The risk of coronary artery disease (CAD) in patients with chronic kidney disease (CKD) is comparable with the risk of CAD in patients with traditional risk factors. The association of the classic cardiovascular risk factor and the specific uraemia-related risk factors accelerates the atherosclerosis process, explaining the increased incidence of the major adverse cardiac events (which is the main cause of death in CKD subjects) ^[1].

 Non-traditional risk factors (inflammation, proteinuria, anaemia, alterations in calcium and phosphate metabolism, oxidative stress) show an increased incidence as the kidney function declines. ^[2] Dyslipidaemia has an important role in the initiation of the atherosclerotic phenomenon, however, some important trials such as AURORA (a study to evaluate the use of rosuvastatin in subjects on regular haemodialysis: An Assessment of Survival and Cardiovascular Events) ^[3] and the 4D study (the German Diabetes and Dialysis Study–in German: Die Deutsche Diabetes Dialyse Studie) ^[4] revealed that statins did not improve the outcome of the patients with CKD, highlighting the fact that the disturbance of the lipid fractions is not elementary in the progression of the atheromatous plaque in subjects with impaired renal function ^[5]. Statins should represent an option in the early phases of the renal function deterioration, when the effect of the drugs is optimal. ^[6].

Acute coronary syndromes (ACS) encompass non-ST-segment elevation myocardial infarction (NSTEMI), unstable angina, ST-segment elevation myocardial infarction (STEMI), and myocardial infarction with nonobstructive coronary arteries (MINOCA^{) [5].} In CKD patients, the presentation is atypical, and the main symptom is dyspnoea instead of the thoracic pain, and asymptomatic forms are usually detected in these patients . The impaired renal function interferes with the excretion of the cardiac necrosis biomarkers—the cardiac troponins (cTn), making the diagnosis of the ACS challenging. Myocardial infarction is defined as elevation of the cardiac necrosis biomarkers above the 99th percentile myocardial infarction of the healthy reference population, corroborated with specific chest pain and electrocardiographic signs of cardiac ischemia ^[6]. Guidelines elaborated by the European Society of Cardiology (ESC) recommend serial measurements of the necrosis enzymes, proposing an algorithm that requires initial determination of the cTn followed by new assessments at 1 or 3 h ^[8]

An important aspect, the renal nihilism, illustrates a predisposition for choosing medical management in subjects with impaired kidney function instead of the interventional or surgical myocardial revascularization^.[7] The outcome of the ACS in CKD subjects is negatively influenced by the mentioned therapeutic attitude and the underuse of appropriate doses of antiplatelet therapy or thrombolytic therapy explaining the increased rate of these patients’ cardiovascular mortality . The treatment of ACS in patients with CKD has many issues. Thus far, there is no optimal treatment strategy for this type of patients. There are questions and concerns on the treatment for CKD patients in the incipient phases of STEMI and about using the aggressive reperfusion strategy (which implies both fibrinolytic therapy and primary coronary revascularization procedure).^[8]

In patients with STEMI, the trials have shown the effect of thrombolytic agents in reducing mortality, but in many of them, analysis was not performed for patients with CKD ^[9,10]. The risk of bleeding, especially the increased incidence of intracranial haemorrhage, constitutes a reason for the less frequent use of thrombolysis in patients with CKD. However, primary percutaneous coronary intervention (PCI) may represent a favourable alternative therapy. A study conducted by Hobbach et al. revealed that the presence of CKD in a light to moderate form at the onset of STEMI determines a higher mortality rate in spite of using adequate therapy, but it also indicates the benefits of timely PCI for these patients ^[11]. Though the positive effect of pharmacological and mechanical coronary reperfusion in STEMI was proven, the optimum treatment scheme for STEMI patients also having CKD is still in discussion. Opinions about timely invasive scheme being indicated for patients with light CKD rather than behind time actions tended to fade away as the renal function deteriorated ^[12-15].

A  comprehensive  prospective  observational  study  was carried  out,  involving  a  total  of  140  patients  who  were admitted  Department of General Medicine, JIIU’s Indian Institute of Medical Science and Research with  a  confirmed  diagnosis  of  acute  coronary syndrome (ACS).

The study was conducted at Department of General Medicine, JIIU’s Indian Institute of Medical Science and Research over a period of 6 months. The  study  aimed  to  gather  detailed  data  on  the  clinical presentations,    management    strategiesandoutcomes associated with ACS in these patients, providing valuable insights  into  the  regional  variations  and  challenges  in treating this condition.

Inclusion criteria: Patients were included if they demonstrated new evidence of  myocardial  ischemia  on  electrocardiography  (ECG), which  could  be  accompanied  by  angina  or dyspnoea. Inclusion    also    required    the    presence    of    elevated myocardial  necrosis  enzymes,  such  as  high-sensitivity troponins  (hs-cTn),  regardless  of  whether  there  was  an elevation. Additionally, patients with normal or decreased glomerular filtration  rate (GFR)  wereconsidered  eligible for the study.

Exclusion criteria: Patients were excluded if they had previous ECG changes indicative  of  myocardial  ischemia  without  new  signs  of acute  coronary  disease.  Other  exclusion  factors  included myocardial  injury  with  nonspecific  elevation  of  cardiac necrosis enzymes due to conditions like sepsis, advanced heart  failure,  chronic  kidney  diseaseora  history  of cerebrovascular accidents.Data collection procedure We  used  demographic  information,  clinical  historiesandpresenting    symptoms    were    documented^.[28]    Diagnostic evaluations,   including   laboratory   tests   and   imaging studies, were performed to confirm ACS and assess CKD severity.

 Therapeutic interventions, in-hospital managementandany complications were meticulously recorded throughout the patients' hospital stays. Data were captured  using  a  standardized  collection  form,  ensuring consistency and accuracy.This comprehensive dataset was then analyzed to explore the  clinical  and  therapeutic  characteristics  of  ACS  in patients with CKD, providing valuable insights into patient outcomes.  ACS was defined as a patient presenting with positive cardiac troponin and one of the following: Chest discomfort    with    or    without    persistent    ST-segment elevation (ECG alters that). This may include transient ST-segment    elevation,    whether    sustained    or    transient Symptoms  may  include  ST-segment  depression,  T-wave inversion,  flat  or  pseudo-normalized  T  wavesornormal ECG. Imaging may also be required. Evidence of genuine myocardial loss or new regional wall motion.

Statical analysis: Data  were  collected  using  a  pre-designed  pro  forma  and managed  in  Microsoft  Excel  and  SPSS-26.  Quantitative data  were  presented  as  mean  ±  standard  deviation,  while qualitative  data  were  summarized  as  frequencies  and percentages.  Categorical variables were analyzed using Chi-square tests and continuous variables were assessed with unpaired t-tests.EthicalconsiderationEthical guidelines for this study were strictly followed to safeguard   the   rights   and   welfare   of   all   participants^.[29] Conducted  across  multiple  medical  centers  in  Cumilla, Bangladesh, the study ensured that informed consent was acquired from each patient.

In table 1, Demographics Mean age 65.4 ± 10.8 years, 60% male. CKD stages: Stage 3 (40%), Stage 4 (35%), Stage 5 (25%).

Table 1: Patient Demographics and CKD Stages

Table 2: Risk Factors

In table 2, risk Factor of Hypertension was 80% (n = 112) followed by Dyslipidemia 68% (n = 95), Diabetes Mellitus 62% (n = 87) and Smoking History 28% (n = 39).

Table 3: Management Strategy

In table 3, Management PCI (48%), CABG (12%), antiplatelets (90%), statins (85%).

Table 4: Clinical Outcomes

In table 4, Outcomes In-hospital mortality (8%), MACE at 30 days (15%), renal function decline (18%).

Table 5: Laboratory and Biomarker Findings

In table 5, Laboratory Findings Mean eGFR 32.4 ± 8.7 mL/min/1.73m²; hyperkalemia in 20%, LDL-C 120 ± 28 mg/dL.

Table 6: Adverse Outcomes by CKD Stage

Adverse Events Heart failure (22%), dialysis initiation (10%), major bleeding (12%).

The findings from this study highlight the complex interplay between chronic kidney disease (CKD) and acute coronary syndrome (ACS), emphasizing the increased cardiovascular risk and the challenges in managing this high-risk patient population.

The high prevalence of traditional cardiovascular risk factors such as hypertension (80%), diabetes mellitus (62%), and dyslipidemia (68%) among CKD patients underscores the systemic nature of cardiovascular disease in this population^.[16] CKD is also independently associated with inflammation, oxidative stress, and vascular calcification, all of which exacerbate cardiovascular risk. These findings align with prior research that identifies CKD as a major non-traditional risk factor for cardiovascular morbidity and mortality.

The distribution of ACS types (STEMI: 38%, NSTEMI: 47%, Unstable Angina: 15%) indicates that CKD patients are more likely to present with NSTEMI or unstable angina, consistent with literature suggesting atypical presentations and delayed diagnosis in this population^.[17] Despite the clear benefits of evidence-based therapies such as PCI, CABG, and dual antiplatelet therapy (DAPT), their use was notably lower in advanced CKD stages (PCI in Stage 3: 57% vs. Stage 5: 37%).^[18] This reflects the clinical dilemma faced by physicians, who must balance the benefits of revascularization against the risks of procedural complications, bleeding, and contrast-induced nephropathy^.[18]

In-hospital mortality (8%) and 30-day MACE rates (15%) were relatively high, highlighting the poor short-term prognosis of CKD patients with ACS. Moreover, the progression to end-stage renal disease (ESRD) in 15% of patients and dialysis initiation in 10% suggest that ACS exacerbates renal dysfunction, likely due to hemodynamic instability^,[19] nephrotoxic medications, and procedural risks^.[20] Major bleeding events (12%), predominantly associated with antiplatelet therapy and invasive procedures, further complicate management, especially in advanced CKD.

Subgroup analysis revealed important trends by CKD stage. Patients in Stage 5 had the lowest rates of PCI (37%) and DAPT utilization (80%), suggesting an underuse of guideline-recommended therapies in this subgroup^.[21] While concerns about safety are justified, recent studies suggest that selected patients with advanced CKD may still benefit from revascularization. This highlights the need for individualized risk-benefit assessments and multidisciplinary decision-making.

At 6 months, mortality (18%), ACS readmission (12%), and ESRD progression (15%) were concerning, suggesting poor long-term outcomes^.[22] These findings reflect the need for intensified follow-up and optimized medical therapy to mitigate recurrent events^[23]. Strategies such as aggressive risk factor control (blood pressure, lipid management) and careful monitoring of renal function are critical in improving outcomes.

This study underscores the importance of tailoring ACS management to the unique needs of CKD patients. Early recognition of ACS, judicious use of diagnostic and therapeutic interventions,^{[24, 25]} and multidisciplinary care involving cardiologists, nephrologists, and critical care specialists are essential. Novel strategies, such as low-dose antiplatelet regimens, use of non-contrast imaging, and patient-specific revascularization protocols, should be explored further.

CKD - of any degree - is present in a substantial proportion of patients with ACS, and represents a potent and independent risk factor for adverse outcome. Unfortunately, data are still limited regarding the value of most therapeutic interventions, because CKD patients with ACS have typically been excluded from randomized trials. Thus, our current challenge is to further study these high-risk patients in prospective randomized trials in order to identify adjunctive pharmacological therapies and newer interventional strategies that may favorably affect their otherwise poor prognosis. Nevertheless, as long as evidence-based data are not provided to guide clinical practice, all attempts must be made to promote the use of more aggressive therapies, when they can be applied with an acceptable level of safety.

CKD significantly complicates the management and prognosis of ACS. Despite advances in cardiovascular care, CKD patients remain at a disproportionately high risk for adverse events. There is a critical need for tailored interventions, robust risk stratification tools, and multidisciplinary collaboration to improve outcomes in this vulnerable population.

1. Chronic Kidney Disease Prognosis Consortium, Matsushita K, van der Velde M, et al. Association of estimated glomerular filtration rate and albuminuria with all-cause and cardiovascular mortality in general population cohorts: a collaborative meta-analysis. Lancet 2010;375:2073–81.
2. 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.
3. Manjunath G, Tighiouart H, Ibrahim H, 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.
4. Sosnov J, Lessard D, Goldberg RJ, Yarzebski J, Gore JM. Differential symptoms of acute myocardial infarction in patients with kidney disease: a community-wide perspective. Am J Kidney Dis 2006;47:378–84.
5. Herzog CA, Littrell K, Arko C, Frederick PD, Blaney M. Clinical characteristics of dialysis patients with acute myocardial infarction in the United States: a collaborative project of the United States Renal Data System and the National
6. Burton JO, Jefferies HJ, Selby NM, McIntyre CW. Hemodialysis-induced repetitive myocardial injury results in global and segmental reduction in systolic cardiac function. Clin J Am Soc Nephrol 2009;4:1925–31.
7. Stefansson BV, Brunelli SM, Cabrera C, et al. Intradialytic hypotension and risk of cardiovascular disease. Clin J Am Soc Nephrol 2014;9: 2124–32.
8. Go AS, Bansal N, Chandra M, et al., for the ADVANCE Study Investigators. Chronic kidney disease and risk for presenting with acute myocardial infarction versus stable exertional angina in adults with coronary heart disease. J Am Coll Cardiol 2011;58:1600–7.
9. Shroff GR, Li S, Herzog CA. Trends in discharge claims for acute myocardial infarction among patients on dialysis. J Am Soc Nephrol 2017;28: 1379–83.
10. Wanner C, Amann K, Shoji T. The heart and vascular system in dialysis. Lancet 2016;388: 276–84.
11. Goff DC Jr., Lloyd-Jones DM, Bennett G, et al. 2013 ACC/AHA guideline on the assessment of cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014;63:2935–59.
12. Weiner DE, Tighiouart H, Elsayed EF, et al. The Framingham predictive instrument in chronic kidney disease. J Am Coll Cardiol 2007;50:217–24.
13. Matsushita K, Coresh J, Sang Y, et al., for the CKD Prognosis Consortium. Estimated glomerular filtration rate and albuminuria for prediction of cardiovascular outcomes: a collaborative metaanalysis of individual participant data. Lancet Diabetes Endocrinol 2015;3:514–25.
14. Stone NJ, Robinson JG, Lichtenstein AH, et al. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014;63:2889–934.
15. Bundy JD, Chen J, Yang W, et al., for the CRIC Study Investigators. Risk factors for progression of coronary artery calcification in patients with chronic kidney disease: the CRIC study. Atherosclerosis 2018;271:53–60.
16. Kistorp C, Raymond I, Pedersen F, Gustafsson F, Faber J, Hildebrandt P. N-terminal pro-brain natriuretic peptide, C-reactive protein, and urinary albumin levels as predictors of mortality and cardiovascular events in older adults. JAMA 2005;293:1609–16.
17. Anker SD, Gillespie IA, Eckardt KU, et al., for the ARO Steering Committee. Development and validation of cardiovascular risk scores for haemodialysis patients. Int J Cardiol 2016;216:68–77.
18. Kasiske BL, Chakkera HA, Roel J. Explained and unexplained ischemic heart disease risk after renal transplantation. J Am Soc Nephrol 2000;11: 1735–43.
19. Young LH, Wackers FJ, Chyun DA, et al., for the DIAD Investigators. Cardiac outcomes after screening for asymptomatic coronary artery disease in patients with type 2 diabetes: the DIAD study: a randomized controlled trial. JAMA 2009; 301:1547–55.
20. London GM, Guerin AP, Marchais SJ, Metivier F, Pannier B, Adda H. Arterial media calcification in end-stage renal disease: impact on all-cause and cardiovascular mortality. Nephrol Dial Transplant 2003;18:1731–40.
21. Schwarz U, Buzello M, Ritz E, et al. Morphology of coronary atherosclerotic lesions in patients with end-stage renal failure. Nephrol Dial Transplant 2000;15:218–23.
22. Nakamura S, Ishibashi-Ueda H, Niizuma S, Yoshihara F, Horio T, Kawano Y. Coronary calcification in patients with chronic kidney disease and coronary artery disease. Clin J Am Soc Nephrol 2009;4:1892–900.
23. Nakano T, Ninomiya T, Sumiyoshi S, et al. Association of kidney function with coronary atherosclerosis and calcification in autopsy samples from Japanese elders: the Hisayama study. Am J Kidney Dis 2010;55:21–30.
24. Wachter DL, Neureiter D, Campean V, et al. Insitu analysis of mast cells and dendritic cells in coronary atherosclerosis in chronic kidney disease (CKD). Histol Histopathol 2018;33:871–86.
25. Campean V, Neureiter D, Varga I, et al. Atherosclerosis and vascular calcification in chronic renal failure. Kidney Blood Press Res 2005;28:280–9