title: Increased lipoproteins and fibrinogen in chronic renal allograft dysfunction.
abstract: Chronic rejection - also called chronic renal allograft dysfunction (CRAD) - is the main cause of long-term loss of the transplanted kidney, but its pathogenesis is not well known. The aim of this study was to know if lipoproteins, fibrinogen, plasminogen activator inhibitor-1 (PAI-1) and platelet aggregation show more abnormalities in renal transplant patients with CRAD than in those with stable renal function. Sixty patients with renal allograft have been studied; 20 patients with CRAD and 40 controls matched for age, gender and time after transplantation. In a univariate analysis patients with CRAD had higher total serum triglycerides (214+/-153 vs. 133+/-39 mg/dl; p = 0.04) and very-low-density lipoprotein (VLDL) triglycerides (128+/-116 vs. 59+/-29 mg/dl; p = 0.04). Apolipoprotein B levels were also increased in patients with CRAD although this difference was only borderline significant (131+/-58 vs. 98+/-16 mg/dl; p = 0.05). Similarly, there was a trend toward increased total, VLDL, and low-density lipoprotein (LDL) cholesterol and reduced high-density lipoprotein (HDL) cholesterol in CRAD patients, but these differences did not reach statistical significance. Apolipoprotein A-1 and lipoprotein(a) levels were similar in both groups. Neither platelet aggregation nor PAI-1 levels differed between both groups. In contrast, fibrinogen was increased in patients with CRAD (373+/-81 vs. 322+/-62 mg/dl; p = 0.01). In a multivariate analysis triglycerides and fibrinogen were positively correlated to CRAD. These findings add further support to the hypothesis that lipid abnormalities may be involved in the pathophysiology of CRAD. In addition, this is the first report showing that fibrinogen levels are increased in patients with CRAD. Further studies are needed to evaluate a potential role of fibrinogen in the development of CRAD.
authors.affiliation: Services of Internal Medicine, Hospital Universitario, Madrid, Spain.
authors.forename: C
authors.initials: C
authors.lastname: Fernandez-Miranda
authors.forename: J M
authors.initials: JM
authors.lastname: Morales
authors.forename: A
authors.initials: A
authors.lastname: Porres
authors.forename: J
authors.initials: J
authors.lastname: Gomez-Gerique
authors.forename: C
authors.initials: C
authors.lastname: Guijarro
authors.forename: J L
authors.initials: JL
authors.lastname: Aranda
authors.forename: A
authors.initials: A
authors.lastname: Andres
authors.forename: J L
authors.initials: JL
authors.lastname: Rodicio
authors.forename: A
authors.initials: A
authors.lastname: Del Palacio
mesh_terms: D000328:Adult; D001055:Apolipoproteins B / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D002908:Chronic Disease; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005340:Fibrinogen / Q000378:metabolism*; D006084:Graft Rejection / Q000097:blood* / Q000209:etiology; D006801:Humans; D016030:Kidney Transplantation; D008074:Lipoproteins / Q000097:blood*; D008077:Lipoproteins, LDL / Q000097:blood; D008079:Lipoproteins, VLDL / Q000097:blood; D008297:Male; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D010974:Platelet Aggregation; D014184:Transplantation, Homologous; D014280:Triglycerides / Q000097:blood
chemical_list: D001055:Apolipoproteins B; D008076:Cholesterol, HDL; D008074:Lipoproteins; D008077:Lipoproteins, LDL; D008079:Lipoproteins, VLDL; D017395:Plasminogen Activator Inhibitor 1; D014280:Triglycerides; D005340:Fibrinogen