Chronic kidney disease (CKD) is a growing global health burden, affecting nearly 10% of the adult population and significantly increasing the risk of cardiovascular morbidity and mortality (1,2). Cardiovascular disease (CVD) remains the leading cause of death among patients with CKD, surpassing the progression to end-stage renal disease in many cases (3). The interplay between kidney dysfunction and cardiovascular complications is multifactorial, involving chronic inflammation, oxidative stress, vascular calcification, and left ventricular hypertrophy (4,5).

Traditional cardiovascular risk assessment tools often underestimate the true risk in CKD patients, necessitating more reliable biomarkers for early detection and risk stratification (6). Cardiac troponins, particularly troponin T (cTnT) and troponin I (cTnI), are well-established markers of myocardial injury and are routinely used in diagnosing acute coronary syndromes (7). However, in CKD patients, baseline troponin levels are frequently elevated even in the absence of acute ischemia, likely due to reduced renal clearance and ongoing subclinical myocardial injury (8,9).

The development of high-sensitivity cardiac troponin (hs-cTn) assays has enabled the detection of even minor degrees of myocardial injury, improving diagnostic accuracy and prognostic evaluation (10). Recent studies have shown that elevated hs-cTn levels in CKD patients are independently associated with an increased risk of adverse cardiovascular outcomes, including myocardial infarction, heart failure, and sudden cardiac death (11,12). Moreover, hs-cTn may reflect chronic structural and functional cardiac changes that precede overt cardiovascular events (13).

Despite its clinical potential, the use of hs-cTn in predicting long-term cardiovascular outcomes in CKD patients remains underexplored, and consensus on appropriate cut-off values for risk stratification is lacking. This study aims to investigate the role of hs-cTn as a prognostic biomarker for cardiovascular events in patients with moderate to advanced CKD and to assess its utility in guiding clinical decision-making.

The study included 150 adult patients aged 30 to 75 years with a confirmed diagnosis of chronic kidney disease (CKD) stages 3 to 5 based on the Kidney Disease Improving Global Outcomes (KDIGO) guidelines. CKD was defined as an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m² for more than three months. Patients with a recent history of acute myocardial infarction (within the past three months), those with active infections, malignancies, liver disease, or on dialysis were excluded to reduce potential confounding factors.

Baseline Evaluation

All participants underwent a detailed clinical evaluation including history, physical examination, and documentation of cardiovascular risk factors such as hypertension, diabetes mellitus, and smoking status. Laboratory investigations included complete blood count, serum creatinine, urea, electrolytes, lipid profile, high-sensitivity C-reactive protein (hs-CRP), and eGFR calculation using the CKD-EPI formula.

Measurement of hs-cTnT

Serum high-sensitivity cardiac troponin T (hs-cTnT) levels were measured at baseline using an electrochemiluminescence immunoassay. Patients were categorized into three groups based on tertiles of hs-cTnT values:

• Group A: <10 ng/L
• Group B: 10–25 ng/L
• Group C: >25 ng/L

Follow-up and Outcomes

Patients were followed for 12 months or until the occurrence of a cardiovascular event, whichever came first. The primary outcome was the occurrence of major adverse cardiovascular events (MACE), which included non-fatal myocardial infarction, stroke, hospitalization for heart failure, and cardiovascular death. Follow-up visits were scheduled every 3 months, and data on outcomes were collected through hospital records, direct interviews, and phone calls.

Statistical Analysis

Data were analyzed using SPSS software version 25.0. Continuous variables were expressed as mean ± standard deviation, and categorical variables as frequencies and percentages. Comparisons between groups were made using ANOVA for continuous variables and chi-square test for categorical data. Kaplan-Meier survival curves were plotted to assess time to MACE, and differences were evaluated using the log-rank test. Cox proportional hazards regression was performed to identify independent predictors of cardiovascular events. A p-value less than 0.05 was considered statistically significant.

A total of 150 patients with chronic kidney disease (CKD) stages 3 to 5 were enrolled in the study, with a mean age of 59.3 ± 10.7 years. The cohort included 88 males (58.7%) and 62 females (41.3%). Based on baseline high-sensitivity cardiac troponin T (hs-cTnT) levels, patients were classified into three tertile groups: Group A (<10 ng/L), Group B (10–25 ng/L), and Group C (>25 ng/L).

Baseline Characteristics

The demographic and clinical profiles across the three hs-cTnT groups are summarized in Table 1. Patients in Group C had a higher prevalence of diabetes mellitus and hypertension compared to Groups A and B. Mean eGFR was significantly lower in Group C (32.8 ± 7.6 mL/min/1.73 m²) compared to Group A (45.2 ± 8.3 mL/min/1.73 m²) (p < 0.001).

Table 1. Baseline Characteristics of Study Participants by hs-cTnT Group

Cardiovascular Events During Follow-up

Over a 12-month follow-up period, 42 patients (28%) experienced at least one major adverse cardiovascular event (MACE). The incidence of MACE was highest in Group C (23 out of 50; 46.0%) compared to Group B (12 out of 50; 24.0%) and Group A (7 out of 50; 14.0%) (p < 0.001), as shown in Table 2.

Table 2. Incidence of Cardiovascular Events by hs-cTnT Group

Kaplan-Meier and Cox Regression Analysis

Kaplan-Meier survival analysis revealed a significantly lower event-free survival in patients with hs-cTnT >25 ng/L compared to the other two groups (log-rank p < 0.001) (Figure 1, not shown here). Cox proportional hazards regression demonstrated that hs-cTnT >25 ng/L was independently associated with increased risk of MACE (HR = 3.4; 95% CI: 1.9–6.1; p < 0.001), even after adjusting for age, diabetes, and eGFR (Table 3).

Table 3. Multivariate Cox Regression for Predictors of Cardiovascular Events

These findings indicate that elevated hs-cTnT levels are significantly associated with increased cardiovascular risk among CKD patients (Tables 1–3).

This prospective study aimed to explore the prognostic utility of high-sensitivity cardiac troponin T (hs-cTnT) in predicting cardiovascular events among patients with chronic kidney disease (CKD) stages 3 to 5. Our findings demonstrate that elevated hs-cTnT levels are significantly associated with higher incidence of major adverse cardiovascular events (MACE), even after adjusting for conventional risk factors such as age, diabetes, and eGFR. These results support the growing body of evidence suggesting that hs-cTnT can serve as a powerful biomarker for cardiovascular risk stratification in patients with CKD.

Cardiovascular disease (CVD) is the predominant cause of mortality in individuals with CKD, with risks increasing as renal function declines (1,2). Traditional markers of myocardial injury, while useful in the general population, have limited reliability in CKD due to altered clearance and baseline elevation, complicating their interpretation (3). The advent of high-sensitivity troponin assays has allowed for the detection of even subtle myocardial damage, making hs-cTnT a promising candidate for early risk detection in high-risk groups such as CKD patients (4-7). This may reflect ongoing subclinical myocardial injury or structural cardiac changes such as left ventricular hypertrophy or fibrosis, which are common in uremic cardiomyopathy (8,9).

The biological basis for hs-cTnT elevation in CKD is multifactorial. Beyond reduced renal clearance, chronic inflammation, endothelial dysfunction, and pressure overload contribute to myocardial stress and microinjury (10,11). Moreover, Erdemoglu and Ozbakir found that even in stable CKD patients, elevated troponin levels could predict future cardiovascular decompensation (12). Importantly, our multivariate analysis revealed that hs-cTnT >25 ng/L conferred a 3.4-fold increased risk of cardiovascular events, highlighting its prognostic strength (13-15).

Despite these strengths, some limitations should be acknowledged. This study was single-centered with a modest sample size, limiting the generalizability of results. Also, the influence of dynamic changes in hs-cTnT over time was not assessed. Future multicentric studies with larger populations and serial hs-cTnT measurements may offer deeper insights into temporal trends and refine its clinical utility.

In conclusion, hs-cTnT is a robust, independent predictor of cardiovascular events in patients with moderate to advanced CKD. Its integration into clinical practice may improve early identification of high-risk individuals and facilitate timely cardiovascular interventions, potentially improving outcomes in this vulnerable population.

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