title: Serum cardiac troponin and subclinical cardiac status in pediatric chronic renal failure.
abstract: BACKGROUND
  Patients with uremia often have elevated serum cardiac troponin T (cTnT) even without clinical heart damage. Pediatric patients are ideal for studies of the relationship between uremia and heart disease because they are unlikely to have cardiac risk factors other than uremia.
  
  
  OBJECTIVE
  To determine the relationship between uremia and cTnT levels.
  
  
  METHODS
  Echocardiograms and blood chemistry results were obtained from 50 pediatric patients with chronic renal failure and without clinical heart disease. Levels of cTnT were tested for correlation with cardiac dysfunction. In multivariate analysis, biochemical aspects of renal disease and its treatment were tested for correlation with cardiac dysfunction.
  
  
  RESULTS
  Forty-nine patients had cardiovascular abnormalities, including increased left ventricular function and mass, elevated heart rate and blood pressure, and reduced LV afterload. LV contractility was inversely correlated with cTnT level (r = -0.36). Higher cTnT also correlated with higher serum creatine kinase-MB mass, lower serum parathyroid hormone, higher blood urea nitrogen and bicarbonate levels, and the use of diuretics, but not with higher cardiac troponin I. Left ventricular contractility was inversely related to serum creatinine, phosphorus, and the use of beta-blockers.
  
  
  CONCLUSIONS
  Elevated cTnT levels are not artifactual, but are genuine indicators of cardiomyocyte damage. Cardiac damage, indicated by either elevated cTnT or low LV contractility, is related to uremia, deranged calcium and phosphorus metabolism, and bicarbonate levels. Serum cTnT and LV contractility identify subclinical cardiac damage that could be treated to hopefully reduce cardiovascular morbidity and mortality in this high-risk population.
authors.affiliation: Department of Cardiology, Children's Hospital, Boston, Massachusetts, USA. steve_lipshultz@urmc.rochester.edu
authors.forename: Steven E
authors.initials: SE
authors.lastname: Lipshultz
authors.forename: Michael J G
authors.initials: MJ
authors.lastname: Somers
authors.forename: Stuart R
authors.initials: SR
authors.lastname: Lipsitz
authors.forename: Steven D
authors.initials: SD
authors.lastname: Colan
authors.forename: Kathy
authors.initials: K
authors.lastname: Jabs
authors.forename: Nader
authors.initials: N
authors.lastname: Rifai
mesh_terms: D000293:Adolescent; D000328:Adult; D015415:Biomarkers; D001806:Blood Urea Nitrogen; D002648:Child; D002675:Child, Preschool; D003402:Creatine Kinase / Q000097:blood; D052279:Creatine Kinase, MB Form; D004452:Echocardiography; D005260:Female; D006331:Heart Diseases / Q000097:blood* / Q000175:diagnosis / Q000000981:diagnostic imaging / Q000209:etiology; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000097:blood / Q000000981:diagnostic imaging / Q000209:etiology; D007223:Infant; D007527:Isoenzymes / Q000097:blood; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000150:complications / Q000628:therapy; D008297:Male; D009200:Myocardial Contraction; D010530:Peritoneal Dialysis; D020033:Protein Isoforms / Q000097:blood; D006435:Renal Dialysis; D014336:Troponin / Q000097:blood*; D014511:Uremia / Q000097:blood* / Q000150:complications / Q000628:therapy
chemical_list: D015415:Biomarkers; D007527:Isoenzymes; D020033:Protein Isoforms; D014336:Troponin; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form