We would like to thank Drs. Giannitsis and Katus for their comment on our report. However, we strongly believe that their harsh critique is unsustainable. By performing the present study we intended to answer a question that is relevant to many clinicians, especially those in the emergency setting, namely how to handle elevations of high-sensitive troponin in patients with renal insufficiency. To make our point clear we want to underline several points:

• 1.
  

  High-sensitive troponin was developed to save time in diagnosing or ruling out acute myocardial infarction and was promoted using this argument by the industry. The current European Society of Cardiology Guidelines for the Management of Acute Coronary Syndromes in patients presenting without persistent ST-segment elevation make the following statement : “Recently, high-sensitivity or ultrasensitive assays have been introduced that have a 10- to 100-fold lower limit of detection and fulfill the requirements of analytical precision. Therefore, MI can now be detected more frequently and earlier in patients presenting with chest pain. The superiority of these new assays, particularly in the early phase of pain onset, was prospectively demonstrated. The negative predictive value for MI with a single test on admission is .95% and thereby at least as high as with previous assays achieved only by serial measurements. Only very early presenters may escape detection. By including a second sample within 3 h of presentation the sensitivity for MI approaches 100%.”

  
  
• 2.
  

  However, the guidelines also make the following statement later : “‘False-positive’ results have been documented in the setting of skeletal myopathies or chronic renal failure. Troponin elevation is frequently found when the serum creatinine level is 2.5 mg/dL (211 mmol/L) in the absence of proven ACS.”

  
  
• 3.
  

  So far no other study has investigated the diagnostic value of a single measurement of high-sensitive troponin T in patients with renal insufficiency.

Given these 3 points, we would like to now reply to the critique by Giannitsis and Katus. The great benefit of high-sensitive troponin was promoted to be the time saving effect, because a single measurement is often sufficient in patients presenting with chest pain (as outlined in the European Society of Cardiology Guidelines). However, from our daily clinical experience we got the impression that this is simply not true for patients with (even moderate) renal insufficiency. Because we found no specific data on this issue when searching the literature and because of the clear statement in the European Society of Cardiology Guidelines on the uncertainty of high-sensitive troponin measurement in renal insufficiency, we decided to perform this study. We strongly believe that the research question posed by us was and still is justified. We believe that our results are important because we could show that single measurement of high-sensitive troponin T has no diagnostic value and serial measurement is indispensable in patients with renal insufficiency. It is just another part in the picture of limited interpretability of biomarkers in renal insufficiency (brain natriuretic peptide and D-dimer). This information is relevant to clinicians, irrespective of what Drs. Giannitsis and Katus’ views are. Also, we want to make clear that this was a pure academic study for which we received no funding. None of the participants in the conduction of the study received lecture fees. We only wanted to bring more light into the relevant question of how to handle troponin elevations in patients with renal insufficiency.