Hyperlipidemia in Stable Renal Transplant Recipients

Abstract

Hyperlipidemia is a major risk factor for atherosclerosis and probably contributes to the increased cardiovascular mortality following renal transplantation. We studied the lipid profiles of 62 adults (29 males) with stable renal function (mean plasma creatinine 0.14 mmol/l, SD 0.07), 7 months to 21 years after renal transplantation. Fifteen patients (24%) were above the age- and sex-adjusted 95th percentile for total triglyceride and 10 (16%) for total cholesterol concentrations when compared with a local reference population. The most common lipoprotein abnormalities were type IIa (19%) and type lib (13%). Multiple regression analysis demonstrated that the use of diuretics and angiotensin-converting enzyme inhibitors were significant factors determining plasma triglyceride concentrations. There were significant bivariate associations between plasma triglyceride concentration and duration since transplantation, plasma creatinine concentration and the use of ciclosporin and diuretics. Duration since transplantation and ciclosporin use were significant factors determining lower plasma cholesterol concentrations. The use of ciclosporin and diuretics was associated with a significantly higher apolipoprotein (apo) B concentration. The cholesterol/HDL cholesterol risk ratio correlated poorly with the apo B/apo A-1 ratio. The value of these ratios as predictors of coronary artery disease need to be established in renal transplant recipients.

Serum Apolipoprotein Profile of Renal-Transplant Patients

“…The results, summarized in table 1, indi cate that postlransplantation changes in se rum lipids were comparable to those de scribed in most studies [4][5][6]. Changes in serum apoproteins were also similar to those described previously by other authors [2,4], When compared to healthy controls, trans planted patients showed higher levels of apo CII (p <0.05).…”

Hyperlipidemia after Renal Transplantation: Treatment with Gemfibrozil

“…Although the relationship between serum TG and car diovascular risks remains controversial, studies in uremic patients and renal transplant recipients have demonstrated the coexistence of hypertriglyceridemia with deleterious qualitative lipoprotein abnormalities and other cardiovas cular risk factors such as reduced HDL-C [32][33][34], Further studies are therefore indicated to examine whether gemfi brozil therapy, which has a greater effect on TG rather than LDL-C and HDL-C, could reduce coronary events in renal transplant recipients [35],…”

Mechanism of tacrolimus-induced chronic renal fibrosis following transplantation is regulated by ox-LDL and its receptor, LOX-1

“…As one of the most effective treatments against end-stage renal disease, renal allografts markedly improve patient survival rates and quality of life (1–3). With developments in transplantation immunobiology and the application of novel immunosuppressants, numerous problems, including acute rejection and short-term graft loss, have been addressed, resulting in decreased mortality rates (2).…”

“…However, improvements in long-term graft survival are not commensurate. With further prolongation of the transplantation period, renal allografts gradually lose their function (3). This irreversible, progressive loss is generally termed chronic renal allograft dysfunction (CRAD) (1), which is caused by immunological and non-immunological factors (2).…”

“…As a non-immunological factor, dyslipidemia leads to cardiovascular disease (CVD) and severely impairs the long-term survival of grafts and patients (4–6). Of note, 40–80% patients have been reported to exhibit hyperlipidemia following renal transplantation (3,7). …”