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Updated: Apr 5, 2026

A Large Animal Model for Acute Kidney Injury by Temporary Bilateral Renal Artery Occlusion
Published on: February 2, 2021
[Troponins and chronic kidney disease]
Insights
High-sensitivity cardiac troponin (hs-cTn) assays present challenges in diagnosing acute myocardial infarction (AMI) in chronic kidney disease (CKD) patients due to elevated baseline levels. This review examines hs-cTn utility for AMI diagnosis and prognosis in CKD.
Area of Science:
- Cardiology
- Nephrology
- Biomarker Research
Background:
- Coronary thrombosis has a long history, with acute myocardial infarction (AMI) distinguished from angina pectoris in 1912.
- Diagnostic tools evolved from ECG and basic labs to cardiac enzymes and finally troponins, with high-sensitivity assays emerging in 2010.
- Chronic kidney disease (CKD) patients face increased cardiovascular risk, complicating the interpretation of cardiac troponin levels.
Purpose of the Study:
- To review the diagnostic role of high-sensitivity cardiac troponin (hs-cTn) in patients with CKD for acute myocardial infarction (AMI).
- To evaluate the prognostic significance of elevated hs-cTn levels in CKD patients without AMI.
Main Methods:
- Literature review focusing on hs-cTn assays in CKD populations.
- Analysis of studies investigating hs-cTn for AMI diagnosis in CKD.
- Examination of research on hs-cTn as a prognostic marker in CKD patients without AMI.
Main Results:
- Elevated baseline hs-cTn levels are common in CKD patients, posing interpretation challenges for AMI diagnosis.
- hs-cTn assays require careful consideration in CKD for accurate AMI detection.
- Elevated hs-cTn levels in CKD patients without AMI may hold prognostic value for cardiovascular events.
Conclusions:
- The interpretation of hs-cTn in CKD requires specific strategies to differentiate AMI from other causes of troponin elevation.
- hs-cTn assays are valuable tools, but their application in CKD necessitates a nuanced approach for both diagnosis and prognosis.
Abstract:
Coronary thrombosis was recognized since 19th century as clinical entity with bad outcomes; only in 1912 it was reported that acute myocardial infarction had to been distinguished from angina pectoris. First diagnostic test was electrocardiogram, while white blood cells count and erythrocytes sedimentation rate were the only available laboratory tests. Late in the 60s and 70s glutammic oxaloacetic and glutamic pyravate transaminase, lactate dehydrogenase and creatine kinase were added to biomarkers pool to provide a diagnosis of myocardial infarction related to myocardial cells injury. Only in 1987 assays for cardiac troponin were developed to assess structural damage of myocardial cells and in 2010 high sensibility troponins first dosage kits became available. It is well known that the population with chronic kidney disease (CKD) is at greater risk for cardiovascular disease and death than the general population. The use and interpretation of high sensitivity cardiac troponin (hs-cTn) assays have been particularly challenging in these patients with the majority having elevated levels at baseline. Aim of this review is to evaluate hs-cTn in patients with CKD for the diagnosis of AMI and for the prognostic significance of elevated levels in CKD patients without AMI.
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