Home About us Current issue Ahead of Print Back issues Submission Instructions Advertise Contact Login   

Search Article 
  
Advanced search 
 
Saudi Journal of Kidney Diseases and Transplantation
Users online: 529 Home Bookmark this page Print this page Email this page Small font sizeDefault font size Increase font size 
 

Table of Contents   
ORIGINAL ARTICLE  
Year : 2018  |  Volume : 29  |  Issue : 3  |  Page : 567-577
Prevalence of cardiac arrhythmia and risk factors in chronic kidney disease patients


1 Department of Nephrology, Faculty of Medicine, Cukurova University, Adana, Turkey
2 Department of Radiology, Faculty of Medicine, Cukurova University, Adana, Turkey
3 Department of Cardiology, Faculty of Medicine, Cukurova University, Adana, Turkey

Click here for correspondence address and email

Date of Submission29-May-2017
Date of Decision19-Jul-2017
Date of Acceptance19-Jul-2017
Date of Web Publication28-Jun-2018
 

   Abstract 

Chronic kidney disease (CKD) patients have a high risk for cardiac arrhythmia. This study aimed to investigate the prevalence of cardiac arrhythmia in CKD patients and to evaluate the relationship between arrhythmia and biochemical and echocardiographic parameters. CKD patients between 18 and 80 years of age were enrolled from the nephrology outpatient clinic. Physical examination, complete blood count, urinalysis biochemical analysis, electrocardiogram, echocardiogram, and 24-h Holter electrocardiogram were performed. Patients with and without cardiac arrhythmia were compared regarding their characteristics, laboratory findings, and echocardiographic parameters. Risk factors for cardiac arrhythmia were also evaluated. The carotid intima-media thickness was measured using Doppler ultrasonography. In our study involving 59 patients, 44 (74%) had atrial arrhythmia (AA) and 40 (68%) had ventricular arrhythmia (VA). Atrial and/or VA were diagnosed in 46 patients (78%), of whom six (10.2%) had AA, two (3.4%) had VA and 38 (64.4%) had AA plus VA. Atrial fibrillation (AF) was present in two patients (3.4%) in the form of paroxysmal AF. Risk factors for AA were low calcium level and posterior wall thickness, while factors associated with VA were age, triglyceride level, leukocyte count, and nonusage of angiotensin 2 receptor blockers. Risk factors for AA and/or VA included increased platelet count, age, and leukocyte count. AA and/or VA were found in as high as 78% of CKD patients. Further studies evaluating course of the disease from early stages are needed to identify risk factors.

How to cite this article:
Kaya B, Paydas S, Aikimbaev K, Altun E, Balal M, Deniz A, Kaypakli O, Demirtas M. Prevalence of cardiac arrhythmia and risk factors in chronic kidney disease patients. Saudi J Kidney Dis Transpl 2018;29:567-77

How to cite this URL:
Kaya B, Paydas S, Aikimbaev K, Altun E, Balal M, Deniz A, Kaypakli O, Demirtas M. Prevalence of cardiac arrhythmia and risk factors in chronic kidney disease patients. Saudi J Kidney Dis Transpl [serial online] 2018 [cited 2022 Jul 6];29:567-77. Available from: https://www.sjkdt.org/text.asp?2018/29/3/567/235178

   Introduction Top


There is a bidirectional interaction between renal and cardiac diseases and co-existence of these diseases has an unfavorable influence on morbidity and mortality.[1] Sudden cardiac death (SCD) is frequently encountered in patients with chronic kidney disease (CKD) and SCD accounts for approximately 25% of all-cause mortality in dialysis patients. CKD patients have a very high risk for cardiac arrhythmia, which is a significant cause of SCD.[2] Cardiac arrhythmias are triggered due to changes in serum levels of electrolytes and metabolites, acid-base imbalance, reduced circulating blood volume, and sympathetic overactivity during dialysis; the risk for cardiac arrhythmia and SCD increase as duration of dialysis therapy and the interval between dialysis sessions are prolonged.[3] Nevertheless, ventricular or supraventricular arrhythmias (VAs) can also be seen in the early period before dialysis in CKD patients. VAs include atrial flutter, atrial fibrillation (AF), atrioventricular re-entry tachycardia, atrioventricular nodal re-entry tachycardia, atrial tachycardia, sinus bradycardia, and premature atrial contraction. AF is the most prevalent arrhythmia with significant prognostic impact in CKD patients.[4] The prevalence of AF is 9%–21% in CKD patients and increases up to 13%–27% in long-term hemodialysis (HD) patients. The five-year mortality in CKD patients with AF is reported to be 80%.[2] VAs included premature ventricular contraction, ventricular tachycardia, ventricular fibrillation, and SCD. While the rate of SCD in general population is one event per 1000 patient-years of follow-up, it increases up to 7.8/1000 patient-years in CKD patients.[2]

Coronary artery disease (CAD) is frequently encountered in CKD patients, as both conditions share common pathophysiological processes such as chronic hyperglycemia, insulin resistance, endothelial dysfunction, and atherosclerosis; increased rate of CAD is probably responsible for a part of the arrhythmias.[2] Moreover, many other factors such as electrolyte disturbances, uremia, inflammatory processes, cardiac autonomic neuropathy, structural cardiac abnormalities, left ventricular disorders and diabetes as well, play a role in the development of arrhythmia.[2]

The present study is aimed to investigate the prevalence of cardiac arrhythmia in CKD patients and to evaluate the relationship between arrhythmia and biochemical and echo-cardiographic parameters.


   Methods Top


Patients

The study included patients with stage 2-5 CKD, between the age of 18 and 80 years, who presented to our nephrology outpatient clinic. Patients with preexisting cardiac arrhythmia, cardiac valve disease, chronic obstructive pulmonary disease, CAD, coronary artery bypass graft, chronic liver disease, cardiomyopathy, clinically overt heart failure, cardiac amyloidosis, hypothyroidism, hyperthyroidism, acute renal insufficiency, obesity [body mass index (BMI) >35 kg/m2] and malignancy were excluded. Approval of the ethics committee of our institution and informed consent of the patients were obtained before starting the study.

Detailed medical history including smoking, alcohol consumption, medication used and, physical examination was recorded. Fibroblast growth factor (FGF-23) level was measured using enzyme-linked immunosorbent assay (ELISA). FGF-23 measurement was performed with USCN Life Science Inc. Wuhan, China ELISA kit in the Chromate microELISA device. Parathormone was measured with Roche Elecys -170 device using the electro chemoluminescence, 25-OH-Vitamin D (25-OH-D) was measured with Agilent-1100 device with the high-pressure liquid chromatography method. Fasting blood glucose (FBG), blood urea nitrogen (BUN), creatinine, uric acid (UA), calcium (Ca), phosphate (P), albumin (alb), magnesium (Mg), sodium (Na) and potassium (K) were measured with Roche Modular DPP device using the enzymatic calorimetry method. Ferritin was measured with Roche Modular system device using the immunoturbidimetric method. C-reactive protein (CRP) was measured with Date Behring BN II device using the immunoturbimetric method. HbA1c was measured with Roche integra 800 device using the immunoturbimetric method. Whole blood count (WBC) was analyzed in a Beckman coulter machine. Chest X-ray, electrocardiography (ECG), exercise ECG, Holter ECG, detailed echocar-diographic examination, carotid intima-media thickness (CIMT) measurement, and abdominal ultrasonography were performed.

Blood pressure was measured in a quiet room in sitting position using the same sphygmomanometer for all patients. BMI was calculated by dividing the body weight (kg) by the square of height (m2). Glomerular filtration rate (GFR) was calculated using the Modification of Diet in Renal Disease formula: GFR = 170 × (serum creatinine)−0.999 × (age)−0.176 × (0.762 if female) × (1.180 if black) × BUN−0.170 × albumin+0.318.

CIMT was measured using Logiq 8 (General Electric Medical Systems) high-resolution B-mode ultrasonography using a linear probe with a frequency of 12.0 MHz, by the same experienced radiologist. CIMT, described by Pignoli et al,[5] was defined as the distance between the inner echogenic line (lumen-intima interface), and the outer echogenic line, which represents the collagen-containing media-adventitia layer. The measurements of CIMT were taken when the patients were in supine position with the head turned 45° to the opposite of the measurement side. Three measurements were taken at the posterior wall of both common carotid arteries 2 cm proximal to the bulbus, the arithmetic mean of these measurements was calculated, and measurements of the right or left side, whichever was higher, was taken as the basis. The presence of calcifications, plaque, or stenosis was noted. Measurements were taken from the places where no atheroma plaque exists.

Echocardiographic measurements were made from appropriate echocardiographic windows by Acuson Sequoia C256 echocardiography system (Acuson Corporation, Mountain view, CA, USA) and 3.5 mHz probe using M-mode, two-dimensional, color Doppler, and pulse wave Doppler echocardiography methods when the patient was lying in a supine or left the lateral position. Parasternal long axis images were obtained by the recommendations of the American Society of Echocardiography (ASE).[6] Normal values of echocardiographic parameters were accepted as follows: ejection fraction (EF, >52%, left ventricular end-systolic diameter (LVESD) <40mm and <35 mm, left ventricular end-diastolic diameter (LVEDD), <58 mm and <52 mm, posterior wall thickness at end-diastole (PWT, <1 cm and <0.9 cm, interventricular septum thickness at enddiastole (IVST, <1 cm and <0.9 cm), left atrial diameter (LAD, <40 mm and <38 mm and left ventricular mass (LVM <224 g and <162 g), left ventricular mass index (LVMI, <115 g/m2 and <95 g/m2 for males and females, respectively according to the ASE and the European Association of Cardiovascular Imaging.[7]

Two-dimensional echocardiography was performed, and the following were analyzed as follows: movement of the ventricular walls, valvular structures and functions, and peri-cardial pathologies. Wall motion abnormalities were investigated by dividing the myocardium into 17 segments by the recommendations of the ASE. The apical four-chamber view was obtained when the patient was lying in the left lateral position. Images showing the largest and the smallest left ventricular cavity area during systole and diastole were obtained. Thereafter, left ventricular EF was calculated automatically by the echocardiography program using the modified Simpson's Rule.

Ventricular and VAs were assessed by 24-h holter ECG. VA was defined as the pre-sence of ventricular extra-systoles and ventri-cular tachycardia. An atrial arrhythmia (AA) was defined as the presence of premature atrial contraction, atrial tachycardia, AF, and sinus bradycardia.


   Statistical Analysis Top


Predictive analytics software Statistics version 18.0 (IBM, Chicago IL. USA) was used for statistical analysis. Descriptive statistics was presented as a mean ± standard deviation for numerical variables and as numbers and percentages for categorical variables. Normality of data was tested using visual (histogram and probability graphics) and analytical methods (Kolmogorov–Smirnov/Shapiro–Wilk tests). Paired and multiple comparisons between categorical variables were made using Chi-square test, or by Fischer's exact test where Chi-square test was not suitable. For numerical variables, the comparison between independent two groups was done using t-test if the normal distribution conditions were met and by Mann–Whitney U-test if the conditions were not met. The factors that influence the presence of cardiac arrhythmia were investigated by logistic regression analysis. A type-1 error <5% was considered statistically significant.


   Results Top


The study included 59 patients; there were 36 males and 23 females. The most common etiological factors for CKD were diabetes (28.8%), polycystic kidney disease (16.9%), and nephrolithiasis (11.9%). The etiology was not known in 18.6% of the patients. Of the study patients three had stage-2 CKD (5.1%), 21 had stage-3 (35.6%), 26 had stage-4 (44.1%), and nine had stage-5 CKD (15.3%).

There were 44 patients (74%) with AA and 40 patients (68%) with VA in our study. AA and/or VA was diagnosed in 46 patients (78.0%), of whom six (10.2%) had only AA, two (3.4%) had VA and 38 (64.4%) had AA plus VA. AF was present in two patients (3.4%) in the form of paroxysmal AF.

No difference was found between the patients with and without AA, VA, and AA and/or VA in terms of age, gender, BMI, smoking, and alcohol consumption, blood pressure (systolic and diastolic), duration of CKD, GFR, presence of concomitant diseases, and the medications used (angiotensin-converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARB), beta-blockers, diuretics, lipid-lowering drugs, Vitamin D, phosphorus binders, and allopurinol) [Table 1].
Table 1: Characteristics of chronic kidney disease patients with and without atrial arrhythmia, ventricular arrhythmia and atrial and/or ventricular arrhythmia.

Click here to view


Patients with AA, VA, and AA and/or VA had significantly lower levels of albumin and calcium when compared to patients without arrhythmia. However, serum levels of P, ALP, FBG, UA, creatinine, hgb, hct, WBC, Plt, ferritin, TSH, HbA1C, total cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL), triglyceride (TG), Na, K, Mg were similar in the two groups [Table 2.
Table 2: Laboratory findings of chronic kidney disease patients with and without atrial arrhythmia, ventricular arrhythmia and atrial and/or ventricular arrhythmia.

Click here to view


With regard to the echocardiographic parameters, LVM, LVMI, and PWT were higher in patients with AA and AA and/or VA [Table 3].
Table 3: Results of echocardiographic parameters in chronic kidney disease patients with and without atrial arrhytmia, ventricular arrhytmia, and atrial and/or ventricular arrhythmia.

Click here to view


No difference was found between the two groups regarding heart rate, EF, LVEDD, LVESD, and IVST. Abnormal findings including higher LAD (left atrium >40 mm) and thicker PWT (PWT >1 cm), were more common in patients with AA and AA and/or VA [Table 3].

CIMT was not different in patients with/or without arrhythmias.

Logistic regression analysis revealed that age, increased platelet count, and lower WBC were statistically significant risk factors, for AA and/or VA. Risk factors for AA were lower calcium, increased ferritin and thicker PWT. Age, lower WBC, TG, and nonuse of ARB were risk factors for VA [Table 4].
Table 4: Risk factors for cardiac arrhythmia in chronic kidney disease patients according to logistic regression analysis.

Click here to view



   Discussion Top


Cardiovascular diseases such as SCD, cardiac arrest, myocardial infarction, and arrhythmias account for 43% of all-cause mortality in HD patients. It is known that along with the traditional cardiovascular risk factors, a number of different risk factors increase the incidence of cardiac events in HD patients.[8] Knowing the incidence of arrhythmia in different stages of the disease, determining the risk factors, understanding the underlying mechanisms, and prevention of modifiable risk factors are necessary measures to reduce the incidence of cardiac arrhythmias and related sudden death in CKD patients. In the present study, we assessed the prevalence of arrhythmia and the risk factors in stage 2–5 CKD patients.

AF has been reported as the most prevalent sustained arrhythmia both in the general population and in CKD patients, and majority of the studies investigating arrhythmia in CKD patients are about AF. Concurrent AF and CKD have a negative effect on prognosis.[9] In the present study, paroxysmal AF was identified in 3.4% of the patients, which is a higher percentage than that reported for the general adult population in Turkey (1.25%).[10] In other studies, the prevalence of AF in CKD patients was found to be 18% and 21.2%.[11],[12] The majority of AF cases in the study of Soliman et al,[11] have been determined based on the patients self-report; the prevalence of AF detected by ECG was reported to be 6.6%. In our study, a lower prevalence of AF (3.4%), when compared to the above-mentioned studies, might have resulted from the exclusion of the patients with pre-existing AF. In CKD patients without pre-existing AF who have been followed for five years, AF was seen in 7.7%.[13] In the same study, AF was associated with 66% increase in relative mortality rate after adjusting for potential confounders.[13] Bonato et al[14] reported the prevalence of VA to be 35% in CKD patients.

Our CKD patients with and without cardiac arrhythmias were similar for age, gender, BMI, blood pressure, biochemical parameters except for lower levels of albumin, and calcium. In another study, it was reported that co-existence of lower BMI and higher LVMI is associated with increased cardiovascular events in stage 3–5 CKD patients. They concluded that measurement of BMI and LVMI might be helpful in identifying CKD patients with poor cardiovascular prognosis.[15] LVMI was higher in patients with AA than that in those without AA (102 g/m2 vs. 90 g/m2) in the present study; the difference was not statistically significant.

AF is known to be an independent risk factor for stroke and death in dialysis patients. Furthermore, fibrotic changes due to systemic inflammation and thromboembolic events due to lower GFR, play an important role in the causation of mortality.[16] In a large, population-based study conducted in the US, decreased renal functions indicated by low GFR and the presence of macroalbuminuria have been reported to be associated with increased risk of AF.[17] In another population-based study performed in Japan in patients who were in an annual check-up program, it was demonstrated that the risk of developing kidney disease was increased in patients with preexisting AF, and the risk of developing incident AF was increased in the patients with baseline renal dysfunction. It was also reported that there is a two-way relationship between AF and renal dysfunction.[18] Deo et al[19] carried out a study in subjects aged >65 years and found the baseline prevalence of AF as 7% with incident AF developing in 13% of the patients during seven-year follow-up. This study concluded that impaired kidney function, as measured by cystatin C, is an independent marker of prevalent AF; but neither cystatin C nor estimated GFR were found to be predictors of incident AF. The study of Ananthapanyasut et al[11] found that GFR levels were not correlated with the presence of AF in nondialysis CKD patients as in our study. Our CKD patients with and without arrhythmia (AA, VA, and AAa/oVA) had similar GFR.

Biomarkers associated with SCD in CKD patients include inflammatory markers such as interleukin-6 (IL-6), CRP and adiponectin and nutritional markers such as albumin and creatinine.[20] In a study investigating the relationship between AF and inflammatory markers including the plasma concentrations of IL-1, IL-1 receptor antagonist, IL-6, tumor necrosis factor-α, transforming growth factor-β, high-sensitive CRP and fibrinogen, the independent and consistent predictive factor for AF in CKD patients, was plasma IL-6 level.[21] Ananthapan-yasut et al[11] found no correlation between CRP levels and presence of AF in nondialysis CKD patients, as in our study. Bonato et al[14] found that CRP and IL-6 levels were similar in those with and without VA. Albumin levels of our CKD patients were significantly lower in patients with AA, VA and AA and/or VA compared with those without arrhythmia.

Changes in electrolyte and mineral concentrations are a risk factor for cardiac arrhythmia. Even minimal changes in potassium levels of CKD patients may result in serious arrhythmias and/or life-threatening conditions. Potassium plays an important role in maintaining the electrical potential across the cellular membrane and in depolarization and repolarization of the cardiac cells.[22] Hypokalemia or hyperkalemia may trigger arrhythmias by altering the transmembrane potential.[23] It has been revealed that hypokalemia is a stronger risk factor than hyperkalemia.[22] Moreover, hypokalemia is the most common electrolyte disturbance in clinical practice.[23] In our study, potassium levels were similar in patients with and without AA, VA and AAOV.

Ananthapanyasut et al[11] found that calcium levels were significantly lower in patients with AF when compared with patients without AF. Hypocalcemia is common among CKD patients and is usually associated with other electrolyte disturbances.[23] We found that the calcium levels were significantly lower in patients with AA, VA and AA and/or VA. However, lower serum calcium level was found as a risk factor only in patients with AA.

Inflammation is another risk factor for the development of cardiac arrhythmias.[24] Decreased pro-inflammatory cytokine clearance, endoto-xemia, oxidative stress, and reduced antioxidant levels are proposed mechanisms for increased inflammation in CKD.[25] In our study, increased platelet count and higher ferritin levels were also risk factors for AA and AA and/or VA, respectively, on logistic regression analysis. Lower serum albumin level related with inflammation was a risk factor for arrhythmias in our study. In contrast to this finding, WBC counts were lower in CKD patients with arrhythmias compared to CKD patients without arrhythmias.

FGF-23 is a hormone produced by osteocytes and regulates phosphate and vitamin D metabolism. The decrease in GFR leads to an increase in serum FGF-23 levels and phosphate levels in CKD patients.[26] The role of FGF-23 in increasing cardiovascular risk, left ventricular hypertrophy (LVH) and vascular calcification is under discussion.[27] Studies are being conducted on the predictive value of FGF-23 in the mortality risk of CKD patients who are either on dialysis or in the predialysis period.[26] Bonato et al[1] found FGF-23 levels to be similar in CKD patients with and without VA. In our study,, FGF-23 levels were not different between the patients with or without AA, VA, and AA and/or VA.

“Accelerated atherosclerosis” has been reported in many dialysis patients.[28] Furthermore, it is known that LVH is seen in CKD patients forming a basis for cardiac diseases such as arrhythmia and heart failure.[28] LVH and cardiac fibrosis lead to cardiac remodeling and structural changes in the heart, which may alter the electrophysiological features of the myocardium in CKD patients.[29] Regarding atherosclerotic risk factors evaluated, no difference was found in total cholesterol, LDL, HDL, FBG, and HbA1c levels of our patients with and without AA, VA, and AA and/or VA. However, TG levels were statistically different only in CKD patients with VA. PWT, LVMI, and LVM and were significantly higher in our CKD patients with AA than that in those without arrhythmia. Our CKD patients with AA had higher PWT and increased LAD. Logistic regression analysis demonstrated that PWT is a significant risk factor for AA. Myocardial fibrosis and hypertrophy provide additional substrate for an increased electrical instability and may contribute to an increased risk of AA. Univariate analyses performed in CKD patients to assess the risk factors for AF revealed a significant relationship with age, white race, increased LAD, lower systolic blood pressure and congestive heart failure in an earlier study,[11] and with older age, female sex, smoking, and history of heart failure and cardiovascular disease in another study.[12] Bonato et al[14] in their study on CKD patients, found that VA was associated with age, increased hemoglobin levels and decreased EF on multiple logistic regression analysis. In our study, logistic regression analysis demonstrated that age increased platelet count and decreased WBC levels are significant risk factors for AA and/or VA. In addition, logistic regression analysis revealed that levels of calcium, ferritin, and PWT are significant risk factors for AA, while factors significantly associated with VA were age, TG level, WBC count, and non-ARB usage. In fact, the process of aging contributes to changes in the cardiovascular system such as increased arterial stiffness, increased systolic ventricular wall stress, and diastolic dysfunction.[30] These structural cardiac alterations over time, along with uremic cardiomyopathy, are potential contributors to the high prevalence of arrhythmias in CKD patients. We found that nonARB use was a significant risk factor for VA. There are several potential mechanisms by which inhibition of the RAS with ACEIs and ARBs may reduce AF. These are a reduction in the atrial stretch, prevention of atrial fibrosis, prevention of electrical remodeling, and direct anti-arrhythmic effects.[31],[32],[33] Nonuse of ARB may increase the risk of cardiac arrhythmia for many reasons.

This study has some limitations to be considered, such as the relatively small sample of prevalent CKD patients. Moreover, the cross-sectional design of the study does not allow us to evaluate the cause-effect relationship to derive conclusions.

In conclusion, cardiac arrhythmias were a frequent finding, as high as 78%, in CKD patients. Paroxysmal AF was found to be higher than in the Turkish healthy population. VA was often accompanied by AA. There was no relationship between FGF-23 and CIMT and cardiac arrhythmias. However, as in other studies, structural cardiac alterations over time, are potential contributors to the high prevalence of arrhythmias in CKD patients. Serum levels of calcium and ferritin and PWT were risk factors for AA, while factors associated with VA were age, TG level, leukocyte count, and nonARB usage.

Conflict of interest: None declared.

 
   References Top

1.
Ronco C. Cardiorenal syndromes: Definition and classification. Contrib Nephrol 2010;164: 33-8.  Back to cited text no. 1
[PUBMED]    
2.
Roberts PR, Green D. Arrhythmias in chronic kidney disease. Heart 2011;97:766-73.  Back to cited text no. 2
[PUBMED]    
3.
Franczyk-Skóra B, Gluba A, Banach M, Kozlowski D, Malyszko J, Rysz J. Prevention of sudden cardiac death in patients with chronic kidney disease. BMC Nephrol 2012; 13:162.  Back to cited text no. 3
    
4.
Bansal N, Hsu CY, Go AS. Intersection of cardiovascular disease and kidney disease: Atrial fibrillation. Curr Opin Nephrol Hypertens 2014;23:275-82.  Back to cited text no. 4
[PUBMED]    
5.
Pignoli P, Tremoli E, Poli A, Oreste P, Paoletti R. Intimal plus medial thickness of the arterial wall: A direct measurement with ultrasound imaging. Circulation 1986;74:1399-406.  Back to cited text no. 5
[PUBMED]    
6.
Sahn DJ, DeMaria A, Kisslo J, Weyman A. Recommendations regarding quantitation in M-mode echocardiography: Results of a survey of echocardiographic measurements. Circulation 1978;58:1072-83.  Back to cited text no. 6
[PUBMED]    
7.
Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: An update from the American Society of Echo-cardiography and the European Association of Cardiovascular İmaging. J Am Soc Echocardiogr 2015;28:1-39.e14.  Back to cited text no. 7
    
8.
Kanbay M, Afsar B, Goldsmith D, Covic A. Sudden death in hemodialysis: An update. Blood Purif 2010;30:135-45.  Back to cited text no. 8
[PUBMED]    
9.
Ferreira C, Providência R, Ferreira MJ, Gonçalves LM. Atrial fibrillation and non-cardiovascular diseases: A systematic review. Arq Bras Cardiol 2015;105:519-26.  Back to cited text no. 9
    
10.
Uyarel H, Onat A, Yüksel H, et al. Incidence, prevalence, and mortality estimates for chronic atrial fibrillation in Turkish adults. Turk Kardiyol Dern Ars 2008;36:214-22.  Back to cited text no. 10
    
11.
Ananthapanyasut W, Napan S, Rudolph EH, et al. Prevalence of atrial fibrillation and its predictors in nondialysis patients with chronic kidney disease. Clin J Am Soc Nephrol 2010;5:173-81.  Back to cited text no. 11
[PUBMED]    
12.
Soliman EZ, Prineas RJ, Go AS, et al. Chronic kidney disease and prevalent atrial fibrillation: The chronic renal insufficiency cohort (CRIC). Am Heart J 2010;159:1102-7.  Back to cited text no. 12
[PUBMED]    
13.
Bansal N, Fan D, Hsu CY, Ordonez JD, Go AS. Incident atrial fibrillation and risk of death in adults with chronic kidney disease. J Am Heart Assoc 2014;3:e001303.  Back to cited text no. 13
[PUBMED]    
14.
Bonato FO, Lemos MM, Cassiolato JL, Canziani ME. Prevalence of ventricular arrhythmia and its associated factors in nondialyzed chronic kidney disease patients. PLoS One 2013;8:e66036.  Back to cited text no. 14
[PUBMED]    
15.
Chen SC, Huang JC, Tsai YC, et al. Body mass index, left ventricular mass index and cardiovascular events in chronic kidney disease. Am J Med Sci 2016;351:91-6.  Back to cited text no. 15
[PUBMED]    
16.
Patel NJ, Patel A, Agnihotri K, et al. Prognostic impact of atrial fibrillation on clinical outcomes of acute coronary syndromes, heart failure and chronic kidney disease. World J Cardiol 2015;7:397-403.  Back to cited text no. 16
[PUBMED]    
17.
Alonso A, Lopez FL, Matsushita K, et al. Chronic kidney disease is associated with the incidence of atrial fibrillation: The atherosclerosis risk in communities (ARIC) study. Circulation 2011;123:2946-53.  Back to cited text no. 17
[PUBMED]    
18.
Watanabe H, Watanabe T, Sasaki S, et al. Close bidirectional relationship between chronic kidney disease and atrial fibrillation: The Niigata preventive medicine study. Am Heart J 2009;158:629-36.  Back to cited text no. 18
[PUBMED]    
19.
Deo R, Katz R, Kestenbaum B, et al. Impaired kidney function and atrial fibrillation in elderly subjects. J Card Fail 2010;16:55-60.  Back to cited text no. 19
[PUBMED]    
20.
Pun PH. The interplay between CKD, sudden cardiac death, and ventricular arrhythmias. Adv Chronic Kidney Dis 2014;21:480-8.  Back to cited text no. 20
[PUBMED]    
21.
Amdur RL, Mukherjee M, Go A, et al. Interleukin-6 is a risk factor for atrial fibrillation in chronic kidney disease: Findings from the CRIC study. PLoS One 2016;11: e0148189.  Back to cited text no. 21
    
22.
Checherită IA, David C, Diaconu V, Ciocâlteu A, Lascăr I. Potassium level changes – Arrhythmia contributing factor in chronic kidney disease patients. Rom J Morphol Embryol 2011;52:1047-50.  Back to cited text no. 22
    
23.
El-Sherif N, Turitto G. Electrolyte disorders and arrhythmogenesis. Cardiol J 2011;18:233-45.  Back to cited text no. 23
[PUBMED]    
24.
Guo Y, Lip GY, Apostolakis S. Inflammation in atrial fibrillation. J Am Coll Cardiol 2012;60:2263-70.  Back to cited text no. 24
[PUBMED]    
25.
Shlipak MG, Fried LF, Crump C, et al. Elevations of inflammatory and procoagulant biomarkers in elderly persons with renal insufficiency. Circulation 2003;107:87-92.  Back to cited text no. 25
[PUBMED]    
26.
Nitta K, Nagano N, Tsuchiya K. Fibroblast growth factor 23/klotho axis in chronic kidney disease. Nephron Clin Pract 2014;128:1-0.  Back to cited text no. 26
[PUBMED]    
27.
Jimbo R, Shimosawa T. Cardiovascular risk factors and chronic kidney disease-FGF23: A key molecule in the cardiovascular disease. Int J Hypertens 2014;2014:381082.  Back to cited text no. 27
[PUBMED]    
28.
Tangri N, Komenda PV, Rigatto C. Chronic kidney disease and heart disease: After 179 years, do we yet understand the link? Kidney Int 2015;88:11-3.  Back to cited text no. 28
[PUBMED]    
29.
Kiuchi MG, Mion D Jr. Chronic kidney disease and risk factors responsible for sudden cardiac death: A whiff of hope? Kidney Res Clin Pract 2016;35:3-9.  Back to cited text no. 29
[PUBMED]    
30.
Oxenham H, Sharpe N. Cardiovascular aging and heart failure. Eur J Heart Fail 2003;5:427-34.  Back to cited text no. 30
[PUBMED]    
31.
Webster MW, Fitzpatrick MA, Nicholls MG, Ikram H, Wells JE. Effect of enalapril on ventricular arrhythmias in congestive heart failure. Am J Cardiol 1985;56:566-9.  Back to cited text no. 31
[PUBMED]    
32.
McEwan PE, Gray GA, Sherry L, Webb DJ, Kenyon CJ. Differential effects of angiotensin II on cardiac cell proliferation and intramyocardial perivascular fibrosis in vivo. Circulation 1998;98:2765-73.  Back to cited text no. 32
[PUBMED]    
33.
Nakashima H, Kumagai K, Urata H, et al. Angiotensin II antagonist prevents electrical remodeling in atrial fibrillation. Circulation 2000;101:2612-7.  Back to cited text no. 33
[PUBMED]    

Top
Correspondence Address:
Dr. Bulent Kaya
Department of Nephrology, Faculty of Medicine, Cukurova University, Adana
Turkey
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1319-2442.235178

Rights and Permissions



 
 
    Tables

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

This article has been cited by
1 Uremic Toxins and Cardiovascular Risk in Chronic Kidney Disease: What Have We Learned Recently beyond the Past Findings?
Carolla El Chamieh, Sophie Liabeuf, Ziad Massy
Toxins. 2022; 14(4): 280
[Pubmed] | [DOI]
2 Computational Models Used to Predict Cardiovascular Complications in Chronic Kidney Disease Patients: A Systematic Review
Alexandru Burlacu, Adrian Iftene, Iolanda Valentina Popa, Radu Crisan-Dabija, Crischentian Brinza, Adrian Covic
Medicina. 2021; 57(6): 538
[Pubmed] | [DOI]



 

Top
   
 
 
    Similar in PUBMED
    Search Pubmed for
    Search in Google Scholar for
    Email Alert *
    Add to My List *
* Registration required (free)  
 


 
    Abstract
   Introduction
   Methods
   Statistical Analysis
   Results
   Discussion
    References
    Article Tables
 

 Article Access Statistics
    Viewed4768    
    Printed38    
    Emailed0    
    PDF Downloaded515    
    Comments [Add]    
    Cited by others 2    

Recommend this journal