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Hyperlipidemia of chronic renal failure
1Department of Medicine, University of California, Davis School of Medicine 95817.
Insights
Patients with advanced renal failure exhibit abnormal lipid profiles, including high triglycerides and altered HDL cholesterol. These lipid changes in chronic renal failure (CRF) are complex and not fully corrected by dialysis.
Area of Science:
- Nephrology
- Clinical Biochemistry
- Cardiovascular Research
Background:
- Patients with advanced renal failure often present with dyslipidemia.
- Key lipid abnormalities include elevated triglycerides and altered high-density lipoprotein (HDL) cholesterol levels.
Purpose of the Study:
- To comprehensively review the lipid abnormalities in chronic renal failure (CRF).
- To explore the underlying mechanisms and clinical implications of these lipid disorders.
Main Methods:
- Analysis of plasma lipid profiles in patients with CRF.
- Evaluation of lipoprotein composition and metabolism.
- Assessment of lipid changes in cell membranes.
Main Results:
- Elevated triglycerides across all lipoprotein fractions; reduced HDL cholesterol, particularly HDL2.
- Decreased lecithin:cholesterol acyltransferase (LCAT) activity and altered apolipoprotein levels (decreased apo A-I/A-II, increased apo B).
- Multifactorial causes including reduced lipoprotein lipase (LPL) activity, increased apo C-III, insulin resistance, and secondary hyperparathyroidism.
Conclusions:
- Dyslipidemia in CRF is complex and not fully corrected by dialysis.
- Lipid profiles improve post-transplantation but may be exacerbated in continuous ambulatory peritoneal dialysis (CAPD) patients.
- While lipid alterations are noted, their direct causal link to atherosclerosis in CRF requires further investigation; pharmacological treatment of qualitative abnormalities is not currently recommended.
Abstract:
Plasma triglycerides are increased in the majority of patients with advanced renal failure but cholesterol is not. HDL cholesterol is reduced while LDL IDL and VLDL cholesterol is increased. Lecithin:cholesterol acyltransferase (LCAT), an enzyme necessary for HDL maturation, is reduced in chronic renal failure (CRF). As a consequence, while all subtypes of HDL are reduced, the small HDL3 subtype is relatively enriched at the expense of the larger, more functional HDL2 subtype. Triglycerides are increased in all lipoprotein fractions. HDL-associated apolipoproteins, apo A-I and A-II are decreased, while apo B is increased. Lipoprotein catabolic rate is reduced, but the cause of hyperlipidemia is multifactorial; reduced lipoprotein lipase (LPL) activity, increased concentration of apo C-III (a specific inhibitor of LPL) in plasma, secondary hyperparathyroidism, insulin resistance. Hyperlipidemia is not corrected by dialysis. Lipid levels are somewhat higher in CAPD patients, possibly as a consequence of increased glucose absorption or as a consequence of transperitoneal HDL losses. Triglycerides decrease and cholesterol increases following transplantation. Oxidized lipids are increased in plasma of patients with CRF. Plasma polyunsaturated fatty acids are decreased and saturated fatty acids increased. The same changes occur in the lipid bilayers composing leukocytes and red blood cell membranes. These changes result in altered membrane fluidity, and are corrected by dialysis. While atherosclerotic disease is a leading cause of death in dialysis patients, it is not certain that the specific lipid disorders of CRF are responsible for this morbidity, nor is it recommended at this time that qualitative abnormalities be treated pharmacologically in the absence of increased lipid levels.