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Cardiac troponin T and I in end-stage renal failure
1Institut für Klinische Chemie und Pathobiochemie, Klinikum rechts der Isar, Technische Universität München, Ismaningerstrasse 22, D-81675 Munich, Germany.
Insights
In end-stage renal failure patients, dialysis affects cardiac troponin T (cTnT) and I (cTnI) levels. Persistently elevated troponin levels may predict cardiac complications, so blood collection before dialysis is recommended.
Area of Science:
- Cardiology
- Nephrology
- Clinical Chemistry
Background:
- Cardiac troponin T (cTnT) and I (cTnI) can be elevated in end-stage renal failure (ESRD) patients without acute myocardial infarction.
- The specificity of these elevated troponin levels in ESRD patients remains unclear.
Purpose of the Study:
- To investigate the time course of cTnT and cTnI levels over one year in ESRD patients undergoing chronic hemodialysis.
- To correlate troponin levels with clinical outcomes over two years, comparing patients with and without a history of cardiac failure.
Main Methods:
- Studied 59 ESRD patients on chronic hemodialysis, dividing them into two groups based on cardiac failure history.
- Measured cTnT and cTnI levels over one year, alongside creatinine and blood urea nitrogen.
- Monitored clinical outcomes, including cardiac complications and mortality, over two years.
Main Results:
- Hemodialysis significantly altered cTnT and cTnI levels, increasing cTnT and decreasing cTnI.
- Elevated cTnT levels were more frequent in patients with a history of cardiac failure, though not statistically significant.
- Five patients (8.5%) died of cardiac complications within two years, all exhibiting elevated cTnT and/or cTnI levels.
Conclusions:
- Dialysis procedures significantly impact measured cTnT and cTnI concentrations.
- Elevated cTnT and cTnI levels in ESRD patients may predict future cardiac complications.
- Blood collection for troponin testing should occur before dialysis in ESRD patients to avoid procedural interference.
Background:
In patients suffering from end-stage renal failure, cardiac troponin T (cTnT) and I (cTnI) may be increased in serum without other signs of acute myocardial damage. Whether these increases are specific to myocardial injury or nonspecific is not completely clear.
Methods:
We investigated time courses of cTnT and cTnI over 1 year and the clinical outcome over 2 years in 59 patients with end-stage renal failure undergoing chronic hemodialysis. At the start of the study, we divided the patients into two groups, group 1, without history of cardiac failure, and group 2, with history of cardiac failure, and looked for differences between the groups in later adverse outcome. cTnT was measured using the Enzymun((R)) troponin T assay on an ES 700 analyzer (Roche). cTnI was measured on a Stratus((R)) II analyzer (Dade Behring). Creatinine and blood urea nitrogen were measured on a Vitros((R)) 950 IRC (Ortho).
Results:
Dialysis acutely increased cTnT (P: <0.01) and decreased cTnI (P: <0.001) regardless of the dialysis membrane used. Although statistically not significant, cTnT but not cTnI was increased more frequently in group 2 than in group 1, in some cases over the whole study period. Five patients (8.5%) died of cardiac complications within 2 years; all of them had mostly increased cTnT and, in one or more samples, increased cTnI.
Conclusions:
Dialysis alters measured cTnT and cTnI concentrations in serum. In patients suffering from end-stage renal failure, sporadic or persistently increased cTnT and cTnI appear to predict cardiac complications. Because of the effects of the dialysis procedure on troponin values, we recommend that blood be collected before dialysis.