Hyperlipidæmia After Renal Transplantation

At present, there are very few studies that look at the effect of uremia, prednisone and cyclosporine therapy on the lipid profiles of children. This effect is important because of the potential association of hyperlipidemia and increased risk of cardiovascular morbidity and mortality and glomerulosclerosis. We measured fasting lipid profiles in 73 children. There were 21 controls, 18 patients treated with cyclosporine and prednisone, 9 patients treated with cyclosporine alone and 25 dialysis patients. Lipoprotein (a) levels were measured using direct binding ‘sandwich’ ELISA. Uremic children had higher levels of triglycerides and very-low-density lipoprotein as compared with the control group. Children receiving combination of cyclosporine and prednisone also had higher total cholesterol, triglycerides, low-density lipoprotein, very-low-density lipoprotein as compared to the control group. However, children receiving cyclosporine monotherapy had lipid profiles similar to the control group. Patients receiving cyclosporine and prednisone had higher total cholesterol, high-density lipoprotein and low-density lipoprotein as compared with the dialysis group. Evaluating lipoprotein (a) levels, children on cyclosporine monotherapy had lower lipoprotein (a) levels as compared with children on dialysis and those receiving both combination therapy. The total cholesterol/ high-density lipoprotein-cholesterol ratio (TC/HDL) was similar among the study groups. In summary, uremic children and children receiving steroids with cyclosporine have elevated lipid levels. However, the increased risk for atherosclerosis is not evident because of similar levels of lipoprotein (a) and TC/HDL ratios among the study groups.

Section: Discussionmentioning

confidence: 99%

Hyperlipidemia in Children: The Role of Uremia, Steroids and Cyclosporine Therapy

Singh¹,

Tejani²

1996

“…Corticoste roids [4,5,[8][9][10][11]13,19], ciclosporin [15,17,[20][21][22], diuretics [12], [$-adrenoreceptor blocking drugs [14], declining renal function [8,9,12,16,18], proteinuria [16,18], obesity [6,8,15] and impaired glucose tolerance [8] have all been impli cated. Other investigators, however, have failed to con firm these observations [23][24][25]. A better understanding of the several confounding clinical factors in which hy perlipidemia occurs may ultimately lead to more effec tive measures for prevention and treatment.…”

Section: Introductionmentioning

confidence: 99%

Hyperlipidemia in Stable Renal Transplant Recipients

Divakar¹,

Bailey²,

Frampton³

et al. 1991

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.

“…Abnormalities in plasma lipoprotein lipids are common in renal allograft recipients and may be important in the pathogenesis of atherosclerosis. The prevalence of dyslipoproteinemia varies, ranging from 16 to 72% of patients [3][4][5][6][7][8][9], These abnormalities include elevated total plasma triglyceride (TG) and cholesterol (C) as well as elevations of very low density lipoprotein (VLDL) and low-density lipoprotein (LDL) cholesterol. High-density lipoprotein (HDL) cholesterol levels have been reported to be low in some studies [9,10] but normal or elevated in others [11,12].…”

Section: Introductionmentioning

confidence: 99%

Lipoprotein Lipid Abnormalities in Healthy Renal Transplant Recipients: Persistence of Low HDL<sub>2</sub> Cholesterol

Ettinger¹,

Bender²,

Goldberg³

et al. 1987

There is disagreement about the prevalence and character of lipoprotein lipid abnormalities in renal transplant patients. To test the hypothesis that these abnormalities may be related to the coexistence of medical conditions and medications which affect lipoprotein metabolism in these patients, triglyceride (TG), cholesterol (C), high-density lipoprotein (HDL) and HDL-C subfractions were measured in 26 transplanted patients (10 F/16 M), control subjects matched for age, sex, weight and race and uremic patients being treated with hemodialysis. Female transplant recipients had higher TG (181 ± 47 vs. 68 ± 6 mg/dl; p < 0.001), C (242 ± 19 vs. 165 ± 9 mg/dl; p < 0.01), and low-density lipoprotein (LDL)-C (155 ± 15 vs. 93 ± 8 mg/dl; p < 0.01) than controls. Levels of HDL-C were similar, but HDL₂ was significantly lower in the transplanted patients (9 ± 2 vs. 19 ± 2 mg/dl; p < 0.01). Compared to the uremic patients, female transplanted patients had higher C (242 ± 19 vs. 178 ± 22 mg/dl; p < 0.01), LDL-C (155 ± 15 vs. 94 ± 18 mg/dl; p < 0.01), HDL-C (51 ± 5 vs. 32 ± 4 mg/dl; p < 0.001) and HDL₃-C (42 ± 4 vs. 26 ± 2 mg/dl; p < 0.001); however, HDL₂-C levels were not significantly different. Similarly, male transplanted patients had higher TG (166 ± 26 vs. 100 + 12 mg/dl; p < 0.01), C (213 ± 10 vs. 158 ± 3 mg/dl; p < 0.01), LDL-C (126 ± 9 vs. 97 ± 3 mg/dl; p < 0.05) and HDL-C (54 ± 4 vs. 41 ± 3 mg/dl; p < 0.05) than controls and higher HDL (54 ± 4 vs. 36 ± 4 mg/dl; p < 0.05) and HDL₃(47 ± 3 vs. 30 ± 2 mg/dl; p < 0.05) than uremic patients. However, HDL₂-C levels did not differ among the transplanted, control or uremic groups. Thus, both male and female renal transplant recipients who are otherwise healthy have elevated plasma TG, C and LDL-C and normal to high levels of HDL-C; however their HDL₂-C levels are low. These abnormalities may explain why renal transplant recipients have an increased incidence of atherosclerotic vascular disease.