Is Atherosclerosis Accelerated by CAPD?

Cardiovascular complications in renal replacement therapy remain prevalent today. The question, “Is atherosclerosis accelerated in peritoneal dialysis (PD) patients,” has not been resolved. Many cross-sectional studies have revealed that there are more atherogenic lipid profiles in continuous ambulatory peritoneal dialysis (CAPD) than in other dialytic modalities. However, it is not certain that CAPD per se may contribute to lipid abnormalities in continuing PD for a long time. Therefore, we tried to assess whether CAPD itself may change lipid profiles in the long-term period on CAPD.

We measured conventional lipid profiles in 16 stable CAPD patients in whom total cholesterol (T.chol.) levels remained under 240 mg/dL at the time of starting observation. Diabetic end-stage renal disease (DMESRD) patients were excluded from this study. Blood sampling was performed under strict conditions indicating overnight fasting with 10 hours dwell of 2 L of 1.5% Dianeal. Plasma levels of T. chol., triglyceride, high-density lipoprotein (HDL), low-density lipoprotein (LDL), and atherogenic lipoprotein (apo B/A-I) did not show significant changes by serial measurements from the sixth month to the thirtieth month following the commencement of CAPD as their initial dialysis treatment.

Recently it is reported that high plasma levels of Lp(a) lipoprotein are an independent risk factor in cardiovascular events in renal replacement therapy because Lp(a) has a close relation to intravascular thrombosis and acceleration of atherosclerosis. We found that the incidence of vascular accidents was five episodes among 33 patients with higher (>31 mg/dL) Lp(a) levels, while there was only one episode in 45 patients with lower «30 mg/dL) Lp(a) levels (p < 0.05, odds ratio: 7.9). However, severity of aortic calcification and incidence of positive treadmill test showed no difference in these two groups. No significant correlation was observed between duration on CAPD and plasma Lp(a) levels. From the fact mentioned above, we speculate that CAPD does not essentially affect lipid profiles if determined under the strict condition of blood sampling.

In order to evaluate atherosclerosis noninvasively, we have measured aortic pulse wave velocity (AoPWV) in 33 stable CAPD patients excluding those with DMESRD by two years’ interval. Fifteen cases (46%) increased in AoPWV, however, lipid profiles did not differ from those of nonadvanced patients.

Calcification of arteries is further evidence of acceleration in atherosclerotic change. Therefore, we have graded severity of abdominal aortic calcification into three categories: grade I denoted nil calcification, grade II denoted patchy calcification, and grade III denoted calcification along the entire abdominal wall, having a lead-pipe shape by lateral view of plain abdominal x-ray film. There were significant differences in the duration of CAPD (grade I: 41 months, grade II: 60 months, grade III: 68 months). AoPWV showed least in the grade I group, faster in grade II, and fastest in grade III, while lipid profiles did not show significant difference in three categories.

From the analysis of serial changes of lipid profiles, AoPWV and aortic calcification, CAPD may present some risk of accelerating atherosclerosis, at least in some patients on long-term treatment. Risk factors contributing to acceleration of atherosclerosis result not from lipid abnormalities, but from other factors which remained to be seen, for example, abnormalities in calcium metabolism.