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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
ORIGINAL ARTICLE  
Year : 2017  |  Volume : 28  |  Issue : 1  |  Page : 51-60
Relation of fibroblast growth factor-23 and cardiovascular calcification in end-stage kidney disease patients on regular hemodialysis


1 Department of Internal Medicine and Nephrology, Faculty of Medicine, Al Azhar University, Cairo, Egypt
2 Department of Nephrology and Internal Medicine, Urology and Nephrology Center, Mansoura University, Mansoura, Egypt
3 Department of Clinical Pathology, Faculty of Medicine, Al Azhar University, Cairo, Egypt

Click here for correspondence address and email

Date of Web Publication12-Jan-2017
 

   Abstract 

More than half of deaths in end-stage kidney disease (ESKD) patients are due to cardiovascular disease. Elevated fibroblast growth factor 23 (FGF-23) was found to be associated with mortality in hemodialysis (HD) patients and correlates with peripheral calcification. Aortic calcification is associated with coronary artery calcification. Both aortic and peripheral vascular calcifications were associated with mortality in chronic kidney disease. We aimed to investigate the relation between intact FGF-23 and cardiovascular calcification in patients with ESKD who were maintained on regular HD. Sixty clinically stable ESKD patients on regular HD were enrolled into this cross-sectional study. They were evaluated by basal abdominal X-ray. They were divided into two groups: (Group A, n = 30), patients with abdominal aortic calcification who underwent multislice computerized tomography scan to measure coronary artery calcification score; and (Group B, n = 30), patients without abdominal aortic calcification. All of them were evaluated by lipid profile and dialysis adequacy parameters. Fifty percent of patients had vascular calcification. We found a significant positive correlation between age and intact FGF-23; significant positive correlations between age, body mass index, duration of HD, and abdominal aortic calcification score. FGF-23 of all patients was elevated and had significant positive correlation with aortic and coronary calcifications in addition to lipid profile, left ventricular mass index (LVMI), and inflammatory markers. Plasma intact FGF-23 was elevated in nondiabetic ESKD patients, and vascular calcification was prevalent in such group of patients with many traditional and nontraditional risk factors. Possibly through its disturbing effects on minerals and parathyroid hormone, FGF-23 might indirectly affect vascular calcification. LVMI was higher in patients with vascular calcification and correlated positively with it.

How to cite this article:
El Baz TZ, Khamis OA, Ahmed Gheith OA, Abd Ellateif SS, Abdallah AM, Abd El Aal HC. Relation of fibroblast growth factor-23 and cardiovascular calcification in end-stage kidney disease patients on regular hemodialysis. Saudi J Kidney Dis Transpl 2017;28:51-60

How to cite this URL:
El Baz TZ, Khamis OA, Ahmed Gheith OA, Abd Ellateif SS, Abdallah AM, Abd El Aal HC. Relation of fibroblast growth factor-23 and cardiovascular calcification in end-stage kidney disease patients on regular hemodialysis. Saudi J Kidney Dis Transpl [serial online] 2017 [cited 2017 May 29];28:51-60. Available from: http://www.sjkdt.org/text.asp?2017/28/1/51/198127

   Introduction Top


Chronic kidney disease (CKD) stage five is associated with an increased risk of cardiovascular mortality which might reach 20 to 30 fold higher than in the general population. The presence and extent of vascular calcification are highly correlated with cardiovascular mortality, and extensive arterial calcification is typical of patients on hemodialysis (HD), even among those younger than 30 years.[1] Vascular calcification could be either intimal calcification of the atherosclerotic plaques, or medial calcification of large elastic arteries and small arterioles and both are associated with an increased risk of myocardial infarction and cardiovascular mortality.[2]

In CKD, the failing kidney is unable to adequately maintain mineral homeostasis, initiating series of events, biochemical changes in serum, altered bone metabolism, vascular calcification, and increased morbidity and mortality.[3]

Increased fibroblast growth factor-23 (FGF-23) levels occur primarily as a result of a net positive phosphate balance leading to increased renal phosphate excretion. The rise in FGF-23 is not merely a response to hyperphosphatemia but also to the increased parathyroid hormone (PTH) level.[4] FGF-23 exerts its biological functions by binding to its cognate FGF receptor in the presence of Klotho which is a transmembrane protein that determines the tissue specificity of FGF-23.[5]

Excess FGF-23 (its level is 25-50 pg/mL in normal subjects using an intact FGF-23) results in renal phosphate wasting, inappropriately low levels of active Vitamin D, and osteomalacia. On the contrary, depletion of FGF-23 leads to hyperphosphatemia, excessive levels of active Vitamin D, and soft tissue calcification.[6]

Factors affecting vascular calcification, a predictor of morbidity and mortality in dialysis patients, are not fully uncovered; FGF-23-null mice suffer severe vascular calcification in conjunction with hyperphosphatemia and increased mortality suggesting that FGF-23 may be protective from vascular calcifications.[7]

On the contrary, the elevated FGF-23 was found to be associated with mortality in HD patients. FGF-23 relation to vascular calcification in CKD patients is more ambiguous; one recent study reported an independent positive correlation between FGF-23 and peripheral vascular calcification,[8] whereas another study reported a negative association.[9] Even less clear is the relation of FGF-23 to aortic calcification which, unlike peripheral calcification, is associated with coronary artery calcification. Both aortic and peripheral vascular calcifications were associated with mortality in CKD.[10]


   Aim Top


We aimed to investigate the relation between intact FGF-23 and cardiovascular calcification in patients with end-stage kidney disease (ESKD) who were maintained on regular HD.


   Patients and Methods Top


Sixty clinically stable chronic renal failure patients undergoing continuous regular HD were enrolled in this cross-sectional study. They were being dialyzed three sessions per week in El-Glaa Military Hospital. Written informed consents were obtained from all participants. According to abdominal aortic calcification by basal abdominal X-ray, patients were divided into two groups: (Group A, n = 30), patients with abdominal aortic calcification who underwent multislice computerized tomography (CT) scan to measure coronary artery calcification score (CACS); and (Group B, n = 30), patients without abdominal aortic calcification.

Patient with the following criteria was included in the study: patients older than 25 years; higher parathormone than 300 pg/mL; serum calcium more than 8.4 mg/dL, and calcium phosphorus (Ca-Ph) product more than 55 mg/dL.

We excluded patients with the following criteria from the study: patients with parathy-roidectomy and/or PTH <150 pg/mL; severely anemic patients (Hb <7 g/dL as severe anemia may interfere with results of ejection fraction (EF) and left ventricular mass index (LVMI); patients with advanced cardiac dysfunction (EF% <35% who may have difficulty to lie flat for long duration); patients on oral anticoagulants; patients on regular HD <6 months and those who are diabetics.

All patients were subjected to (1) full history taking, especially age, sex, duration of HD, original kidney disease, and history of hypertension, diabetes, detailed medical treatment including oral anticoagulant, type and dosage of phosphate binder and active Vitamin D intake; and (2) complete physical examination.

Hemodialysis prescription

All patients were under continuous regular HD (12 h per week on 3 divided sessions), using polysulfone hemodialyzer and bicarbonatebased dialysate. The adequacy of dialysis was assessed using Kt/V formula.

Laboratory evaluation

All patients were evaluated by the following laboratory parameters: serum calcium, phosphorus, albumin, cholesterol, high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C), triglycerides (TG), in addition to plasma intact FGF-23, serum intact PTH, serum creatinine, serum urea, calculated Kt/V, serum C-reactive protein (CRP), and blood hemoglobin.

Radiological evaluation

It was performed through:

  1. Echocardiography which was used to measure different cardiac parameters especially left ventricular diameters and EF
  2. Lateral abdominal X-radiography of the aorta for grading of calcifications as follows: 0 - no aortic calcific deposits; 1 - small scattered calcific deposits less than one-third of the corresponding length of the vertebral level; 2 - medium quantity of calcific deposits about one-third or more, but less than two-thirds of the correspon- ding vertebral length; 3 - severe quantity of calcifications of more than two-third or more of the corresponding vertebral lengths. To detect abdominal aortic calcification, we used a validated 24-point abdominal aortic calcification score (AACS). For the 24-point score, calcified deposits along the anterior and posterior longitudinal walls of the abdominal aorta adjacent to each lum- bar vertebra from L1 to L4 were assessed using the midpoint of the intervertebral space above and below the vertebrae as the boundaries. The scores obtained separately for the anterior and posterior walls resulted in a range from 0 to 6 for each vertebral level and 0 to 24 for the total score [11]
  3. Multislice CT scan to measure CACS using Agatston score. The score was calculated using a weighted value assigned to the highest density of calcification in a given coronary artery. The density was measured in Hounsfield units, and score of 1 for 130-199 HU, 2 for 200-299 HU, 3 for 300-399 HU, and 4 for 400 HU and greater. This weighted score was then multiplied by the area (in square millimeters) of the coronary calcification. The tomographic slices of the heart were 3 mm thick and average about 64 slices from the coronary artery ostia to the inferior wall of the heart. The calcium score of every calcification in each coronary artery for all of the tomographic slices was then summed up to give the total coronary artery calcium score (CAC score). [Figure 1], [Figure 2][12]
    Figure 1. Varying degrees of abdominal aortic calcifications ranging from score 8 to 12 to 24
    respectively.


    Click here to view
    Figure 2. Multislice images of the patients enrolled in the study show the presence of the coronary artery
    calcification.


    Click here to view



   Statistical Analysis Top


All statistical calculations were done using computer programs SPSS (Statistical Package for the Social Science; SPSS Inc., Chicago, IL, USA) version 15 for Microsoft Windows. Data were statistically described in terms of mean and standard deviation, median and range, or frequencies (number of cases) and percentages when appropriate. Comparison of numerical variables between the study groups was done using Student's t-test for independent samples. For comparing categorical data, Chi-square test was performed. The exact test was used instead when the expected frequency is <5. Correlation between various variables was done using Pearson moment correlation equation. P <0.05 was considered statistically significant.


   Results Top


The age of patients enrolled in our study ranged from 28 to 72 years old with mean age 54.1 ± 9.35 years, (28) patients were males and (32) were females, their mean body mass index (BMI) was 27.5 ± 2.5 kg/m2, mean duration of HD was 4.48 ± 2.2 years, and the most common etiology of renal failure was hypertension which represented 38.3% of all patients as shown in [Table 1].
Table 1. Demographic, laboratory, and echocardiographic data of patients in the two groups.

Click here to view


Group A included 30 patients, their mean age was 55.8 ± 9.4 years, 13 patients were males, and 17 were females, mean BMI was 27.6 ± 2.3 g/m2, mean duration of HD was 4.9 ± 2.2 years, and most common etiology of renal failure was hypertension and represented 40% of patients group as shown in [Table 1]. In Group B, the included patients number was 30, their mean age was 52.5 ± 9.1 years, 15 patients were males and 15 were females, mean BMI was 27.4 ± 2.7 g/m2, mean duration of HD was 4.07 ± 2.2 years, and most common etiology of renal failure was also hypertension and represented 36.7% of patients as shown in [Table 1]. The number of patients with vascular calcification was 30 patients representing 50% of patients. Both groups were matched regard mean age, gender, BMI, original kidney disease, and duration of HD (P >0.05, [Table 1]). We found significant positive correlation between age and intact FGF-23 (P <0.005) but no significant correlation with either duration of HD or BMI (P >0.05). In addition, there were significant positive correlations between age, BMI, duration of HD, and AACS (P <0.05). Moreover, there were significant positive correlations between age, duration of HD, BMI, and CACS (P < 0.005). FGF-23 of all patients was elevated (280.7 ± 193.3 pg/mL) and had significant positive correlation with normal value of controls (13.3 ± 19 pg/mL) (P <0.05). It was higher in group A compared to group B, but this did not rank to significance (P >0.05). Despite the fact that there was no significant difference between the two groups regarding serum creatinine and urea (P >0.05), we found that mean KT/V, albumin, and hemoglobin were significantly higher in Group B in addition to lower serum phosphorus, calcium, Ca-Ph product, serum PTH, and CRP (P <0.05). We found a significant positive correlation between AACS and intact FGF-23, CRP, corrected serum calcium, serum phosphorus, Ca-Ph product, serum cholesterol, triglyceride, LDL, and LVMI; but it correlated negatively with hemoglobin, HDL, EF (P <0.05). However, it did not correlate with renal function or Kt/V (P >0.05, [Table 2]).
Table 2. Correlations between FGF-23 and other laboratory variables.

Click here to view


Similarly, CACS correlated positively with intact FGF-23, CRP, corrected serum calcium, serum phosphorus, Ca-Ph product, serum cholesterol, triglyceride, LDL, and LVMI; but it correlates negatively with hemoglobin, HDL, EF (P <0.05). However, it did not correlate with renal function and Kt/V (P >0.05, [Table 2]).


   Discussion Top


We observed that plasma intact FGF-23 was elevated in all studied patients, especially those with vascular calcification (Group A).

This was coinciding with Stubbs et al,[13] who found that circulating FGF-23 levels were elevated in CKD patients and its levels were often increased thousand-fold.[14] Moreover, a cross-sectional study performed on 128 maintenance HD patients reported similar findings compared to age- and gender-matched healthy controls[15] and irrespective of the level of phosphorus.[16] In our study, FGF-23 showed significant positive correlations with age, serum phosphorus, corrected serum calcium, Ca-Ph product, serum PTH, serum cholesterol, serum TG, serum LDL, CRP, and had significant negative correlations with Kt/V, hemoglobin, and serum HDL. However, it did not correlate with serum creatinine, blood urea, or serum albumin. These findings were matched with that reported by Unsal et al,[17] who found significant positive correlations between FGF- 23 and serum phosphate, log PTH, and Ca-Ph product. In addition, significant correlations were observed between FGF-23 levels and serum phosphate, intact PTH levels,[15] and duration of HD.[16] On the other hand, both Wesseling-Perry et al[18] and Kojima et al[19] did not find a relation between plasma C-terminal FGF-23 levels and serum PTH in their cohorts. These contradictory results might be explained by different FGF-23 assay, relatively small- sized pediatric samples on different dialysis modalities. Using the log of FGF-23 in Kojima et al,[19] study might have resulted in higher magnitude of data which could explain the positive correlations of serum creatinine and serum albumin with FGF-23. In addition, heterogeneity of their group, especially those with adynamic bone disease who were treated with relatively high dose of calcium carbonate and Vitamin D, might have influenced plasma FGF-23 and serum PTH levels.

The prevalence of LVH was variable in different studies. In our study, we observed that plasma intact FGF-23 was positively correlated with elevated LVMI detected in all our patients with hypertension as the most common cause of ESKD and negatively correlated with EF. Both Strózecki et al[20] and Kutlay et al[21] reported LVH in 86% of hypertensive HD patients while the former reported LVH in 55% of normotensive HD patients. However, LVH prevalence in HD patients was reported as 43.6%, and FGF-23 was independently associated with LVH.[22] Similar results were reported in dialysis patients by Kirkpantur et al[15] and in predialysis CKD patients by Gutiérrez et al.[23] The higher prevalence of LVMI might be due to uremia-related factors such as hypervolemia, anemia (although severe anemia was excluded from the study) and uncontrolled hypertension which may strongly influence LV geometry in HD patients.[21] Moreover, Seiler et al[24] concluded that patients who underwent coronary angiography with lower EF <40% had significantly higher FGF-23 levels even with multivariate analysis compared with patients with lower EF. In the same direction, Faul et al[25] found that left ventricular EF was modestly lower in the highest versus the lower quartiles of FGF-23 levels while the LVMI - with multivariate analysis - increased with increasing FGF-23 quartiles. Using stepwise regression analysis, we found that serum phosphorus and Ca-Ph product were the only independent predictors of FGF-23. This matched with the results of Imanishi et al,[16] Unsal et al,[17] Kojima et al,[19] and Marsell et al.[26]

Abdominal aortic calcification was detected only in 50% of all our patients which was lower than that reported in most of studies[27] ,[28] ,[29] ,[30] ,[31] which reported up to 94% vascular calcification. This might be explained by the relatively younger age and shorter dialysis duration in our patients and the heterogeneity of patients in other cohorts with diabetes, adynamic bone disease and those on oral anticoagulant which were considered major causes of vascular calcification in HD patients. The use of plain X-ray for detection of abdominal aortic calcification is used in most of the studies.[32] In the present study, AACS showed significant positive correlations with other variables rather than age, duration of HD such as BMI, serum phosphorus, corrected serum calcium, and Ca-Ph product, serum PTH, serum lipid profile, and CRP but showed significant negative correlation with hemoglobin and serum HDL. However, in multivariate regression analysis, we found that PTH, hemoglobin, serum phosphorus, and CRP were the only predictors of AACS. Toussaint et al[32] reported that age, dialysis duration, and the presence of cardiovascular disease were independent predictors for the presence and severity of abdominal aortic calcification. Other studies added some vascular calcification risk factors as age, gender, diabetes, dialysate calcium, serum calcium and Vitamin D treatment, CaPh product, PTH, CRP, and high phosphate in nondiabetic ESKD patients;[33] advanced age, longer duration of HD, high phosphate, and lower predialysis diastolic pressure;[34] in addition to higher serum PTH and FGF-23 Levels.[7] ,[35] Similarly, Gelev et al[36] added that risk factors for arterial calcifications were age, BMI, lower dialysis adequacy, serum CRP, serum TG, serum calcium, and PTH. Again in nondiabetic Caucasian HD patients, Schlieper et al[37] found that Ca-Ph product, high-sensitivity CRP, and lower Kt/V were independent risk factors. Increased levels of CRP were significantly associated with the presence of vascular calcification in both aorta and hand arteries indicating evident relationship between inflammation and vascular calcification in HD patients.[38] On the other hand, Yamada et al,[39] found that serum calcium, serum phosphorus and the Ca-Ph product were not associated with aortic calcification possibly because of good mineral control of their patients.

In our study, CACS was positively correlated with age, duration of HD, serum phosphorus, corrected serum calcium, Ca-Ph product, PTH levels, and CRP. This result has been documented before by many studies[17] ,[40] ,[41] ,[42] which all supported the concept that disturbances in mineral metabolism contribute to coronary artery calcification in patients with ESKD. On the other hand, Nitta et al[43] reported that the CACS correlated only with age and CRP but not with mineral parameters or PTH. The heterogeneity of the study population, study design as single baseline laboratory value may lessen the strength of some significant predictors of CAC, especially those that vary widely from day-to-day (e.g., serum phosphorus levels).

In addition, we found that CACS showed significant positive correlations with BMI, cholesterol, TG, LDL, and blood urea and had significant negative correlation with hemoglobin, and HDL but no significant correlation with serum creatinine, Kt/V, or serum albumin. Unsal et al[17] reported significant relationship between CAC and age, LVMI, dialysis duration, serum phosphorus levels, and Ca-Ph product but no correlation was found between LVMI and log FGF-23. However, significant relationships were found between LVMI, CAC, and aortic calcification. The patients with coronary calcification had higher LVMI than those without and the severity of calcification was significantly related to LVMI. Moreover, in multiple linear regression analysis, CACS was an independent predictor of LVMI.[44]

The present study showed significant positive correlations between intact serum FGF-23 and AACS and CACS; significant positive correlations between LVMI, AACS, and CACS. However, the role of FGF 23 as vascular calcification predictor was not proven. Many studies verified the role of FGF-23 in vascular calcification and reported conflicting results[7] ,[36] ,[45] ,[46] ,[47] ,[48] ,[49] and no consensus have been developed yet.

Moreover, serum phosphorus and Ca-Ph product were the only independent predictors of FGF-23, while PTH, hemoglobin level, calcium, and CRP were the only independent predictors of AACS. Moreover, PTH, hemoglobin level, and Ca-Ph product were the only independent predictors of CACS. Thus, serum calcium, serum phosphorus, and PTH derangement in accordance with high plasma FGF-23 levels, contribute to the development of vascular calcification. Calcium-phosphorus product in HD patients raised the possibility of a specific effect of FGF-23 on medial calcification of the aorta.


   Conclusion Top


Plasma intact FGF-23 was elevated in nondiabetic ESKD patients, and vascular calcification was prevalent in such group of patients with many traditional and nontraditional risk factors. Possibly through its disturbing effects on minerals and PTH, FGF-23 might indirectly affect vascular calcification. LVMI was higher in patients with vascular calcification and correlated positively with it.

Conflict of interest: None declared.

 
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Inaba M, Okuno S, Imanishi Y, et al. Role of fibroblast growth factor-23 in peripheral vascular calcification in non-diabetic and diabetic hemodialysis patients. Osteoporos Int 2006;17:1506-13.  Back to cited text no. 48
    
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Roos M, Lutz J, Salmhofer H, et al. Relation between plasma fibroblast growth factor-23, serum fetuin-A levels and coronary artery calcification evaluated by multislice computed tomography in patients with normal kidney function. Clin Endocrinol (Oxf) 2008;68:660- 5.  Back to cited text no. 49
    

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Correspondence Address:
Osama Ashry Ahmed Gheith
Department of Nephrology and Internal Medicine, Urology and Nephrology Center, Mansoura University, Mansoura
Egypt
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DOI: 10.4103/1319-2442.198127

PMID: 28098103

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