Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
October 16, 2026 · via Europe PMC
Long forms of cardiac troponin T are independent of kidney function and improve the diagnosis of myocardial infarction.
Hellman T, Teppo K, Linko-Parvinen A, +9 more, Wittfooth S.
AI summary — for doctors, generated from the abstract only
Long forms of cardiac troponin T were unaffected by kidney function and diagnosed myocardial infarction better than standard hs-cTnT, especially at lower eGFR.
What was studied
Prospective emergency department study of consecutive patients with hs-cTnT of 14 ng/L or higher, comparing a long cTnT assay with hs-cTnT across kidney function estimated by creatinine, cystatin C and combined equations.
Key findings
- 1811 patients were included; 205 (11.3%) had myocardial infarction and 204 (11.3%) had a history of CKD
- In patients without MI, long cTnT showed no consistent association with eGFR, whereas hs-cTnT was inversely associated with kidney function
- The conclusions state long cTnT outperforms hs-cTnT for MI detection, with the greatest advantage at lower eGFR, but the diagnostic accuracy numbers are cut off in the abstract
Clinical relevance
Could reduce false-positive troponin results in patients with kidney dysfunction presenting with suspected MI.
Who should care
Limitations
Abstract is truncated in the results, so discrimination statistics and P values are not available; single-population emergency cohort that was enrolled only with elevated hs-cTnT.
Long cTnT looks like a more kidney-independent MI marker, pending confirmation of the exact accuracy gains.
This is an AI-generated summary of the published abstract, not a clinical recommendation. It may not reflect the full text or subsequent updates — verify against the original source before acting on it.
Abstract
Background and hypothesis
A recently developed cardiac troponin T (cTnT) assay measuring intact or mildly fragmented cTnT (long cTnT) has shown promise in improving the accuracy of myocardial infarction (MI) detection compared to the commercial high sensitivity cTnT (hs-cTnT) assay. However, data on patients with kidney dysfunction are limited. We compared the performance of long and hs-cTnT in MI diagnostics across the full spectrum of kidney function.
Methods
In this prospective study, consecutive patients presenting at the emergency department with an elevated (≥14 ng/L) hs-cTnT were recruited. Long and hs-cTnT were measured on admission and kidney function was determined with plasma creatinine (Crea), cystatin C (CysC) and estimated glomerular filtration rate (eGFR) using contemporary equations with Crea, CysC or both (Crea-CysC) together. The association of eGFR with hs-cTnT and long cTnT concentrations and the discriminative ability of hs-cTnT and long cTnT for type 1 MI and any MI were evaluated.
Results
In total, 1811 patients were included, 205 (11.3%) had a MI and 204 (11.3%) had a history of chronic kidney disease. The overall median (interquartile range) Crea-eGFR, CysC-eGFR and Crea-CysC-eGFR were 71 (51-87), 52 (36-69) and 63 (44-79) ml/min/1.73m2. In patients without MI, long cTnT showed no consistent association with kidney function (β=0.0008, P = 0.050; β=0.0005, P = 0.222; β=0.0006, P = 0.182 for Crea-eGFR, CysC-eGFR and Crea-CysC-eGFR, respectively), whereas hs-cTnT was inversely associated with kidney function (β=-0.0032, -0.0035 and - 0.0035; all P < 0.001). Long cTnT demonstrated superior diagnostic performance compared with hs-cTnT for the detection of MI (P < 0.001), with the advantage becoming progressively more pronounced with lower eGFR irrespective of equation used.
Conclusions
In contrast to hs-cTnT, long cTnT is unaffected by kidney function and outperforms hs-cTnT in the detection of MI, with the greatest diagnostic advantage observed in patients with lower eGFR.
DOI
10.1093/ndt/gfag239
PMID
42886060
Research metadata (titles, abstracts, authors, publication dates) is sourced from Europe PMC, which aggregates content from PubMed/MEDLINE, PubMed Central, and other providers under the U.S. National Library of Medicine (NLM/NCBI). NLM does not claim copyright on abstracts; the original journal publishers or authors may hold rights to the full articles. AI-generated summaries are derived only from the abstract, never the full text, and are always labeled as AI-generated.
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