YKL-40, a marker of cardiovascular disease and endothelial dysfunction, in kidney transplant recipients.
BACKGROUND
YKL-40 is an inflammatory glycoprotein involved in endothelial dysfunction and expressed in macrophages in the earliest lesion of atherosclerosis. Because cardiovascular mortality is the main cause of death, there are no data on kidney transplant recipients, so the aim of the study was to assess YKL-40 in that population, with particular attention being paid to the relationship with endothelial damage.


METHODS
We studied 68 patients after kidney transplantation. Complete blood count, creatinine, lipids, and fasting glucose were studied with the use of standard laboratory methods. We assessed YKL-40; markers of inflammation high-sensitivity C-reactive protein (hs-CRP), von Willebrand factor, thrombomodulin, interleukin-6, intracellular adhesion molecule, and vascular cell adhesion molecule; markers of hemostasis plasmin-antiplasmin complexes, thrombin-antithrombin complexes, prothrombin fragments 1+2; and marker of kidney function neutrophil gelatinase-associated lipocalin (NGAL) with the use of commercially available assays.


RESULTS
Mean levels of YKL-40 were significantly higher in kidney allograft recipients than in the control group (P < .001). YKL-40 was also significantly higher in patients with coronary artery disease, hypertension, and diabetes compared with their counterparts without these diseases. YKL-40, in univariate analysis, was related to NGAL, protein Z, plasmin-antiplasmin complex, mean corpuscular volume, cyclosporine level, and hs-CRP. YKL-40 was not related to serum lipids, markers of endothelial cell injury, or causes of end-stage renal failure. YKL-40 was predicted by cyclosporine level, NGAL, and hs-CRP, explaining 37% of the variation.


CONCLUSIONS
Elevated YKL-40 may contribute to enhanced risk of cardiovascular complication, mainly owing to endothelial cell injury and inflammation in patients after kidney transplantation treated with calcineurin inhibitors.
2nd Department of Nephrology, Medical University, Bialystok, Poland. Electronic address: jolmal@poczta.onet.pl.
Jolanta
J
Malyszko
2nd Department of Nephrology, Medical University, Bialystok, Poland.
E
E
Koc-Zorawska
2nd Department of Nephrology, Medical University, Bialystok, Poland.
Jacek
J
Malyszko
D054392:Adipokines / Q000097:blood*; D000328:Adult; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein; D002318:Cardiovascular Diseases / Q000401:mortality* / Q000473:pathology; D000071451:Chitinase-3-Like Protein 1; D004730:Endothelium, Vascular / Q000166:cytology / Q000293:injuries; D005260:Female; D006801:Humans; D015850:Interleukin-6; D007676:Kidney Failure, Chronic / Q000473:pathology; D007677:Kidney Function Tests; D016030:Kidney Transplantation; D037102:Lectins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D066027:Transplant Recipients; D014184:Transplantation, Homologous
D054392:Adipokines; D015415:Biomarkers; C084533:CHI3L1 protein, human; D000071451:Chitinase-3-Like Protein 1; D015850:Interleukin-6; D037102:Lectins; D002097:C-Reactive Protein