Contribution of renal function impairment to unexplained troponin T elevations in congestive heart failure
Nur Aksoy1, Orhan Ozer, Ibrahim Sari
1Gaziantep University, School of Medicine, Department of Biochemistry, Gaziantep, Turkey. naksoy@gantep.edu.tr
Insights
Impaired renal function, not just cardiac disease, contributes to elevated troponin T (TnT) levels in severe congestive heart failure (CHF) patients. This finding highlights the importance of kidney function in managing CHF and interpreting TnT results.
Area of Science:
- Cardiology
- Nephrology
- Biochemistry
Background:
- Severe congestive heart failure (CHF) patients often exhibit unexplained elevations in serum troponin T (TnT).
- Cardiac TnT release due to underlying cardiac disease is the proposed cause.
- This study investigates impaired renal function as an additional contributing factor.
Purpose of the Study:
- To determine if impaired renal function contributes to elevated serum troponin T (TnT) levels in patients with severe congestive heart failure (CHF).
Main Methods:
- Sixty-two patients with nonischemic CHF (NYHA class III-IV) and normal serum creatinine were studied.
- Glomerular filtration rate (GFR) was calculated using the Cockcroft Gault equation.
- Serum TnT levels were measured and correlated with clinical parameters.
Main Results:
- Despite normal mean creatinine, mean GFR was low (56 mL/min).
- Elevated TnT levels were found in 53% of patients.
- Serum TnT levels were independently and negatively associated with GFR (p=0.005), more strongly than with cardiac function (LVEF).
Conclusions:
- Impaired renal function (GFR) is a significant factor in elevated serum TnT levels in severe CHF patients.
- Renal function's correlation with TnT was stronger than cardiac function (LVEF).
- Impaired renal function likely causes troponin accumulation, explaining unexplained TnT elevations in severe CHF.
Background:
Patients with severe congestive heart failure (CHF) often have unexplained elevations in serum concentrations of troponin T (TnT), and it is proposed that this is due to cardiac TnT release because of underlying cardiac disease. We investigated whether impaired renal function is an additional underlying phenomenon contributing to increased TnT levels in patients with CHF.
Methods:
Sixty-two patients with nonischemic CHF, New York Heart Association (NYHA) class III-IV, with normal coronary angiogram and normal serum creatinine were included in the study. Baseline glomerular filtration rate (GFR) was calculated using the Cockcroft Gault equation.
Results:
Although mean creatinine level was normal (0.92 +/- 0.17 mg/dL), mean GFR was low (56 +/- 16 mL/min) in the cohort. Elevated (>or=0.02 microg/L) TnT was measured in 33 patients (53%). Compared with patients with normal (<0.02 microg/L) TnT levels, patients with elevated TnT had significantly higher NYHA class (p = 0.02), longer duration of disease (p = 0.02), lower GFR (p = 0.0001), and lower LVEF (p = 0.0001). There were significant associations between TnT levels and duration of disease (r = 0.29, p = 0.01), creatinine (r = 0.30, p = 0.01), GFR (r = -0.55, p < 0.0001), and LVEF (r = -0.39, p = 0.001). Independence of these associations was evaluated in multiple linear regression analysis, and serum TnT was independently and negatively associated only with GFR (p = 0.005).
Conclusions:
Renal function (GFR) correlated significantly and more strongly than cardiac function (LVEF) with the serum TnT levels in patients with CHF. This supports our hypothesis that impaired renal function causes the accumulation of troponin and is very likely the cause of unexplained elevations of serum TnT in patients severe CHF.
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