INTERPRETATION OF TROPONIN IN CHRONIC KIDNEY DISEASE AS PREDICTOR OF CARDIOVASCULAR DISEASE

14/02/2025 Views : 12

Ni Made Dharma Laksmi

Introduction

Chronic Kidney Disease (CKD) is an independent risk factor for cardiovascular disease. More than 50% of deaths in CKD patients are attributed to cardiovascular diseases (1). Coronary heart disease is the leading cause of morbidity and mortality in CKD patients, with acute myocardial infarction accounting for approximately 50% of all deaths among patients undergoing hemodialysis (2). In addition to traditional risk factors, uremia-related risk factors such as inflammation, oxidative stress, endothelial dysfunction, coronary artery calcification, and hyperhomocysteinemia contribute to accelerated atherosclerosis. The atypical clinical presentation and the adverse effects of cardiovascular disease treatments in CKD often lead to delayed diagnosis and therapy initiation (3,4).

Troponin is a cardiac biomarker that is currently used to aid in the diagnosis of acute coronary syndrome (ACS). However, troponin elevation can also occur in conditions associated with chronic structural heart disease, particularly when the increase remains persistent. Patients with chronic kidney disease (CKD) tend to have higher troponin levels. Studies have shown that CKD patients without ACS who exhibit chronically elevated troponin levels have an increased risk of cardiovascular morbidity and mortality (5). In ACS cases, there is currently no well-defined cutoff value for troponin reference levels to establish a diagnosis. Some studies suggest that a >20% increase or decrease in troponin levels from baseline may be considered in diagnosing ACS in CKD patients (6).

Cardiovascular Disease in Chronic Kidney Disease (CKD)

Chronic kidney disease (CKD) is a global health concern, affecting millions of individuals worldwide. It is estimated that 20 million adults in the United States suffer from CKD. According to the United States Renal Data System (USRDS), in 2009, a total of 571,414 patients were diagnosed with end-stage CKD, and 172,553 patients underwent kidney transplantation (3).  

The correlation between cardiovascular disease and CKD can be described through the concept of cardiorenal syndrome, in which CKD contributes to impaired cardiac function, ventricular hypertrophy, diastolic dysfunction, and an increased incidence of adverse cardiovascular events (4). CKD patients are at high risk for cardiovascular disease, with more than 50% of deaths in this population attributed to cardiovascular causes. The two-year mortality rate for CKD stage 5 patients with acute myocardial infarction is estimated to be as high as 50% (3,4). In contrast, the 10-year post-myocardial infarction mortality rate in the general population without CKD is only 25%. Even milder stages of CKD have been associated with an increased risk of cardiovascular disease (4).

Adverse cardiovascular outcomes in CKD patients are associated with specific biomarker levels in plasma. Biomarkers such as troponin, asymmetric dimethylarginine, plasminogen-activator inhibitor type 1, homocysteine, natriuretic peptides, C-reactive protein, serum amyloid, hemoglobin, and albumin have been linked to cardiovascular outcomes in CKD patients (4). However, only Troponin T is considered a potential biomarker indicative of myocardial disease in CKD, whereas other biomarkers primarily reflect chronic disease, inflammation, and malnutrition (7).

The strong relationship between CKD and cardiovascular disease is based on several factors: (1) cardiovascular risk factors are frequently present in CKD patients, (2) CKD is associated with an increased prevalence of traditional cardiovascular risk factors, (3) CKD patients have additional non-traditional risk factors, (4) CKD is an independent risk equivalent for cardiovascular disease, and (5) the presence of CKD predicts a more rapid decline in kidney function, creating a worsening cycle (8).

Myocardial and arterial remodeling are the primary pathogenesis of cardiovascular disease in CKD. Myocardial remodeling primarily results from secondary effects of excessive pressure and volume load. Increased pressure load arises from prolonged hypertension, aortic stenosis, atherosclerosis, diabetes mellitus, and anemia, leading to left ventricular hypertrophy. Excessive volume load results from arteriovenous shunting during hemodialysis, salt and water overload, anemia, ischemic heart disease, hypertension, and hypoalbuminemia, ultimately causing left ventricular dilation. Additionally, uremic conditions and ischemic heart disease promote increased apoptosis, accelerating cardiomyopathy and resulting in both systolic and diastolic dysfunction (8).

Vascular pathology in CKD includes accelerated atherosclerosis, arteriosclerosis, vascular calcification, and endothelial dysfunction. Vascular wall damage, hypertension, dyslipidemia, prothrombotic factors, increased oxidative stress, and hyperhomocysteinemia contribute to these pathological changes. Vascular remodeling occurs in both the arterial lumen and vascular wall components, leading to atherosclerosis and arteriosclerosis. While atherosclerotic lesions in the general population are typically fibroatheromatous, in CKD patients, these lesions tend to be more extensive, unstable, frequently calcified, and characterized by medial layer thickening (8).

In addition to traditional risk factors, various non-traditional risk factors, such as albuminuria, anemia, inflammation, oxidative stress, endothelial dysfunction, homocysteine, lipoprotein(a) [Lp(a)], malnutrition, thrombogenic factors, sympathetic overactivity, and insulin resistance, have also been linked to the atherosclerosis process. Arteriosclerosis is characterized by diffuse arterial dilation, hypertrophy of large arteries, and arterial wall stiffness, which occurs secondary to excessive pressure and volume load commonly observed in CKD (8).

Vascular calcification is a hallmark characteristic of CKD. The pathogenesis of vascular calcification in CKD is not yet fully understood and, similar to the general population, is multifactorial in nature. Several studies have demonstrated that uremic toxins stimulate vascular smooth muscle cell proliferation and their transformation into an osteoblast-like phenotype, leading to vascular calcification. Disturbances in calcium and phosphate metabolism, hyperhomocysteinemia, and genetic factors also play a role in vascular calcification. Hyperphosphatemia and hypercalcemia are independent risk factors for cardiovascular disease in CKD. Additionally, hyperphosphatemia accelerates the progression of secondary hyperparathyroidism, leading to bone fragility, which is associated with calcium-phosphate deposition in the vasculature.

Calcification of atherosclerotic plaques (intimal arterial calcification, an occlusive condition) frequently extends into the medial layer, forming medial calcinosis (medial arterial calcification, a non-occlusive condition). Medial layer calcification reduces arterial elasticity, contributing to macroangiopathy. This condition is commonly observed in elderly CKD patients and those with diabetes. Medial calcinosis is associated with increased cardiovascular and all-cause mortality in dialysis patients, and vascular calcification has been linked to left ventricular hypertrophy (8,9).

CKD patients exhibit a wide range of abnormalities that adversely impact endothelial dysfunction, with oxidative stress and chronic inflammation playing key roles. The end result of this process includes impaired endothelial proliferation, a procoagulant state (due to increased activator inhibitor 1 and von Willebrand factor, and decreased tissue plasminogen activator), and dysregulation of vascular homeostasis due to impaired nitric oxide synthesis caused by elevated dimethylarginine, homocysteine, and oxidized LDL (8).

The Role of Troponin in Diagnosing Myocardial Injury

In the early 1900s, troponin T and I assays were introduced. Initial studies suggested that the detection of troponin in the bloodstream was an indication of myocardial injury. Consequently, clinicians at that time quickly recognized troponin as a biomarker with 100% accuracy for myocardial infarction (4).  

Although troponin testing was proposed as a replacement for CK-MB measurement, an exact equivalence between these two tests has not been established. Approximately 12% to 39% of patients with negative CK-MB results present with positive troponin levels. This discrepancy raised questions about whether discordant CK-MB and troponin results indicate a false positive or if troponin represents a more sensitive biomarker capable of accurately classifying patients. Subsequent meta-analyses addressed this issue by demonstrating that positive troponin results indicate a higher risk of poor outcomes, even in the absence of recurrent ischemic injury. The evolving definition of myocardial infarction as any myocardial necrosis caused by ischemia, along with advancements in the sensitivity and specificity of diagnostic technologies such as troponin testing, necessitates a reevaluation to establish a clear definition of myocardial infarction (4).

In 2007, a global consensus meeting represented by the ESC, ACCF, AHA, and WHF was held to revise the definition of myocardial infarction (MI). The outcome of this meeting established that the term "myocardial infarction" should be used when there is evidence of myocardial necrosis in a clinical setting consistent with ischemia, accompanied by specific diagnostic criteria: (1) a rise or fall in biomarkers (particularly troponin); (2) sudden cardiac death; (3) an increase in biomarkers following percutaneous coronary intervention (PCI) in patients with normal pre-procedural troponin levels; (4) an increase in biomarkers in patients undergoing coronary artery bypass grafting (CABG) who previously had normal troponin levels; and (5) pathological findings of acute myocardial infarction (4,6).

Based on these criteria, myocardial infarction is classified into five types, as outlined in Figure 2: Type 1 is defined as spontaneous myocardial infarction associated with coronary ischemia due to plaque rupture, erosion, fissure, or dissection; Type 2 is associated with ischemia due to an imbalance between oxygen supply and demand; Type 3 is linked to sudden cardiac death; Type 4a is related to PCI, while Type 4b is associated with stent thrombosis; and Type 5 is related to CABG (4).

Troponin is widely recognized as a biomarker of myocardial injury. Cardiac troponin is a protein that regulates the calcium-mediated interaction between actin and myosin, facilitating muscle contraction and relaxation. The troponin complex consists of three subunits: troponin C, which binds to calcium; troponin I, which inhibits actin-myosin interaction; and troponin T, which anchors the troponin complex by binding to tropomyosin and facilitating contraction. While troponin C is found in both cardiac and skeletal muscle cells, the amino acid sequences of troponin I and T are specifically expressed in cardiac muscle (10,11).

The normal plasma troponin level in healthy individuals is estimated to be 0.1–0.2 ng/L, which results from the continuous microscopic loss of cardiomyocytes during the normal life cycle. Troponin is primarily bound to the myofibrillar apparatus, where it functions in contraction; however, approximately 7% of troponin T and 3%–5% of troponin I exist freely in the cytoplasm. Following myocardial injury, troponin levels increase in a biphasic manner, initially due to the rapid release of free cytoplasmic troponin, followed by a gradual release of the myofibril-bound troponin complex. Acute transmural myocardial necrosis typically takes 2–4 hours to develop, though this process may be prolonged in specific conditions, such as the presence of collateral circulation or intermittent coronary artery occlusion.

Troponin terdeteksi sekitar 2-4 jam setelah cedera miokard. Kadar troponin dalam serum tetap meningkat selama 4-7 hari pada troponin I dan 10-14 hari pada troponin T. Walaupun proses eliminasi dari troponin ini masih belum diketahui dengan jelas karena ukuran molekul troponin yang relatif besar, namun diperkirakan troponin dibersihkan melalui sistem retikuloendotelial. Walaupun demikian, bukti terbaru memperkirakan bahwa troponin T dipecah menjadi molekul yang cukup kecil untuk diekskresikan oleh ginjal, hal ini menjelaskan tingginya prevalensi peningkatan troponin T pada gagal ginjal (10).

Pada pemeriksaan konvensional untuk infark miokard akut, sensitivitas troponin T yang diperiksa saat baru masuk rumah sakit yaitu 25%-65% dan meningkat menjadi 59%-90% pada 2 hingga 6 jam setelahnya. Sensitivitas mencapai 100% setelah 6 hingga 12 jam setelah saat awal masuk. Sedangkan sensitivitas troponin I saat pertama masuk kurang dari 45%, dan meningkat 69%-82% setelah 2 hingga 6 jam kemudian, dan mencapai 100% setelah 6-12 jam. Oleh sebab itu, sensitivitas maksimal dari pemeriksaan standar troponin belum bisa didapatkan hingga 6 jam atau lebih setelah proses inisiasi nekrosis miokard. Oleh sebab itu, sampel darah yang digunakan untuk mengukur kadar troponin disarankan untuk diambil saat datang dan diulang 6-9 jam kemudian untuk mengoptimalisasi baik sensitivitas dan spesifisitas dari diagnosis infark miokard (10).  Saat ini sudah berkembang pemeriksaan troponin yang lebih baik yaitu hs-troponin. Pemeriksaan hs-troponin ini memiliki akurasi diagnostik yang lebih besar sehingga memberikan kesempatan untuk memulai lebih cepat dalam diagnosis dan pemberian terapi (10).

Troponin becomes detectable approximately 2–4 hours after myocardial injury. Serum troponin levels remain elevated for 4–7 days for troponin I and 10–14 days for troponin T. Although the exact elimination process of troponin remains unclear due to its relatively large molecular size, it is believed to be cleared via the reticuloendothelial system. However, recent evidence suggests that troponin T is broken down into smaller molecules that can be excreted by the kidneys, which explains the high prevalence of elevated troponin T levels in patients with renal failure (10).In conventional testing for acute myocardial infarction, the sensitivity of troponin T at initial hospital admission ranges from 25% to 65%, increasing to 59%–90% within 2 to 6 hours and reaching 100% after 6 to 12 hours. Similarly, the sensitivity of troponin I is less than 45% at initial admission, increasing to 69%–82% after 2 to 6 hours and reaching 100% after 6–12 hours. Therefore, maximum sensitivity of standard troponin testing is not achieved until at least 6 hours after the onset of myocardial necrosis. For optimal sensitivity and specificity in diagnosing myocardial infarction, it is recommended to collect an initial blood sample upon admission and repeat testing 6–9 hours later (10).

Advancements in troponin testing have led to the development of high-sensitivity troponin (hs-troponin) assays. These tests offer greater diagnostic accuracy, allowing for earlier detection and initiation of appropriate therapy (10).

In conditions other than acute myocardial infarction, several other clinical scenarios can also present with elevated troponin levels as an indication of myocardial injury. In these cases, troponin elevation remains relatively constant across different sampling intervals (initial measurement, repeated at 6–9 hours, and again at 12–24 hours), a pattern referred to as "smoldering," which is commonly associated with chronic conditions such as renal failure, heart failure, myocarditis, or amyloidosis. Conversely, although clinical data are limited, a dynamic change from baseline values is more suggestive of an acute myocardial infarction process. 
According to the guidelines from the National Academy of Clinical Biochemistry (NACB), a 20% change (increase or decrease in troponin levels) within 3–6 hours from baseline indicates myocardial infarction (6,12,13). However, while such a pattern suggests acute myocardial injury, it does not distinguish whether the injury is due to acute coronary syndrome or other causes such as pulmonary embolism or myocarditis. Therefore, the degree of troponin elevation plays a crucial role in clinical decision-making (6).

The Role of Troponin in CKD Patients
Although the exact pathophysiology underlying elevated troponin levels in patients with impaired renal function remains unclear, its association with clinical outcomes is well established. Troponin serves as a reliable biomarker for diagnosing acute coronary syndrome (ACS); however, its diagnostic accuracy is less definitive in the context of CKD. As previously described, CKD is a significant contributor to cardiovascular events. A study analyzing coronary angiography findings in dialysis patients reported that approximately 40–50% had significant coronary artery disease (15,16).  
Despite these challenges, troponin remains the primary biomarker for diagnosing ACS. The National Academy of Clinical Biochemistry (NACB) recommends using troponin for diagnosing myocardial infarction in all CKD patients, regardless of disease stage, when ischemic symptoms or electrocardiographic evidence of ischemia are present. The guideline suggests that a dynamic change in troponin levels of ≥20% within 6 to 9 hours after initial presentation can confirm acute myocardial infarction in end-stage CKD patients. Additionally, the guideline states that troponin can be used for risk stratification in end-stage CKD and as a baseline reference for comparison when acute clinical changes occur (6,12,13,17).

However, the implementation of dynamic troponin changes as a diagnostic criterion still faces challenges. A 2016 study in Japan aimed to establish a single-measurement troponin threshold that could be used for diagnosing acute coronary syndrome (ACS). This study was conducted to assist clinicians working in resource-limited areas or small clinics with limited diagnostic facilities. The findings suggested that the optimal troponin threshold varies according to CKD stage.
For CKD stages 1–2, where renal function is nearly normal, the recommended threshold was 0.047 ng/mL, slightly higher than the normal population threshold of 0.03 ng/mL when using conventional cardiac troponin T assays. In CKD stage 3, characterized by moderate renal impairment, the suggested threshold was 0.088 ng/mL, nearly twice the cutoff used for CKD stages 1–2. This threshold was based on study data indicating that a cardiac troponin T level of 0.075 ng/mL was a potential marker for significant coronary stenosis, with a sensitivity of 51% and a specificity of 89%.
For CKD stages 4–5, the optimal threshold for diagnosing ACS was 0.180 ng/mL, nearly four times higher than that for CKD stage 1. An even higher cutoff of 0.280 ng/mL was proposed for end-stage CKD. A retrospective study in Korea identified a troponin level of 0.35 ng/mL as useful for detecting ACS in end-stage CKD patients. The Japanese study ultimately concluded that a cardiac troponin T level of 0.3 ng/mL was the most reliable threshold for diagnosing ACS in end-stage CKD (15).

There is strong evidence that troponin T has significant prognostic value in patients with end-stage renal disease (ESRD). A 2005 meta-analysis reported that elevated troponin T levels were significantly associated with all-cause mortality, with a relative risk of 2.64 (95% CI: 2.17–3.20). A significant association was also observed for cardiovascular mortality, with a relative risk of 2.55 (95% CI: 1.93–3.37) (6). Patients with troponin T levels exceeding the 99th percentile had a two- to five-fold higher risk of all-cause mortality compared to those without elevated troponin levels.
A meta-analysis by Khan et al., which analyzed data from 28 studies (3931 patients), concluded that troponin T holds promising prognostic value for risk stratification in ESRD patients and may aid in therapeutic decision-making. This study indicated that elevated troponin T levels (>0.1 µg/L) could be useful in identifying asymptomatic ESRD patients at higher risk for poor survival and cardiovascular mortality. However, the clinical interpretation of troponin I remains unclear due to the limited number of standardized studies (11).

The Food and Drug Administration (FDA) recently approved the use of troponin T as a biomarker for mortality risk stratification in ESRD patients, and the Kidney Disease Outcomes Quality Initiative (KDOQI) also recommends its use for prognostic purposes (11). However, it is crucial to measure troponin levels before dialysis, as evidence suggests that dialysis can affect troponin concentrations. Troponin I levels may decrease by approximately 86% post-dialysis, whereas troponin T levels may increase. The mechanisms underlying these differences remain unclear but are thought to be related to the release, degradation, and clearance of troponin in circulation (11).

Cardiac abnormalities, particularly geometric and left ventricular (LV) functional abnormalities, are frequently observed in CKD patients and have been strongly associated with increased morbidity, all-cause mortality, and cardiovascular mortality. Echocardiography is the primary non-invasive modality used to assess cardiac function and structure. Left ventricular hypertrophy (LVH) is found in approximately 16–50% of patients with CKD stages 1–3, 50–70% in CKD stages 4–5, and 70–90% in patients undergoing routine dialysis (18). Diastolic dysfunction is also commonly observed in CKD patients and serves as a strong predictor of mortality, particularly in those with advanced CKD (18,19). Although most CKD patients maintain a preserved left ventricular ejection fraction (LVEF >50%), a decline in LVEF has been shown to be an independent prognostic factor in CKD patients (18,20).  

Recent studies have demonstrated that troponin T provides significant prognostic value beyond clinical, biochemical, dialysis-related, and echocardiographic parameters such as LV mass and ejection fraction in patients undergoing chronic peritoneal dialysis. Dialysis patients have an increased risk of circulatory congestion, with underlying factors such as systolic dysfunction further exacerbating this condition. A prospective study involving 222 patients undergoing chronic peritoneal dialysis investigated the utility of a single-time troponin T measurement in identifying patients at risk for circulatory congestion over a three-year follow-up period. The study concluded that troponin T enhances predictive value when combined with LV mass and ejection fraction in assessing the risk of circulatory congestion. When comparing patients with troponin T ≤ 0.06 µg/L (median) and preserved LV systolic function to those with troponin T > 0.06 µg/L but with preserved LV systolic function, the latter group exhibited nearly twice the risk of developing circulatory congestion (11,21).

Thus, troponin plays a significant role as a prognostic marker for cardiovascular disease. However, no studies have yet demonstrated the utility of elevated troponin levels in CKD patients as a basis for more aggressive therapeutic strategies to prevent the progression of cardiovascular disease. Therefore, further research is needed to explore the potential benefits of intensified treatment approaches aimed at reducing cardiovascular morbidity and mortality in CKD patients.

Conclusion
CKD is a significant risk factor and predictor of cardiovascular disease. Various mechanisms contribute to the pathophysiology of cardiovascular disease in CKD, one of which is the elevation of serum troponin levels. While troponin elevation has long been used as a primary diagnostic modality for acute coronary syndrome (ACS), its role as a biomarker for ACS in CKD patients remains less definitive. One of the recommended diagnostic criteria for ACS in CKD includes a ≥20% increase or decrease in troponin levels within 6–9 hours.  
Troponin is well recognized for its prognostic value in cardiovascular disease. Therefore, routine troponin assessment in CKD patients is crucial, both as a baseline reference for potential acute changes in patient condition and as a subject for future research. Further studies are needed to explore the potential role of troponin in guiding more aggressive therapeutic interventions aimed at reducing cardiovascular morbidity and mortality in CKD patients.

References
1. Seidman JG, Pyeritz RE, Seidman CE. Inherited Cardiovascular Disease. In : Mann DL, Zipes DP, Libby P, Bonow RO. 9th ed. Braunwald's heart disease: a textbook of cardiovascular medicine. Philadelphia: Elsevier Health Sciences; 2014. pp 70-80.
2. Huang HL, Zhu S, Wang WQ, Nie X, Shi YY, He Y, et al. Diagnosis of Acute Myocardial Infarction in Hemodialysis Patients With High-Sensitivity Cardiac Troponin T Assay. Archives of pathology & laboratory medicine. 2016;140(1):75-80.
3. Cai Q, Mukku VK, Ahmad M. Coronary artery disease in patients with chronic kidney disease: a clinical update. Current cardiology reviews. 2013;9(4):331-9.
4. Ronco C, Haapio M, House AA, Anavekar N, Bellomo R. Cardiorenal Syndrome. Journal of the American College of Cardiology. 2008;52(19):1527-39.
5. Michos ED, Wilson LM, Yeh HC, Berger Z, Suarez-Cuervo C, Stacy SR, et al. Prognostic value of cardiac troponin in patients with chronic kidney disease without suspected acute coronary syndrome: a systematic review and meta-analysis. Annals of internal medicine. 2014;161(7):491-501.
6. Newby LK, Jesse RL, Babb JD, Christenson RH, De Fer TM, Diamond GA, et al. ACCF 2012 expert consensus document on practical clinical considerations in the interpretation of troponin elevations: a report of the American College of Cardiology Foundation task force on Clinical Expert Consensus Documents. J Am Coll Cardiol. 2012;60(23):2427-63.
7. Herzog CA, Asinger RW, Berger AK, Charytan DM, Diez J, Hart RG, et al. Cardiovascular disease in chronic kidney disease. A clinical update from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney international. 2011;80(6):572-86.
8. Ardhanari S, Alpert MA, Aggarwal K. Cardiovascular disease in chronic kidney disease: risk factors, pathogenesis, and prevention. Advances in peritoneal dialysis Conference on Peritoneal Dialysis. 2014;30:40-53.
9. Moe SM, Chen NX. Pathophysiology of Vascular Calcification in Chronic Kidney Disease. Circulation Research. 2004;95(6):560-7.
10. Daubert MA, Jeremias A. The utility of troponin measurement to detect myocardial infarction: review of the current findings. Vascular Health and Risk Management. 2010;6:691-9.
11. Wang AY-M, Lai K-N. Use of Cardiac Biomarkers in End-Stage Renal Disease. Journal of the American Society of Nephrology. 2008;19(9):1643-52.
12. Morrow DA, Cannon CP, Jesse RL, Newby LK, Ravkilde J, Storrow AB, et al. National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Clinical Characteristics and Utilization of Biochemical Markers in Acute Coronary Syndromes. Circulation. 2007;115(13):e356-e75.
13. Wu AH, Apple FS, Gibler WB, Jesse RL, Warshaw MM, Valdes R, Jr. National Academy of Clinical Biochemistry Standards of Laboratory Practice: recommendations for the use of cardiac markers in coronary artery diseases. Clin Chem. 1999;45(7):1104-21.
14. Agewall S, Giannitsis E, Jernberg T, Katus H. Troponin elevation in coronary vs. non-coronary disease. European Heart Journal. 2010;32:404-411.
15. Iwasaki M, Yamazaki K, Ikeda N, Tanaka Y, Hayashi T, Kubo S, et al. Point of care assessment of cardiac troponin T level in CKD patients with chest symptom. Renal failure. 2016;10:1-7.
16. Sung J-M, Su C-T, Chang Y-T, Su Y-R, Tsai W-C, Wang SPH, et al. Independent Value of Cardiac Troponin T and Left Ventricular Global Longitudinal Strain in Predicting All-Cause Mortality among Stable Hemodialysis Patients with Preserved Left Ventricular Ejection Fraction. BioMed Research International. 2014;14:1-12.
17. Stacy SR, Suarez-Cuervo C, Berger Z, Wilson LM, Yeh HC, Bass EB, et al. Role of troponin in patients with chronic kidney disease and suspected acute coronary syndrome: a systematic review. Annals of internal medicine. 2014;161(7):502-12.
18. Liu Y-W, Su C-T, Song E-J, Tsai W-C, Li Y-H, Tsai L-M, et al. The role of echocardiographic study in patients with chronic kidney disease. Journal of the Formosan Medical Association.114(9):797-805.
19. Farshid A, Pathak R, Shadbolt B, Arnolda L, Talaulikar G. Diastolic function is a strong predictor of mortality in patients with chronic kidney disease. BMC Nephrology. 2013;14(1):280-288.
20. Nagueh SF, Smiseth OA, Appleton CP, Byrd BF, Dokainish H, Edvardsen T, et al. Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography: An Update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. European Heart Journal – Cardiovascular Imaging. 2016;29:277-314.
21. Pecoits-Filho R, Bucharles S, Barberato SH. Diastolic heart failure in dialysis patients: mechanisms, diagnostic approach, and treatment. Seminars in dialysis. 2012;25(1):35-41.

Related Article

INOTROPICS IN ACUTE HEART FAILURE AND CARDIOGENIC SHOCK

Ni Made Dharma Laksmi