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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Roles of hypoalbuminemia and lipoprotein lipase on hyperlipoproteinemia in continuous ambulatory peritoneal dialysis.

To assess the mechanism of serum lipoprotein abnormalities in continuous ambulatory peritoneal dialysis (CAPD), we measured serum lipids, apolipoproteins, and postheparin lipases in 46 patients with end-stage renal disease (ESRD) treated on CAPD, 26 patients on hemodialysis (HD), and 29 healthy subjects. HD patients had higher serum triglyceride levels than the healthy controls, showing type IV and type III phenotypes. They had significantly lower activities of hepatic triglyceride lipase (HTGL) in postheparin plasma compared with controls, and postheparin lipoprotein lipase (LPL) was also decreased by 15%, although the latter change was not statistically significant. CAPD patients had elevated levels in triglyceride, total cholesterol, low-density lipoprotein cholesterol (LDL-C), and apolipoprotein (apo) B, showing type IV, III, and II (IIb and IIa) phenotypes. The mean LPL and HTGL activities in CAPD patients were not different from those of HD patients. CAPD patients with hyperlipoproteinemia had significantly higher serum albumin levels than those with normolipidemia. There was a significant positive correlation between albumin and apo B levels in CAPD patients. In hyperlipidemic CAPD patients, there was no difference in serum albumin concentrations or HTGL activities among lipoprotein phenotypes, whereas LPL activities were significantly higher in the patients with type II than those with type IV hyperlipoproteinemia. These results suggest that there was some linkage between alterations in serum albumin and lipoproteins, and that LPL was related to phenotypic variation of hyperlipoproteinemia in CAPD.[1]

References

  1. Roles of hypoalbuminemia and lipoprotein lipase on hyperlipoproteinemia in continuous ambulatory peritoneal dialysis. Shoji, T., Nishizawa, Y., Nishitani, H., Yamakawa, M., Morii, H. Metab. Clin. Exp. (1991) [Pubmed]
 
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