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ACTH lowers serum lipids in steroid-treated hyperlipemic patients with kidney disease
1Department of Nephrology, University Hospital, Lund, Sweden.
Insights
Adrenocorticotropic hormone (ACTH) significantly reduced lipids in hyperlipidemic kidney disease patients. This suggests iatrogenic ACTH deficiency may contribute to secondary hyperlipidemia in these patients.
Area of Science:
- Endocrinology
- Nephrology
- Lipid Metabolism
Background:
- Secondary hyperlipidemia mechanisms in chronic inflammatory diseases are unclear.
- Adrenocorticotropic hormone (ACTH) has demonstrated hypolipidemic effects in healthy individuals.
- Steroid treatment in kidney disease patients can lead to hyperlipidemia.
Purpose of the Study:
- To investigate the clinical relevance of ACTH's hypolipidemic effects in hyperlipidemic patients with kidney disease.
- To determine if ACTH administration can improve lipid profiles in this patient population.
Main Methods:
- Nine hyperlipidemic, steroid-treated patients with kidney disease received ACTH for three weeks.
- Plasma ACTH concentrations were measured before treatment.
- Serum lipid levels (triglycerides, cholesterol, LDL, HDL, Apo B, Apo A1, Lp(a)) and enzyme activities (HL, LPL) were assessed.
Main Results:
- ACTH administration resulted in significant reductions (20-50%) in triglycerides, cholesterol, LDL cholesterol, Apo B, and Lp(a).
- HDL cholesterol and Apo A1 concentrations increased by 10-25%.
- Hepatic lipase (HL) activity decreased by ~40%, while lipoprotein lipase (LPL) activity increased by ~140%.
Conclusions:
- Hyperlipidemia in steroid-treated kidney disease patients may be partly caused by iatrogenic ACTH deficiency.
- ACTH treatment demonstrates potential therapeutic benefits for lipid management in this cohort.
- The findings support a role for ACTH in regulating lipid metabolism in patients with kidney disease.
Abstract:
The mechanisms behind secondary hyperlipidemia in patients with various chronic inflammatory diseases are not known in detail. We have recently demonstrated that ACTH exerts strong hypolipidemic effects in healthy volunteers. To test the clinical relevance of this finding, we administrated ACTH during three weeks to nine hyperlipidemic steroid-treated patients with kidney disease. Before administration of ACTH 1-24, plasma ACTH concentrations were low. Treatment with ACTH led to 20 to 50% reductions in serum concentrations of triglycerides, cholesterol, LDL cholesterol and Apo B as well as of Lp(a). HDL cholesterol and Apo A1 concentrations increased by 10 to 25%. HL activity in postheparin plasma decreased by about 40% and LPL activity, which was initially low, increased by about 140%. The effects of ACTH were similar in kidney transplant recipients and in patients with inflammatory kidney disease. Our results indicate that hyperlipidemia in steroid treated patients with kidney disease may at least partly be due to iatrogenic ACTH deficiency.