.[20]

   Conclusion Top

This study has affirmed that the prevalence and extent of AAC are critical in incident HD patients. Serum FGF-23 level is the sole statistically significant correlate of AAC in incident HD patients. Hypertension was noticed in most patients with AAC. FGF-23 was significantly elevated in incident HD patients with significant correlation with iPTH and phosphorus.

   Ethical Committee Approval Top

The Local Ethical Committee of the Internal Medicine department, School of Medicine, Cairo University, approved this work.

Conflict of interest: None declared.

   References Top

USRDS. Annual Report: Atlas of End Stage Renal Disease in the USA; 2007.  Back to cited text no. 1
de Jager DJ, Grootendorst DC, Jager KJ, et al. Cardiovascular and noncardiovascular mortality among patients starting dialysis. JAMA 2009;302:1782-9.  Back to cited text no. 2
Iijima K, Hashimoto H, Hashimoto M, et al. Aortic arch calcification detectable on chest X-ray is a strong independent predictor of cardiovascular events beyond traditional risk factors. Atherosclerosis 2010;210:137-44.  Back to cited text no. 3
Shimoyama Y, Tsuruta Y, Niwa T. Coronary artery calcification score is associated with mortality in Japanese hemodialysis patients. J Ren Nutr 2012;22:139-42.  Back to cited text no. 4
Matsuoka M, Iseki K, Tamashiro M, et al. Impact of high coronary artery calcification score (CACS) on survival in patients on chronic hemodialysis. Clin Exp Nephrol 2004;8:54-8.  Back to cited text no. 5
Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Work Group. KDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease-mineral and bone disorder (CKD-MBD). Kidney Int Suppl 2009;113:S1-130.  Back to cited text no. 6
Sinha S, Eddington H, Kalra PA. Vascular calcification: Mechanisms and management. Br J Cardiol 2008;15:316-21.  Back to cited text no. 7
Nasrallah MM, El-Shehaby AR, Salem MM, Osman NA, El Sheikh E, Sharaf El Din UA. Fibroblast growth factor-23 (FGF-23) is independently correlated to aortic calcification in haemodialysis patients. Nephrol Dial Transplant 2010;25:2679-85.  Back to cited text no. 8
Foley RN, Gilbertson DT, Murray T, Collins AJ. Long interdialytic interval and mortality among patients receiving hemodialysis. N Engl J Med 2011;365:1099-107.  Back to cited text no. 9
Górriz JL, Molina P, Cerverón MJ, et al. Vascular calcification in patients with nondialysis CKD over 3 years. Clin J Am Soc Nephrol 2015;10:654-66.  Back to cited text no. 10
Goldsmith DJ, Covic A, Sambrook PA, Ackrill P. Vascular calcification in long-term haemo-dialysis patients in a single unit: A retrospective analysis. Nephron 1997;77:37-43.  Back to cited text no. 11
Hashim Al-Saedi AJ, Jameel NS, Qais A, Kareem AH, Mohssen TS. Frequency of abdominal aortic calcification in a group of Iraqi hemodialysis patients. Saudi J Kidney Dis Transpl 2014;25:1098-104.  Back to cited text no. 12
Bellasi A, Raggi P. Vascular imaging in chronic kidney disease. Curr Opin Nephrol Hypertens 2012;21:382-8.  Back to cited text no. 13
Tatami Y, Yasuda Y, Suzuki S, et al. Impact of abdominal aortic calcification on long-term cardiovascular outcomes in patients with chronic kidney disease. Atherosclerosis 2015; 243:349-55.  Back to cited text no. 14
McCullough PA, Sandberg KR, Dumler F, Yanez JE. Determinants of coronary vascular calcification in patients with chronic kidney disease and end-stage renal disease: A systematic review. J Nephrol 2004;17:205-15.  Back to cited text no. 15
Bellasi A, Ferramosca E, Muntner P, et al. Correlation of simple imaging tests and coronary artery calcium measured by computed tomography in hemodialysis patients. Kidney Int 2006;70:1623-8.  Back to cited text no. 16
Desjardins L, Liabeuf S, Renard C, et al. FGF23 is independently associated with vascular calcification but not bone mineral density in patients at various CKD stages. Osteoporos Int 2012;23:2017-25.  Back to cited text no. 17
Olauson H, Qureshi AR, Miyamoto T, et al. Relation between serum fibroblast growth factor-23 level and mortality in incident dialysis patients: Are gender and cardiovascular disease confounding the relationship? Nephrol Dial Transplant 2010;25:3033-8.  Back to cited text no. 18
Krajisnik T, Björklund P, Marsell R, et al. Fibroblast growth factor-23 regulates parathyroid hormone and 1alpha-hydroxylase expression in cultured bovine parathyroid cells. J Endocrinol 2007;195:125-31.  Back to cited text no. 19
Sharaf El Din UA, Salem MM, Abdulazim DO. FGF23 and inflammation. World J Nephrol 2017;6:57-8.  Back to cited text no. 20

Correspondence Address:
Ahmed Fayed
Dr. Ahmed Fayed, Department of Internal Medicine, Nephrology Unit, School of Medicine, Cairo University, Cairo
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DOI: 10.4103/1319-2442.265457

PMID: 31464238

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  [Table 1], [Table 2], [Table 3], [Table 4]


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