Why the study?
Are plasma levels and peritoneal loss of Lipoprotein (a) altered in patients undergoing continuous ambulatory peritoneal dialysis?
Are plasma levels and peritoneal loss of Lipoprotein (a) altered in patients undergoing continuous ambulatory peritoneal dialysis?
Patients undergoing CAPD have significantly elevated plasma Lp(a) levels, which may be driven by continuous peritoneal loss of proteins and contribute to accelerated atherosclerosis.
Elevated Lp(a) may heighten CV risk in CAPD; hypothesis-generating for peritoneal loss mechanisms and needs prospective confirmation.
Cerebrovascular and cardiovascular diseases are important predictors for survival in patients undergoing continuous ambulatory peritoneal dialysis (CAPD). Recently, increased levels of Lp (a) were documented in nephrotic syndrome and renal failure. We quantified the plasma levels and peritoneal loss of lipids and lipoproteins, and studied the composition of plasma and effluent lipoproteins in 19 patients on CAPD (10 females and 9 males, 26 to 73 years old). Median levels of plasma Lp (a) were significantly elevated in CAPD patients compared to controls (30.5 vs. 10.7mg/dl, P<0.05). We found no statistically significant correlations of Lp (a) with age, blood pressure, plasma lipoprotein, apoprotein, glycated hemoglobin, BUN, creatinine, plasma protein levels, or the duration of CAPD treatment. All plasma lipoproteins, (VLDL, IDL, LDL, Lp (a), and HDL) were present in the peritoneal effluent. There were significant positive correlations between plasma Lp (a) levels & peritoneal loss of Lp (a) and total cholesterol. Positive correlation was observed between peritoneal loss of Lp (a) & proteins and other lipoproteins. Autopsy material from the left coronary artery and from the thoracic aorta has been examined by means of immunohistochemistry. Most of plasma Lp (a) accumulates in the arterial wall intima. We suggest, based on our findings, that the increased hepatic synthesis of Lp (a) due to the continuous peritoneal loss of Lp (a) & proteins and/or impaired catabolism of Lp (a) contribute to the high levels of plasma Lp (a) in CAPD patients, and such factors may have led to the accelerated atherosclerosis observed in these patients.
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Takegoshi et al. (1994) studied this question.
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