Effects of Lipid Abnormalities on Arteriosclerosis and Hemostatic Markers in Patients under Hemodialysis

Abstract

Vascular events caused by arteriosclerosis are the major cause of death in patients under hemodialysis (HD). Arteriosclerosis is associated with lipoprotein abnormalities such as increased serum levels of low-density lipoprotein (LDL), especially of modified LDL (M-LDL) and oxidized LDL (Ox-LDL). We examined the relationship between markers of arteriosclerosis, hemostasis, and lipid metabolism in patients with chronic renal failure, hyperlipidemia, and healthy volunteers. In patients under HD, the serum levels of total cholesterol, LDL, and triglyceride (TG) were decreased, but the serum levels of M-LDL were increased compared to HL and healthy volunteers. In patients with CRF, the serum levels of Ox-LDL in patients under HD were lower than in those under continuous ambulatory peritoneal dialysis or conservative therapy. The plasma levels of antithrombin and protein C were significantly lower and the plasma levels of thrombomodulin were significantly higher in patients under HD compared to those under conservative therapy. These data show that patients under HD were more in hypercoagulable state than those under conservative therapy. Among patients under HD, only the plasma levels of von Willebrand factor were significantly increased in patients with more than 30 U/L of Ox-LDL compared to those with less than 30 U/L of Ox-LDL. There was no significant difference in the tests of arteriosclerosis among M-LDL values and Ox-LDL values. These findings suggest that abnormalities of lipid are not the main risk factor for arteriosclerosis disease in patients under HD.

Low Plasma Activated Protein C-Protein C Inhibitor Complex Concentration Is Associated with Vascular Access Failure in Hemodialysis Patients

“…We performed a cross-sectional study of plasma concentrations of vWF:Ag, APC-PCI complex, Hcy, TM-ag and TM-act in 35 patients participating in a maintenance HD program. We were able to confirm previously published results [5,6,7,8,9,10] showing significantly elevated plasma levels of TM-ag in HD patients and, in addition, we showed that this is also the case with plasma TM-act. An elevated level of P-TM-ag, together with elevated P-TM-act, is considered a marker of vascular endothelial damage.…”

“…Thrombin in complex with its endothelial cell membrane-bound cofactor thrombomodulin (TM) activates the anticoagulant protein C, creating activated protein C (APC), which is inactivated by protein C inhibitor (PCI). Significantly elevated predialysis plasma levels of soluble plasma TM fragments (P-TM-ag) have been demonstrated in HD patients relative to healthy controls [5,6,7,8,9,10]. In addition, postdialysis P-TM-ag levels have been shown to be significantly elevated compared to predialysis levels [11,12,13].…”

Effect of Rosuvastatin on Outcomes in Chronic Haemodialysis Patients: Baseline Data from the AURORA Study

“…Documented CVD and/or diabetes were present in half of the patients. The main lipid parameters at baseline were close to those observed in other studies of haemodialysis populations [19,37,38] , although they did appear to differ from those reported in the 4D study: Mean 8 SD baseline lipid levels in 4D: TC 220 8 42 mg/dl in placebo and 218 8 43 mg/dl in atorvastatin patients, LDL-C 127 8 30 mg/dl in placebo and 125 8 29 mg/dl in atorvastatin patients and TG 267 8 168 mg/dl in placebo and 261 8 165 mg/dl in atorvastatin patients -all higher lev- RRT = Renal replacement therapy; Kt/V = dialysis adequacy calculated from pre-and post-urea results [34]. els than in the AURORA patients at baseline; HDL-C was 36 8 14 mg/dl in placebo and 36 8 13 mg/dl in atorvastatin patients -lower than in AURORA patients at baseline [29,39] .…”

Thrombophilias and arteriovenous fistula dysfunction in maintenance hemodialysis

“…Alterations in haemostatic plasma factors create a hypercoagulable state in HD patients [11,25]. In recent years, alterations in several haemostatic plasma protein factors have been suggested to create a hypercoagulable state in patients on regular HD therapy, although their role in the arteriovenous fistula (AVF) failure is still debated [11].…”