Nakayama M, Yamada K, Yamamoto Y, Yokoyama K, Nakano H, Kubo H, Shigematsu T, Kawaguchi Y, Sakai O
Tokyo Jikei University School of Medicine, Second Department of Internal Medicine, Japan.
Clin Nephrol. 1994 Aug;42(2):117-20.
Circulating plasma immunoreactive thrombomodulin (i-TM) reflects the injury of vascular endothelium, and desmopressin stimulates tissue plasminogen activator (tPA) release from endothelium. Therefore, in order to estimate the damage of vascular endothelium in patients on regular dialysis treatment (RDT), we studied 1) basal plasma levels of i-TM and 2) a capability to release tPA by desmopressin. The basal plasma i-TM levels of the patients (n = 23) were significantly higher than those of the normal controls (p < 0.001). The basal plasma tPA levels of the patients (n = 8) were significantly lower than those of the controls (p < 0.05). The maximum increments of tPA from the basal levels by desmopressin in the patients were significantly reduced compared to those of the controls (p < 0.001). There was a significant inverse correlation in those cases between the maximum increments of tPA and the basal plasma levels of i-TM (p < 0.05, r = -0.75). The results actually suggested that there is a vascular endothelial damage in patients on RDT.
