Elevated troponin I levels but not low grade chronic inflammation is associated with cardiac-specific mortality in stable hemodialysis patients
Bibliographic record
Abstract
BACKGROUND: Elevated cardiac troponin I (TnI) levels are associated with all-cause mortality in stable hemodialysis patients. Their relationship to cardiac-specific death has been inconsistent, and the reason for their elevation is not well understood. We hypothesized that elevated TnI levels in chronic stable hemodialysis patients more specifically track with cardiac mortality, and this mechanism is independent of other contributors of cardiac mortality, such as inflammation. METHODS: We conducted a single-centre, cohort study of prevalent hemodialysis patients at a tertiary care hospital. Plasma TnI levels were measured with routine monthly blood tests in clinically stable patients for two consecutive months. Plasma TnI was measured by immunoassay and a value above the laboratory reference range (0.06 μg/L) was considered elevated. The primary outcome of death was adjudicated separately for this study, and classified as cardiac, non-cardiac, or unknown. Cox proportional hazard models were used to examine the association of TnI with the all-cause and cardiac-specific mortality, adjusting for potential confounders, including C-reactive protein (CRP) as a marker of inflammation. RESULTS: Of 133 patients followed for a median of 1.7 years, there were 38 deaths (58% non-cardiac, 39% cardiac, 3% unknown). Elevated TnI was associated with adjusted HR for all-cause mortality of 2.57 (95% CI 1.30-5.09) and an adjusted HR for cardiac death of 3.14 (95% CI 1.07-9.2), after accounting for age, time on dialysis, diabetes status, prior coronary artery disease history, and C-reactive protein. Although CRP was also independently associated with all-cause mortality, it did not add prognostic information to TnI for cardiac-specific death. CONCLUSION: Elevated TnI levels are independently associated with cardiac and all-cause mortality in asymptomatic hemodialysis patients. The mechanism for this risk is likely independent of inflammation, but may reflect chronic subclinical myocardial injury or unmask those with subclinical atherosclerotic heart disease. Whether those with elevated TnI levels may benefit from additional investigations or more aggressive therapies to treat cardiovascular disease remains to be determined.
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How this classification was reachedexpand
Full frame distilled prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.
Codex and Gemma teacher scores by category
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.001 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.000 |
| Bibliometrics | 0.000 | 0.001 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.001 |
| Insufficient payload (model declined to judge) | 0.001 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one teacher head, not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".