INCREASED LIPOPROTEINS AND FIBRINOGEN IN CHRONIC RENAL-ALLOGRAFT DYSFUNCTION

Chronic rejection - also called chronic renal allograft dysfunction (C RAD)- 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 k now if lipoproteins, fibrinogen, plasminogen activator inhibitor-1 (PA I-1) and platelet aggregation show more abnormalities in renal transpl ant patients with CRAD than in those with stable renal function. Sixty patients with renal allograft have been studied; 20 patients with CRA D and 40 controls matched for age, gender and time after transplantati on. In a univariate analysis patients with CRAD had higher total serum triglycerides (214 +/- 153 vs. 133 +/- 39 mg/dl; p = 0.04) and very-l ow-density lipoprotein (VLDL) triglycerides(128 +/- 116 vs. 59 +/- 29 mg/dl; p = 0.04). Apolipoprotein B levels were also increased in patie nts with CRAD although this difference was only borderline significant (131 +/- 58 vs. 98 +/- 16 mg/dl; p = 0.05). Similarly, there was a tr end toward increased total, VLDL, and low-density lipoprotein (LDL) ch olesterol and reduced high-density lipoprotein (HDL) cholesterol in CR AD patients, but these differences did not reach statistical significa nce. Apolipoprotein A-1 and lipoprotein(a) levels were similar in both groups. Neither platelet aggregation nor PAI-I levels differed betwee n both groups. In contrast, fibrinogen was increased in patients with CRAD (373 +/- 81 vs. 322 +/- 62 mg/dl; p = 0.01). In a multivariate an alysis triglycerides and fibrinogen were positively correlated to CRAD . These findings add further support to the hypothesis that lipid abno rmalities 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 poten tial role of fibrinogen in the development of CRAD.