Aberrant lipoprotein composition is the primary driver of dyslipoproteinemia in renal failure, with low lipoprotein lipase activity playing a contributory role.
Does not alter lipid management in uremia; leaves open the relative primacy of lipoprotein composition versus lipase activity.
The lipoprotein pattern, observed in patients with renal failure, suggests impaired catabolism of triglyceride-rich lipoproteins. This is supported by the findings of numerous studies addressing the pathogenesis of the dyslipoproteinemia of uremia. Aberrant lipoprotein composition, resulting in disturbed substrate characteristics for lipoprotein lipase and unfavourable receptor ligand function, probably constitutes the primary pathology. The structural details of the lipoproteins that are responsible for this dysfunction are not yet established. In this regard, abnormal apolipoprotein pattern and, possibly more important, biological modifications must be taken into consideration. Low activity of lipoprotein lipase does not seem to be a primary pathogenetic factor. However, there is little doubt that it plays a contributory part. The role of hepatic lipase is controversial.
No takes yet. Share an insight, caveat, or question.
Margrét Árnadóttir (1997) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: