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Göteborgs universitets publikationer

Dyslipidemia of kidney disease.

Författare och institution:
Per-Ola Attman (Institutionen för medicin, avdelningen för molekylär och klinisk medicin); Ola Samuelsson (Institutionen för medicin, avdelningen för molekylär och klinisk medicin)
Publicerad i:
Current opinion in lipidology, 20 ( 4 ) s. 293-9
Artikel, refereegranskad vetenskaplig
Sammanfattning (abstract):
PURPOSE OF REVIEW: Chronic kidney disease is associated with specific alterations of lipoprotein metabolism that may be linked to accelerated atherosclerosis and cardiovascular disease. This review summarizes current knowledge of the pathophysiology of renal dyslipidemia and the therapeutic options. RECENT FINDINGS: The renal dyslipidemia is characterized by accumulation of intact and partially metabolized triglyceride-rich apoB-containing and apoC-containing lipoproteins. Increased concentrations of atherogenic apoC-III rich lipoproteins, the hallmark of renal dyslipidemia, may result from disturbances of insulin metabolism and action in chronic kidney disease. Novel findings strongly suggest that apoC-III triggers a cascade of pro-inflammatory events, which ultimately can result in endothelial dysfunction and vascular damage. Disappointingly, recently reported intervention trials with statins have failed to show any benefit on cardiovascular disease in patients with advanced renal failure. SUMMARY: During recent years, our understanding of the character and biological significance of the dyslipidemia of chronic kidney disease, and its link to cardiovascular disease, has increased. However, our knowledge about its proper management is still very limited.
Ämne (baseras på Högskoleverkets indelning av forskningsämnen):
Apolipoprotein C-III, metabolism, Cardiovascular Diseases, metabolism, Chronic Disease, Dyslipidemias, complications, metabolism, Humans, Kidney Diseases, complications, metabolism, Lipoproteins, metabolism, Models, Theoretical
Postens nummer:
Posten skapad:
2010-01-25 13:25
Posten ändrad:
2012-08-17 14:17

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