Decrease in lipoprotein(a) after renal transplantation is related to the glucocorticoid dose

Ahsen, Nico von; Helmhold, M.; Eisenhauer, T.; Armstrong, Victor W.; Oellerich, Michael

doi:10.1111/j.1365-2362.1996.tb02151.x

Cited by 11 publications

(4 citation statements)

References 27 publications

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“…Our data are consistent with other prospective studies that have shown decreases of Lp(a) after transplantation several months to years post-transplant [24,25,26,27]. Prevalence of Lp(a) >25 mg/dl was 31–37% after 2–10 months post-transplant [28, 29] and >12 mg/dl in approximately 60% of patients 1 year post-transplant [29].…”

Section: Discussionsupporting

confidence: 81%

Effects of Renal Replacement Therapy on Plasma Lipoprotein(a) Levels

Rosas¹,

Joffe

Wolfe

et al. 2007

Am J Nephrol

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Patients with end-stage renal disease (ESRD) have significantly higher levels of lipoprotein(a) [Lp(a)] when compared to control populations. Elevated levels of Lp(a) may play a role in the high incidence of cardiovascular disease in ESRD. We conducted a prospective study to test the hypothesis that plasma levels of Lp(a) decline rapidly after renal transplantation proportional to the improvement in renal function, but are not affected by hemodialysis. All adults that initiated hemodialysis or received a renal transplant from our institution during a 10-month period were invited to participate in the study. Lp(a) levels were obtained immediately prior to the initiation of renal replacement therapy. In transplant recipients, repeat Lp(a) measures were done at 3 days, 5 days, 1 week, 2 weeks, 3 weeks and 4 weeks post-transplant. In hemodialysis patients, repeat Lp(a) measures were done after 3 months. We used a mixed effects model to analyze the effect of time, race and creatinine on Lp(a) after transplant. Lp(a) levels decreased rapidly after renal transplantation. Mean Lp(a) levels at 2 weeks were 35.3% lower than prior to transplantation. Each reduction of 50% in creatinine was associated with a 10.6% reduction in Lp(a) (p < 0.001). In contrast, there was no significant change in Lp(a) after initiation of hemodialysis. The rapid decrease of Lp(a) levels after renal transplantation provides support for a metabolic role of the kidney in Lp(a) catabolism and suggests that the increase in Lp(a) seen in chronic kidney disease is due to loss of functioning renal tissue.

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Section: Discussionsupporting

confidence: 81%

Effects of Renal Replacement Therapy on Plasma Lipoprotein(a) Levels

Rosas¹,

Joffe

Wolfe

et al. 2007

Am J Nephrol

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“…In addition, dexamethasone treatment after renal transplantation has been shown to induce a dose-dependent reduction in Lp(a). 47 Therefore, the changes in Lp(a), IGF-I, and IGFBP-1 and the observed association between Lp(a) and IGFBP-1 during alcohol withdrawal are possibly not related to cortisol. Unfortunately, neither plasma nor urinary catecholamines and cortisol were measured in the present study.…”

Section: Discussionmentioning

confidence: 99%

Alcohol Withdrawal–Induced Change in Lipoprotein(a)

Paassilta

Kervinen

Linnaluoto

et al. 1998

ATVB

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Abstract-Lipoprotein(a) [Lp(a)] is an important risk factor for cardiovascular disease. Alcohol is one of the few nongenetic factors that lower Lp(a) levels, but the metabolic mechanisms of this action are unknown. Alcohol inhibits the growth hormone (GH)/insulin-like growth factor-I (IGF-I) axis. Alcohol might also affect IGF-binding protein-1 (IGFBP-1), which is an acute inhibitor of IGF-I. We studied how alcohol withdrawal affects Lp(a) levels and the GH/IGF-I/IGFBP-1 axis. Male alcohol abusers (nϭ27; 20 to 64 years old) were monitored immediately after alcohol withdrawal for 4 days. Twenty-six healthy men, mainly moderate drinkers, served as control subjects. Fasting blood samples were drawn to determine Lp(a), IGF-I, and IGFBP-1 (by ELISA, RIA, and immunoenzymometric assay, respectively). Nocturnal (12 hours) urine collection was performed in 9 alcoholics and 11 control subjects for GH analyses (RIA). The groups were similar in age and body mass index. Lp(a), GH, and IGF-I tended to be lower and IGFBP-1 higher in the alcoholics immediately after alcohol withdrawal than in the control subjects. During the 4-day observation in alcoholics, Lp(a) levels increased by 64% and IGF-I levels by 41%, whereas IGFBP-1 levels decreased by 59% (PϽ.001 after ANOVA for all comparisons). Urinary GH levels tended to decline. The increase in Lp(a) correlated inversely with the changes in IGFBP-1 (rϭϪ.63, PϽ.001, nϭ27) and GH (rϭϪ.70, PϽ.05, nϭ9), but not with IGF-I. In multiple regression analysis, the main predictors for the increase in Lp(a) were IGFBP-1 and urinary GH.

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“…Lp(a) was quantified using a specific polyclonal noncompetitive enzyme-linked immunosorbent assay (21). Apo(a) isoforms were separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis on commercially available 4-15% polyacrylamide gradient gels (PHAST-System; Pharmacia, Freiburg, Germany) followed by immunoblotting as described elsewhere (22). Apo(a) polymorphs were numbered 1 to 10 with increasing molecular weight (21).…”

Section: Methodsmentioning

confidence: 99%

The effect of recombinant human GH replacement therapy on lipoprotein(a) and other lipid parameters in adults with acquired GH deficiency: results of a double-blind and placebo-controlled trial

Nolte

Rädisch

Armstrong

et al. 1997

European Journal of Endocrinology

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The effect of GH substitution on serum lipids and lipoproteins, and in particular lipoprotein(a) (Lp(a)), was investigated in 32 adults with postoperative (acquired) GH deficiency as part of a double-blind, placebo-controlled trial. Seventeen men and fifteen women, aged 18-59 years (mean 42 years) from two centres (Hannover and Göttingen) were randomly assigned to two groups. Group P (placebo) received placebo for the first 12 months and recombinant human GH (rhGH) for the following 12 months (open phase). Group V (verum) was treated with rhGH for two consecutive periods of 12 months each. The target dose of rhGH was 2 U/m 2 per day, given subcutaneously daily at bedtime. Serum concentrations of Lp(a), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) and triglycerides were determined at 0, 12 and 24 months. In group V, Lp(a) increased significantly in the first as well as in the second year of treatment (P=0.02, 12 months versus baseline; P=0.016, 24 months versus 12 months). In contrast, Lp(a) levels remained unchanged in group P during the first 12 months (P=0.826 versus baseline), but increased significantly (P=0.002) during the second year, when all patients were administered GH. The increase in Lp(a) after 12 months of rhGH replacement therapy in all 32 patients was significant for Lp(a) baseline concentrations both above and below 20 mg/dl and was independent of the apolipoprotein(a) isoforms. Total and LDL-C decreased significantly after 1 year and triglycerides after 2 years in group V. A significant reduction was also observed in the TC/HDL-C and the LDL-C/HDL-C ratios. Our study shows an unfavorable effect of rhGH replacement therapy on Lp(a) levels, which is, however, counteracted by a favorable effect of rhGH on TC, LDL-C and the TC/LDL-C and LDL-C/HDL-C ratios.

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Decrease in lipoprotein(a) after renal transplantation is related to the glucocorticoid dose

Cited by 11 publications

References 27 publications

Effects of Renal Replacement Therapy on Plasma Lipoprotein(a) Levels

Effects of Renal Replacement Therapy on Plasma Lipoprotein(a) Levels

Alcohol Withdrawal–Induced Change in Lipoprotein(a)

The effect of recombinant human GH replacement therapy on lipoprotein(a) and other lipid parameters in adults with acquired GH deficiency: results of a double-blind and placebo-controlled trial

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