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Using Extraordinary Optical Transmission to Quantify Cardiac Biomarkers in Human Serum
Published on: December 13, 2017
Cardiac troponin I concentration is commonly increased in nondialysis patients with CKD: experience with a sensitive
Edmund J Lamb1, Claire Kenny, Nasir A Abbas
1Clinical Biochemistry, East Kent Hospitals NHS Trust, Canterbury, Kent. edmund.lamb@ekht.nhs.uk
Background:
Cardiac troponin (cTn) concentrations commonly are increased in patients with chronic kidney disease (CKD) in the absence of an acute coronary syndrome. cTn T (cTnT) concentration reportedly is increased more commonly than cTn I (cTnI). Using a sensitive cTnI assay, we studied cTnI concentrations in predialysis patients with CKD who did not have an acute coronary event.
Study Design:
Observational cohort study.
Setting And Participants:
Nondialysis patients with CKD attending an outpatient clinic.
Predictor:
Plasma cTnI was measured using the cTnI-Ultra assay (Bayer HealthCare LLC, Diagnostics Division, Tarrytown, NY), the same manufacturer's standard cTnI assay, and a cTnT assay (Roche Diagnostics PLC, East Sussex, UK).
Outcomes And Measurements:
Prevalence of increased cTn concentration, effect of clinical variables on cTnI-Ultra concentration, and independent associations between cTn assays and all-cause mortality by using multiple regression modeling.
Results:
Plasma cTnI-Ultra concentration exceeded the upper limit of normal in 33% of patients compared with 18% with the cTnI-standard assay and 43% with the cTnT assay. Age, vascular disease, parathyroid hormone concentration, and left ventricular mass, but not kidney function, had independent effects on plasma cTnI-Ultra concentrations. There were 39 deaths during follow-up. Survival was decreased in patients with baseline cTnI-Ultra concentrations of 0.040 ng/mL or greater (54% versus 83%; P < 0.001), cTnI-standard concentrations of 0.07 ng/mL or greater (55% versus 78%; P = 0.02), and cTnT concentrations of 0.01 ng/mL or greater (59% versus 89%; P < 0.001). Only cTnT concentration was an independent predictor of death.
Limitation:
Only all-cause mortality was recorded.
Conclusion:
Using a sensitive assay, we found that the prevalence of increased cTnI concentrations in patients with CKD is similar to that observed for cTnT. cTnT concentration, but not cTnI, was independently associated with death.
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