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Letters |
1
Depts. of Pathol. and Lab. Med. and
2
Surgery Hartford Hosp. 80 Seymour St. PO Box 5037 Hartford, CT 06102-5037
a Author for correspondence.
To the Editor:
Cardiac troponins T (cTnT) and I (cTnI), structural proteins of the thin filament, are sensitive markers for myocardial injury (1). In unstable angina, abnormal cTnT and cTnI concentrations have been linked to a high short-term incidence (within 6 months) of adverse cardiac events [acute myocardial infarction (AMI) and death] (2). Studies of serum of patients with chronic renal failure have shown that cTnT [Cardiac T; Boehringer Mannheim (BMC), Indianapolis, IN] is abnormally increased more frequently than cTnI, suggesting that cTnT may be more nonspecific (3)(4). High troponin T concentrations in these patient groups could be caused by reexpression of troponin T in regenerating skeletal muscles (as observed by Bodor et al. in patients with Duchenne muscular dystrophy (5)), nonspecificity of the existing cTnT assay, or minor myocardial injury (6). Recently, BMC has released a second generation ELISA cTnT assay modified by moving the capture antibody to become the labeled antibody and using an entirely new capture antibody (7).
We evaluated both cTnT assays on the BMC ES300 analyzer (instrument supplied and supported by BMC) against a cTnI assay (cTnI; Behring Diagnostics, Westwood, MA) on the Opus Plus (supplied and supported by Behring) using serum of 26 patients collected before and after renal transplantation. The upper reference limit (URL) for both cTnT assays was 0.1 µg/L (8). The URL for cTnI was 0.5 µg/L, although a cutoff of 2.5 µg/L is recommended for diagnosing AMI (9). Previous comparisons of cTnT and cTnI in hemodialysis patients have been criticized because cTnT cutoff limits for AMI were set at the URL whereas recommended cutoffs for cTnI were above the URL (6). A retrospective clinical follow-up of these patients was conducted for the presence of AMI or cardiac death by the attending physician 6 weeks after the collection of the posttransplant sample.
Fig. 1
A and B show results of samples containing at least one abnormal
cTnT result. The original cTnT assay produced positive results in 14 of
26 (54%) pretransplant samples and 3 of 26 (12%) posttransplant
samples. Corresponding results for the modified assay were 4 of 26
(15%) and 1 of 26 (4%), respectively. In all but two cases,
posttransplant serum results were lower than pretransplant values. When
a cTnT cutoff of 0.2 µg/L is used (as recommended for the BMC Rapid
cTnT assay (10)), the number of positive results decreased
to 1 (4%) pretransplant and 1 (4%) posttransplant. cTnI was below the
AMI cutoff concentration for all pre- and posttransplant samples.
However, if the URL is used as the cutoff (0.5 µg/L), 2 (8%) and 1
(4%) of pre- and posttransplant samples, respectively, were positive
(Fig. 1C
). In case no. 2, posttransplant values were higher than
pretransplant for all three markers, suggesting that real myocardial
injury might exist. This patient did suffer from an aortic valve
insufficiency within 6 weeks of the transplant. However, none of the 26
transplant patients died or suffered a diagnosed AMI during the
followup period.
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Unlike the results observed in patients with unstable angina, abnormal results either before or after transplantation do not appear to reflect a poor prognosis in this limited study. The source of positive troponin results remains unknown. If release is due to occult cardiac injury, renal transplantation might have reduced the injury in these patients (e.g., case no. 1), although the underlying vascular disease prompting the need for transplantation (e.g., diabetic nephropathy) was still present. Decreasing concentrations after transplantation could also be due to improved clearance of released proteins. This study suggests that the first-generation cTnT assay produced falsely high results in renal failure, a problem that may have been corrected with the second-generation assay.
References
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