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Renal biomarkers and prognosis in acute pulmonary embolism
  1. Thomas M Berghaus,
  2. Martin Schwaiblmair,
  3. Wolfgang von Scheidt
  1. Department of Cardiology, Respiratory Medicine and Intensive Care, Klinikum Augsburg, Ludwig-Maximilians-University Munich, Germany
  1. Correspondence to Dr Thomas M Berghaus, Klinikum Augsburg, Stenglinstrasse 2, D – 86156 Augsburg, Germany; thomas.berghaus{at}klinikum-augsburg.de

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Renal dysfunction has become a validated prognostic factor indicating increased morbidity and mortality in different cardiovascular diseases, such as acute coronary syndrome1 or chronic heart failure.2 Impaired kidney function may not only reflect chronic renal disease but also deterioration secondary to haemodynamic disturbances, as decreased cardiac output and elevated central venous pressure may contribute to renal insufficiency.3 Kidney dysfunction has previously been observed in patients with acute pulmonary embolism (APE) and was found to be associated with worse short-term outcomes.4 ,5 However, those studies were not able to distinguish between acute kidney injury due to haemodynamic compromise cause by APE or chronic pre-existing renal insufficiency.

Kostrubiec and co-workers6 investigated markers of acute kidney injury such as cystatin C and serum neutrophil gelatinase-associated lipocalin (N-GAL) and their association with left and right heart function, disease severity, and prognosis in patients with APE. Cystatin C is a 13 kDa endogenous cysteine proteinase inhibitor and is produced by nucleated cells at a constant rate. It is freely filtered by the glomerulus, reabsorbed and catabolised, but it is not secreted by the tubules. Earlier studies demonstrated the superiority of serum cystatin C compared with creatinine, especially to detect minor changes in glomerular filtration rate …

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