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  3. Liver and Kidney Function Markers as Non-Predictors of Coronary Artery…
Original Article Open Access

Liver and Kidney Function Markers as Non-Predictors of Coronary Artery Disease

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Annals of Medicine and Medical SciencesVol. 05, No. 06, (2026) June 27, 2026pp. 905 - 912
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Abstract

Background: Several studies have assessed liver and kidney functions in patients with coronary artery disease (CAD). However, the association of liver and kidney function markers with CAD remains unclear. Aim and Objective: To determine the potential of liver and kidney parameters in detecting and predicting the occurrence of CAD. Methods: This retrospective case-control study included 131 males and 97 females. Participants were categorized as cases or controls based on coronary angiography findings from the Department of Cardiology, Kasturba Hospital, Manipal, Karnataka. Relevant liver and kidney function test values were obtained from medical records and correlated with angiographic findings. Results: Mann–Whitney U test and receiver operating characteristic (ROC) curve analyses were used to assess diagnostic accuracy for predicting CAD. Correlation analysis was performed to evaluate the relationship between the jeopardy score and liver and kidney function indices. A significant increase in direct bilirubin, aspartate aminotransferase, and serum urea was observed among males, whereas females showed elevated serum albumin and creatinine levels. Conclusion: Despite these gender-specific variations, most liver and kidney function indices showed no significant association with angiographic findings. These results suggest that liver and kidney function markers have limited value in detecting or predicting the development of CAD.

Keywords

liver function test kidney function test coronary artery disease coronary angiogram prediction.

Introduction

Cardiovascular diseases (CVD) are a major cause of death among patients with advanced renal diseases [1,2]. However, the risk of developing cardiac dysfunction is not limited to end-stage kidney disease [3,4]. Several studies have shown that serum creatinine is an independent predictive marker for assessing renal function (GFR) [5]. Patients undergoing dialysis have a higher prevalence of coronary artery plaques [6,7], but the direct association of renal function with plaque severity remains unclear. It is therefore important to investigate whether renal function indices can directly predict the risk of CAD.

Liver function tests are routinely performed in clinical practice. Although chronic low serum albumin concentration is not directly related to the occurrence of CVD, a sudden decrease may serve as an early warning sign for cardiac disorders. Studies have reported a significant correlation between the aspartate aminotransferase/alanine aminotransferase ratio (AAR) and chronic liver diseases, as well as adverse long-term cardiac outcomes [8]. However, another study found no association between liver function indices and coronary atherosclerosis [L/C]. These conflicting findings suggest that a combination of liver and renal function markers may be useful in predicting CAD.

Inflammation plays a crucial role in the development and progression of cardiovascular disorders. Serum albumin is uniquely affected by inflammation and infection [9]. Lower serum albumin levels have been associated with a higher risk of myocardial infarction (MI), stroke and poor CAD outcomes [10-12]. Low albumin and globulin concentrations have also been shown to predict adverse cardiovascular events in patients with stable CAD [13-15]. Furthermore, decreased serum albumin concentration has independently proven to be a useful predictor of CAD in patients with preserved kidney function [16]. These outcomes have also been linked to cigarette smoking, which increases susceptibility to inflammatory responses [8,17].

Atherosclerotic disease, a leading cause of mortality worldwide, is characterized by chronic arterial inflammation and lipid peroxidation [18]. Bilirubin acts as a potent antioxidant and restricts lipid peroxidation [19-22]. However, the role of serum bilirubin in adverse cardiovascular events remains controversial [23]. Kunutsor et al.,(2015) suggested an independent inverse association between serum bilirubin concentrations and cardiovascular disorders [24], while other evidence indicates a possible non-linear relationship with CAD occurrence [25].

Transaminases have long been used to assess liver function [26]. Aspartate aminotransferase (AST) is present in several tissues, including the liver, kidney and lungs, whereas alanine aminotransferase (ALT) is mainly found in hepatocytes. Hepatocellular injury results in the release of AST and ALT into the bloodstream [27]. A study evaluating the alanine aminotransferase-to-lymphocyte ratio (ALR) concluded that ALR can independently predict coronary angiogram plaques in CAD patients undergoing percutaneous coronary investigations [28].

Although creatinine is primarily considered a renal marker, it has also been linked to insulin resistance, dyslipidemia and coronary artery disorders. Bagheri et al. (2019) reported a significant correlation between serum creatinine and renal function markers, but not with insulin or inflammatory markers [29]. Based on existing evidence, this study aims to investigate whether a combination of liver and kidney function indices can predict the risk of CAD incidence.

Methodology

In this cross-sectional retrospective study, we included patients who had undergone a coronary angiogram due to angina or chest pain. These patients were admitted to the cardiology department at a tertiary hospital in southern India. We conducted the study after receiving ethical clearance from the Manipal Institutional Ethics Committee (IEC 503/2017). The study was conducted in the Department of Physiology at Kasturba Medical College over an 11-month period in 2017. The study population included participants between 35 and 70 years of age, with no history of acute or chronic cardiac, liver, or renal disorders. We enrolled 131 age-matched male cases and controls, as well as 97 age-matched female cases and controls, for a total of 528 participants.

In the presented scientific article, competent researchers were enlisted to conduct a retrospective case-control study that gathered a comprehensive assemblage of data from electronic medical databases. The data curation process included basic demographic details, past hospitalizations and medical histories, and family histories of diseases. Coronary angiography was performed as a routine check-up for each individual, as advised by the cardiology consultant. Based on the angiogram report, individuals were categorized as cases or controls. Cases were defined as individuals with at least 50% stenosis in the epicardial artery, while controls were individuals with less than 50% stenosis.

Blood samples were collected from each participant, and serum was prepared and tested to evaluate liver and kidney function. Liver function test (LFT) parameters included total bilirubin, direct bilirubin, serum albumin, serum globulin, aspartate aminotransferase (AST), alanine transaminase (ALT), and alkaline phosphatase (ALP). Kidney function test (KFT) parameters included serum urea, creatinine, sodium, and potassium. The aim of the study was to assess liver and renal function indices for early detection and prediction of CAD.

Statistical Analysis

The curated data were analyzed using Graphpad Prism version 5.0, and the results were reported as median (interquartile range) due to the non-skewed distribution of data. Receiver operating characteristic (ROC) analysis was performed to determine the diagnostic performance of liver and renal function parameters. The ROC analysis involved determining the optimal cut-off, area under the curve (AUC), sensitivity, specificity, and Youden Index. The level of significance was set at a p-value of less than 0.05.

Results

Comparison of liver and kidney function indices in CAD cases and controls

Table I summarizes the general profile measurements of the liver function test and kidney function test in the study sample (males and females). The total number of study population included 228 subjects, out of which 57% (n=131) were males and 43% (n=97) were females. Both male and female cases and controls were matched by age, wherein the mean age are such as: 55.27±8.59 (male cases), 55.34±8.58 (male controls), 57.84±7.72 (female cases) and 57.90±7.85 (female controls) respectively. Statistical analysis exhibits a statistical significant difference in bilirubin direct, AST and serum urea in male cases compared to controls, whereas a significant difference in serum albumin and serum creatinine in female cases as and when compared to controls.

Table 1
Characteristics Male cases (n=131) Male controls (n=131) p-value Female cases (n=97) Female controls (n=97) p-value
Total bilirubin 0.60(0.40-0.78) 0.60(0.40-1.00) 0.0531 0.40(0.30-0.60) 0.38(0.10-0.50) 0.0737
Bilirubin direct 0.10(0.10-0.20) 0.20(0.20-0.30) 0.0002 0.10(0.10-0.20) 0.20(0.10-0.20) 0.4421
Serum albumin 4.32(4.20-4.60) 4.33(4.08-4.60) 0.8138 4.32(4.05-4.59) 4.10(3.78-4.41) 0.0468
Serum globulin 2.80(2.53-3.10) 2.90(2.61-3.30) 0.1766 3.14(2.70-3.31) 3.00(2.60-3.26) 0.3056
AST 31.0(20.0-60.0) 24.0(19.0-38.0) 0.0254 30.0(21.0-41.5) 28.0(19.0-42.0) 0.6830
ALT 25.00(18.00-42.25) 26.00(17.00-42.75) 0.9147 20.50(16.00-36.75) 19.00(15.00-36.00) 0.5129
ALP 82.00(67.50-98.50) 79.00(67.00-92.00) 0.4236 84.0(68.0-105.8) 84.0(71.0-103.5) 0.7920
TSH 1.85(1.13-2.97) 2.21(1.50-3.17) 0.0520 2.485(1.195-3.450) 2.32(1.48-3.82) 0.5841
Troponin T hs 0.066(0.011-0.737) 0.009(0.006-0.020) <0.001 0.039(0.009-0.390) 0.011(0.005-0.027) 0.0002
Serum urea 20.0(17.0-26.0) 23.0(18.0-30.0) 0.0230 21.00(17.50-27.00) 24.00(16.00-30.25) 0.4432
Serum creatinine 1.0(0.9-1.2) 1.0(0.8-1.2) 0.0736 0.8(0.7-1.0) 0.7(0.7-0.9) 0.0317
Serum sodium 139.0(137.0-141.0) 140.0(138.0-142.0) 0.3140 139.0(136.0-140.0) 139.5(137.0-141.0) 0.1920
Serum potassium 4.30(4.08-4.50) 4.30(4.00-4.60) 0.6521 4.360±0.5139 4.314±0.5096 0.5288

ROC curves for assessing accuracy of predictors for CAD

Table II indicates the AUC, optimal cut-off, measurements of sensitivity and specificity, Youden Index for encapsulating the diagnostic accuracy of liver and kidney function indices in prediction of CAD for both males and females. The ROC curve analysis was performed so as to evaluate the diagnostic predictability of a parameter and effectively correlate it with other markers. Outliers from the male and female control group were culminated and optimal cut-off points were determined. Both liver and kidney function indices could not demonstrate acceptable discrimination in ROC with value >0.7 in AUC.

Table 2
Characteristics Males/Females AUC Optimal Cut-off Sensitivity (%) Specificity (%) Youden Index
Total bilirubin Males 0.5398 <0.65 68.48 38.42 0.06
Females 0.5895 <0.45 62.67 51.72 0.15
Bilirubin direct Males 0.5679 <0.15 51.09 69.86 0.21
Females 0.5361 <0.15 57.33 51.72 0.09
Serum albumin Males 0.5021 <4.415 62.16 45.21 0.07
Females 0.6146 >4.13 71.67 54.55 0.27
Serum globulin Males 0.05051 <2.765 45.95 55.00 0.01
Females 0.5589 >3.125 57.63 62.22 0.20
AST Males 0.5954 >30.5 50.54 63.74 0.14
Females 0.5206 >25.5 60.53 44.07 0.05
ALT Males 0.5008 <29.5 59.78 45.65 0.06
Females 0.5331 >19.5 56.58 53.45 0.1
ALP Males 0.5342 >86.5 41.94 65.93 0.08
Females 0.5135 <78.5 40.79 63.16 0.04
TSH Males 0.5760 <2.265 58.18 51.38 0.09
Females 0.5257 <2.81 64.10 44.0 0.08
Troponin T hs Males 0.7505 >0.0105 77.67 64.52 0.43
Females 0.6832 >0.0135 67.09 61.29 0.29
Serum urea Males 0.5815 <22.5 61.83 52.71 0.15
Females 0.5325 <22.5 58.06 55.32 0.13
Serum creatinine Males 0.5636 >0.95 70.00 43.08 0.13
Females 0.5878 >0.75 56.84 56.84 0.14
Serum Sodium Males 0.5359 <139.5 53.85 53.85 0.08
Females 0.5546 <139.5 67.71 50.0 0.19
Serum Potassium Males 0.5162 >4.25 56.92 47.69 0.05
Females 0.5300 >4.45 45.83 64.21 0.1
Figure
Figure Figure 1: ROC Curves of liver function indices in prediction of CAD in males
Figure
Figure Figure 2: ROC Curves of kidney function indices in prediction of CAD in males
Figure
Figure Figure 3: ROC Curves of liver function indices in prediction of CAD in females
Figure
Figure Figure 4: ROC Curves of kidney function indices in prediction of CAD in females

Discussion

A reversed interconnection of increased serum bilirubin concentration with the appearance and severity of coronary artery plaques have been intimidated. The protective effects of serum bilirubin with regard to the existence and intensity of plaques or stenosis have recently been established wherein serum bilirubin levels were inversely proportional to atherosclerosis in a dose-dependent format [30]. Atherosclerosis causes attenuation of vascular nitric oxide via oxidization of low-density lipoproteins (LDL) which further leads to the stiffening of the arterial wall thereby ultimately leading to platelet aggregation and thrombus formation. On the contrary, the anti-oxidative properties of bilirubin inhibits systemic inflammatory response therewith inhibiting the aggregation of platelets [31].

Evidence proves bilirubin to have an anti-inflammatory, anti-oxidative and anti-proliferative properties. A causal relationship between the presence of CAD and low serum bilirubin concentration is yet to be established. In our study, the total bilirubin concentration between the cases and controls were comparable whereas direct bilirubin concentration displays a significant fall among the male cases as compared to the controls. The anti-oxidative effect of bilirubin might be partly related to the inhibition of xanthine oxidase, which is a common phenomenon in hyperuricemia [32]. As hyperuricemia is closely associated with dyslipidemia and insulin resistance, the linkage between serum levels of bilirubin and the occurrence of coronary artery plaques might be underlined in these mechanisms.

As discussed, severe pathological conditions can lead to tissue damage which further accelerates the release of AST thereby denoting AAR as a potential biomarker. Elevated AAR has proven to be an independent predictive biomarker in patients with arrhythmogenic cardiomyopathy [33], which is at par with the outcome in our study. Our results are consistent with previously published study wherein the authors have conducted a multivariate regression analysis so as to conclude AAR as an independent predictive marker for adverse cardiovascular mortality and cardiac mortality [34]. The probable explanation for this mechanism is an elementary, underlying cardio-hepatic inter-linkage that correlates the reduced hepatic blood flow and decreased concentration of ALT with myocardial dysfunction thereby further correlating the AAR with coronary artery plaques.

Lower levels of serum albumin is typically in association with all cardiac-related myopathies and related deaths [35,36]. On other words, an increase in serum albumin level expedites into a marked reduction in coronary heart disease and cardiovascular mortality rate [37]. Our study displays a contradictory result as the serum albumin concentration decreases in the male cases compared to controls, whereas significantly rises among the female cases compared to the respective controls. Scientists recommends the correlation to be a reason for the enormous conventional risk factors associated with CAD [35]. Even though serum albumin has never been identified as a marker of the coronary arterial dysfunction, the substantial lack of possible pathogenesis of the effect of albumin on CAD prevalence makes it a potential research topic.

Serum creatinine is considered to be a traditional potential risk factor of CAD among Chinese population [2]. In our study, the serum creatinine levels are comparable among the male cases and controls. Although among females, the serum creatinine concentration significantly improved the risk of CAD prediction. Our study therefore concurs with previous studies [38-40], thereby validating the results. Contrarily, a glance at the serum urea concentration which normally rises in case of CAD has drastically reduced among the cases in our study group. The elevation of serum urea in cardiovascular events usually takes places as a result of decreased glomerular filtration rate (GFR), increased tubular reabsorption of urea as well as rise in the uptake of urea concentration for excretion. The reduction in serum urea in patients with CAD remains open for a debate.

Despite of the extensive nature of our study design and the effort to simultaneously correlate the liver and kidney function parameters with CAD, there are some major potent limitations in our study. First of all, our study patients are only those individuals who have undergone a coronary angiogram in a single-centric, tertiary care unit of South India. As such, these patients represents only a sub-set of the population affected by CVD thereby do not exactly reflects the actual scenario of patients with adverse cardiac events. Secondly, the sample size is not adequate enough. Even though it was appropriately generated, most of the liver and kidney function indices fails to detect the exact correlation with the incidences of CAD. Hence, it is recommended to conduct a similar study plan in a large-scale cohort. Third, a prospective randomized clinical trial would prove to be more effective. Fourth, it is paramount to apply a similar study design even in the younger generation to validate the generalization of the study. Fifth, owing to the observational nature of the study design, the correlation of the liver and kidney function indices along with the mortality rate of the patients were not possible.

Conclusion

To summarize, we conclude that patients with at least 50% stenosis in the epicardial artery displays very little changes in liver or kidney function indices. We fail to enumerate an inter-relationship between the liver or renal dysfunction with the incidence or severity of CAD and risk of mortality. Probably an all-inclusive, wide ranged prospective study would be able to find out the associated co-relationship.

Declarations

Acknowledgement

All the authors who are directly involved in the study would sincerely like to thank the participants of the study for successful data curation and completion of the work. We would also like to show our sincerest gratitude to all the staffs of the Department of Physiology and Department of Cardiology of Kasturba Medical College, Manipal, for their immeasurable help during data collection.

Conflict of Interest

The authors declare that there are no competing interests related to this study.

Financial support

There were no financial support received during the conduct of this study.

Authors’ Contributions

All authors contributed substantially to the conception and design of the study, literature review, data acquisition, data curation, statistical analysis, interpretation of findings and manuscript preparation. The authors were also involved in scientific advising, critical revision of the manuscript for important intellectual content, and overall supervision of the work. All authors have reviewed, approved and agreed to the final version of the manuscript and accept responsibility for the integrity and accuracy of the work.

Ethical Clearance

The study was conducted in compliance with the ethical guidelines established by the Institutional Ethics Committee and adhered to the principles outlined in the Declaration of Helsinki (1964), along with its later revisions and amendments. Prior to commencement, ethical approval was obtained from the Institutional Ethics Committee (Approval No. IEC 503/2017).

References

  1. Na KY, Kim CW, Song YR, Chin HJ, Chae DW. The association between kidney function, coronary artery disease, and clinical outcome in patients undergoing coronary angiography. J Korean Med Sci. 2009; 24 Suppl (Suppl 1): S87-94. DOI ↗ Google Scholar ↗
  2. Salim A, Tai ES, Tan VY, Welsh AH, Liew R, et al. C-reactive protein and serum creatinine, but not haemoglobin A1c, are independent predictors of coronary heart disease risk in non-diabetic Chinese. Eur J Prev Cardiol. 2016; 23(12): 1339-49. DOI ↗ Google Scholar ↗
  3. Muntner P, He J, Hamm L, Loria C, Whelton PK. Renal insufficiency and subsequent death resulting from cardiovascular disease in the United States. J Am Soc Nephrol. 2002; 13: 745-53. DOI ↗ Google Scholar ↗
  4. Go AS, Chertow GM, Fan D, McCulloch CE, Hsu CY. Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization. N Engl J Med. 2004; 351: 1296-305. DOI ↗ Google Scholar ↗
  5. Manjunath G, Tighiouart H, Ibrahim H, MacLeod B, Salem DN, et al. Level of kidney function as a risk factor for atherosclerotic cardiovascular outcomes in the community. J Am Coll Cardiol. 2003; 41: 47-55. DOI ↗ Google Scholar ↗
  6. Ansari A, Kaupke CJ, Vaziri ND, Miller R, Barbari A. Cardiac pathology in patients with end-stage renal disease maintained on hemodialysis. Int J Artif Organs. 1993; 16: 31-6. PMID: 8458668. Google Scholar ↗
  7. Rostand SG, Kirk KA, Rutsky EA. Dialysis-associated ischemic heart disease: insights from coronary angiography. Kidney Int. 1984; 25: 653-9. DOI ↗ Google Scholar ↗
  8. Nelson JJ, Liao D, Sharrett AR, Folsom AR, Chambless LE, et al. Serum albumin level as a predictor of incident coronary heart disease: the Atherosclerosis Risk in Communities (ARIC) study. Am J Epidemiol. 2000; 151(5): 468-77. DOI ↗ Google Scholar ↗
  9. Don BR, Kaysen G. Serum albumin: relationship to inflammation and nutrition. Semin Dial. 2004; 17(6): 432-7. DOI ↗ Google Scholar ↗
  10. Djoussé L, Rothman KJ, Cupples LA, Levy D, Ellison RC. Serum albumin and risk of myocardial infarction and all-cause mortality in the Framingham Offspring Study. Circulation. 200; 106(23): 2919-24. DOI ↗ Google Scholar ↗
  11. Gillum RF, Ingram DD, Makuc DM. Relation between serum albumin concentration and stroke incidence and death: the NHANES I Epidemiologic Follow-up Study. Am J Epidemiol. 1994; 140(10): 876-88. DOI ↗ Google Scholar ↗
  12. Suzuki S, Hashizume N, Kanzaki Y, Maruyama T, Kozuka A, et al. Prognostic significance of serum albumin in patients with stable coronary artery disease treated by percutaneous coronary intervention. PLoS One. 2019; 14(7): e0219044. DOI ↗ Google Scholar ↗
  13. Qin F, Sun C, Ma Y, Liu C, Bai F, et al. Is low serum albumin concentration associated with the adverse cardiovascular events in stable coronary heart disease? Int J Cardiol. 2018; 266: 260. DOI ↗ Google Scholar ↗
  14. Wang M, Liu J, Ma C, Wang W, Liu X, et al. Synergistic association of serum albumin and globulin with coronary heart disease. J Atheroscler Thromb. 2012; 19(7): 619-32. DOI ↗ Google Scholar ↗
  15. Wada H, Dohi T, Miyauchi K, Shitara J, Endo H, et al. Long-term clinical impact of serum albumin in coronary artery disease patients with preserved renal function. Nutr Metab Cardiovasc Dis. 2018; 28(3): 285-290. DOI ↗ Google Scholar ↗
  16. Shaper AG, Wannamethee SG, Whincup PH. Serum albumin and risk of stroke, coronary heart disease, and mortality: the role of cigarette smoking. J Clin Epidemiol. 2004; 57(2): 195-202. DOI ↗ Google Scholar ↗
  17. Gimbrone MA Jr, Topper JN, Nagel T, Anderson KR, Garcia-Cardeña G. Endothelial dysfunction, hemodynamic forces, and atherogenesis. Ann N Y Acad Sci. 2000; 902: 230-40. DOI ↗ Google Scholar ↗
  18. Troughton JA, Woodside JV, Young IS, Arveiler D, Amouyel P, et al. Bilirubin and coronary heart disease risk in the Prospective Epidemiological Study of Myocardial Infarction (PRIME). Eur J Cardiovasc Prev Rehabil. 2007; 14(1): 79-84. DOI ↗ Google Scholar ↗
  19. Geographical variation in the major risk factors of coronary heart disease in men and women aged 35-64 years. The WHO MONICA Project. World Health Stat Q. 1988; 41(3-4): 115-40. PMID: 3232405. Google Scholar ↗
  20. Scarabin PY, Arveiler D, Amouyel P, Dos Santos C, Evans A, et al. Prospective Epidemiological Study of Myocardial Infarction. Plasma fibrinogen explains much of the difference in risk of coronary heart disease between France and Northern Ireland. The PRIME study. Atherosclerosis. 2003; 166(1): 103-9. DOI ↗ Google Scholar ↗
  21. Neuzil J, Stocker R. Bilirubin attenuates radical-mediated damage to serum albumin. FEBS Lett 1993; 331: 281–284. DOI ↗ Google Scholar ↗
  22. Kunutsor SK. Serum total bilirubin levels and coronary heart disease--Causal association or epiphenomenon? Exp Gerontol. 2015; 72:63-6. DOI ↗ Google Scholar ↗
  23. Kunutsor SK, Bakker SJ, Gansevoort RT, Chowdhury R, Dullaart RP. Circulating total bilirubin and risk of incident cardiovascular disease in the general population. Arterioscler Thromb Vasc Biol. 2015; 35(3): 716-24. DOI ↗ Google Scholar ↗
  24. Li C, Wu W, Song Y, Xu S, Wu X. The Nonlinear Relationship Between Total Bilirubin and Coronary Heart Disease: A Dose-Response Meta-Analysis. Front Cardiovasc Med. 2022; 8: 761520. DOI ↗ Google Scholar ↗
  25. Newsome PN, Cramb R, Davison SM, Dillon JF, Foulerton M, et al. Guidelines on the management of abnormal liver blood tests. Gut. 2018; 67(1): 6-19. DOI ↗ Google Scholar ↗
  26. Rej R. Aspartate aminotransferase activity and isoenzyme proportions in human liver tissues. Clin Chem. 1978; 24(11): 1971-9. PMID: 213206. Google Scholar ↗
  27. Zheng RJ, Guo QQ, Tang JN, Yang XM, Zhang JC, et al. ALT-to-Lymphocyte Ratio as a Predictor of Long-Term Mortality in Patients with Normal Liver Function Presenting Coronary Artery Disease after Undergoing PCI: A Retrospective Cohort Study. J Interv Cardiol. 2020; 2020: 4713591. DOI ↗ Google Scholar ↗
  28. Bagheri B, Radmard N, Faghani-Makrani A, Rasouli M. Serum Creatinine and Occurrence and Severity of Coronary Artery Disease. Med Arch. 2019; 73(3): DOI ↗ Google Scholar ↗
  29. Kang SJ, Kim D, Park HE, Chung GE, Choi SH, et al. Elevated serum bilirubin levels are inversely associated with coronary artery atherosclerosis. Atherosclerosis. 2013; 230(2): 242-8. DOI ↗ Google Scholar ↗
  30. Jain V, Ghosh RK, Bandyopadhyay D, Kondapaneni M, Mondal S, et al. Serum Bilirubin and Coronary Artery Disease: Intricate Relationship, Pathophysiology, and Recent Evidence. Curr Probl Cardiol. 2021; 46(3): 100431. DOI ↗ Google Scholar ↗
  31. Kawada T. Serum bilirubin concentrations, type 2 diabetes and incident coronary heart disease. Acta Diabetol. 2019; 56(3): 381-382. DOI ↗ Google Scholar ↗
  32. Liu X, Liu P. Elevated AST/ALT ratio is associated with all-cause mortality in patients with stable coronary artery disease: a secondary analysis based on a retrospective cohort study. Sci Rep. 2022; 12(1): 9231. DOI ↗ Google Scholar ↗
  33. Bezan A, Mrsic E, Krieger D, Stojakovic T, Pummer K, et al. The Preoperative AST/ALT (De Ritis) Ratio Represents a Poor Prognostic Factor in a Cohort of Patients with Nonmetastatic Renal Cell Carcinoma. J Urol. 2015; 194(1): 30-5. DOI ↗ Google Scholar ↗
  34. Wu CC, Lu YC, Yu TH, Wang CP, Hung WC, et al. Serum albumin level and abnormal corrected QT interval in patients with coronary artery disease and chronic kidney disease. Intern Med J. 2018; 48(10): 1242-1251. DOI ↗ Google Scholar ↗
  35. Chien SC, Chen CY, Leu HB, Su CH, Yin WH, et al. Association of low serum albumin concentration and adverse cardiovascular events in stable coronary heart disease. Int J Cardiol. 2017; 241: 1-5. DOI ↗ Google Scholar ↗
  36. Gillum RF, Makuc DM. Serum albumin, coronary heart disease, and death. Am Heart J. 1992; 123(2): 507-13. DOI ↗ Google Scholar ↗
  37. Buckley DI, Fu R, Freeman M, Rogers K, Helfand M. C-reactive protein as a risk factor for coronary heart disease: a systematic review and meta-analyses for the U.S. Preventive Services Task Force. Ann Intern Med. 2009; 151(7): 483-95. DOI ↗ Google Scholar ↗
  38. Wannamethee SG, Shaper AG, Perry IJ. Serum creatinine concentration and risk of cardiovascular disease: a possible marker for increased risk of stroke. Stroke. 1997; 28(3): 557-63. DOI ↗ Google Scholar ↗
  39. Mazza A, Pessina AC, Tikhonoff V, Montemurro D, Casiglia E. Serum creatinine and coronary mortality in the elderly with normal renal function: the Cardiovascular Study in the Elderly (CASTEL). J Nephrol. 2005; 18(5): 606-12. PMID: 16299689. Google Scholar ↗