In the present cohort study based on community population, we aimed to further investigate the association between eGFR and hs-cTnT. We found that baseline eGFR were independently and negatively associated with follow-up hs-cTnT. Furthermore, baseline eGFR was an independent and positively predictor of the change in hs-cTnT (hs-cTnTδ) after 4.8 years of follow-up. However, we couldn’t prove the association between eGFRδ and hs-cTnTδ. Together with the results from our present study, we confirmed that renal function was related to myocardial injury, and decreased renal function could lead to increased myocardial injury in community-based population without overt CVD.
Troponins are thin myofilament proteins including three isoforms: cardiac troponin I, C and T (cTnI, cTnC and cTnT). They are coded by separate genes differed in structure, and cTnT is cardio-specific. They form a complex to regulate the contraction of striated muscles, and release quickly from cytoplasm when cardiomyocytes get injured [17–19]. The measurement of circulating cTnT assists in diagnosing myocardial injury including acute coronary syndromes and acute myocardial infarction, facilitating risk stratification, and evaluating treatment strategies [20–22]. However, with the development of highly sensitive assays, the detection limit of hs-cTnT is much lower than before, and the prevalence of detectable hs-cTnT is greatly improved in general population without overt CVD [23–24]. In our current study, among 1354 participants aged 61.28 ± 11.27 years old, 740 (54.65%) of them had detectable hs-cTnT concentrations above 3 pg/mL. The prevalence of hs-cTnT concentrations above 13.3 pg/mL was approximately 12.0%, which is similar to the prevalence in another study conducted in the majority of community-dwelling older adults .
As is well known, CVD accounts for nearly half of the deaths in patients with ESRD, and patients with renal insufficiency also have a high risk for CVD and progress early to CVD before reaching dialysis . The mutual effect between renal function and CVD is evident. As a specific and sensitive biomarker of myocardial injury, hs-cTnT elevation was found in patients with renal insufficiency, and associated with increased risk for mortality, even in the absence of clinically suspected ischemic heart disease [26–28]. Thus, in the current study we sought to further explore the relationship between renal function and myocardial injury, and the predictive value of eGFR on hs-cTnT in a community-based population after 4.8 years of follow-up. Pearson’s correlation analysis revealed that baseline eGFR showed a negative association with follow-up hs-cTnT (r=-0.439; P < 0.001), and this association remained independently and negatively in multiple linear regression analysis (β=-0.310, P = 0.005). Additionally, after stepwise adjusting for conventional cardiovascular prognostic indicators, such as plasma lipid levels, hypertension, BMI, and FBG, baseline eGFR was independently and positively associated with hs-cTnTδ (quartile 1: OR, 4.447; 95% CI, 2.279–8.678; P < 0.001, quartile 2: OR, 1.818; 95% CI, 1.124–2.941; P = 0.015, and quartile 3: OR, 1.831; 95% CI, 1.068–3.138; P = 0.028). These results implied that impaired renal function could lead to increased myocardial injury, and the worse the renal function at baseline, the more serious the myocardial injury as time progressed.
The pathophysiologic mechanisms responsible for the release of hs-cTnT in patients with renal insufficiency still need further exploration. Several reasons that may help explain this correlation are provided below. Firstly, except for some major clinical presentations of CVD like acute coronary syndromes , patients with renal insufficiency also suffer from repeated episodes of clinically silent myocardial necrosis, which could result in elevated hs-cTnT [29–30]. Secondly, some studies proposed a theory that cTnT could resolve into small immunoreactive fragments and be cleared by kidney. This may partly illustrate the high prevalence of elevated hs-cTnT in patients with reduced renal excretion [31–32]. Thirdly, uremic-induced myocardial ischemia or injury is another factor that should be taken into consideration .