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(Circulation. 2004;109:23-25.)
© 2004 American Heart Association, Inc.
Brief Rapid Communications |
From the Departments of Clinical Chemistry (J.H.C.D., C.M.H., M.P.v.D.-V.), Nephrology (J.P.K.), and Cardiology (Y.M.P.), University Hospital Maastricht, and the Cardiovascular Research Institute Maastricht (W.T.H), The Netherlands.
Correspondence to J.H.C. Diris, Department of Clinical Chemistry, University Hospital Maastricht, PO Box 5800, 6202 AZ Maastricht, The Netherlands. E-mail Diris{at}klinchem.azm.nl
Received May 20, 2003; de novo received October 1, 2003; revision received November 11, 2003; accepted November 14, 2003.
Background Patients with severe renal dysfunction often have unexplained elevated serum concentrations of cardiac troponin T (cTnT). We investigated whether in vivo fragmentation of cTnT could explain these increases.
Methods and Results cTnT, creatine kinase isoenzyme MB, and myoglobin serum concentrations were measured in all 63 dialysis patients of our in-hospital dialysis department. A highly sensitive immunoprecipitation assay, followed by electrophoresis and Western blotting, was used to extract and concentrate cTnT and its possible fragments from serum of these 63 hemodialysis patients. Although creatine kinase isoenzyme MB values excluded recent ischemic myocardial events in 55 of the 63 cases, cTnT fragments ranging in size from 8 to 25 kDa were present in the serum samples of all dialysis patients.
Conclusions cTnT is fragmented into molecules small enough to be cleared by the kidneys of healthy subjects. Impaired renal function causes accumulation of these cTnT fragments and is very likely the cause of the unexplained elevations of serum cTnT found in patients with severe renal failure.
Key Words: kidney troponin T plasma
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