title: Renalase, kidney function, and markers of endothelial dysfunction in renal transplant recipients.
abstract: BACKGROUND
  Renalase is an enzyme released by the kidneys, which breaks down catecholamines in the blood and thus may regulate blood pressure. In kidney transplant recipients, endothelial dysfunction is often present.
  
  
  OBJECTIVE
  The aim of the study was to assess associations between renalase, blood pressure, and kidney function in kidney allograft recipients.
  
  
  METHODS
  We studied 62 kidney allograft recipients. Complete blood count, urea and creatinine levels, serum lipids, and fasting glucose were measured by standard laboratory methods. We also assessed markers of coagulation: prothrombin fragments 1+2; fibrinolysis: tissue plasminogen activator (tPA), plasminogen activator inhibitor, plasmin-antiplasmin complexes; endothelial function/injury: von Willebrand factor (vWF), thrombomodulin, intercellular adhesion molecule, vascular cell adhesion molecule (VCAM); and inflammation: high‑sensitivity C‑reactive protein and interleukin 6. Renalase levels were assessed using a commercially available kit.
  
  
  RESULTS
  Mean serum renalase levels in kidney allograft recipients correlated with age, time after transplantation, soluble CD44 (sCD44), VCAM, serum creatinine, estimated glomerular filtration rate (eGFR; measured by CKD-EPI, MDRD, and Cockcroft‑Gault formulas), serum phosphate, urea, sCD146, vWF, and thrombomodulin and tended to correlate with tPA. In patients with eGFR above 60 ml/min, renalase was lower than in those with lower eGFR. In hypertensive allograft recipients, renalase was significantly higher than in normotensives. A multiple regression analysis showed that renalase was predicted in 58% by serum creatinine.
  
  
  CONCLUSIONS
  Renalase, which is highly elevated in kidney transplant recipients, is dependent primarily on kidney function, which deteriorates with age and time after transplantation. Further studies are needed to establish the putative role of renalase in the pathogenesis of hypertension after transplantation and its possible use in novel targeted therapies.
authors.affiliation: Department of Nephrology and Transplantology, Medical University of Białystok, Poland. edzbroch@poczta.onet.pl
authors.forename: Edyta
authors.initials: E
authors.lastname: Zbroch
authors.forename: Jolanta
authors.initials: J
authors.lastname: Małyszko
authors.forename: Jacek
authors.initials: J
authors.lastname: Małyszko
authors.forename: Ewa
authors.initials: E
authors.lastname: Koc-Żórawska
authors.forename: Michał
authors.initials: M
authors.lastname: Myśliwiec
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000097:blood; D007674:Kidney Diseases / Q000201:enzymology*; D007677:Kidney Function Tests; D016030:Kidney Transplantation; D008297:Male; D008875:Middle Aged; D008995:Monoamine Oxidase / Q000097:blood*; D015849:Plasminogen Inactivators / Q000097:blood; D010959:Tissue Plasminogen Activator / Q000097:blood; D014184:Transplantation, Homologous
chemical_list: D015415:Biomarkers; D036341:Intercellular Signaling Peptides and Proteins; D015849:Plasminogen Inactivators; D008995:Monoamine Oxidase; C521557:renalase; D010959:Tissue Plasminogen Activator