Wayand D, Baum H, Schätzle G, Schärf J, Neumeier D
Institut für Klinische Chemie und Pathobiochemie, Klinikum rechts der Isar, Technische Universität München, Ismaningerstrasse 22, D-81675 Munich, Germany.
Clin Chem. 2000 Sep;46(9):1345-50.
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.
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).
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.
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.
