The impact of an amino acid-based peritoneal dialysis fluid on plasma total homocysteine levels, lipid profile and body fat mass.
BACKGROUND
The caloric load from glucose-based peritoneal dialysis (PD) fluids contributes to hypertriglyceridaemia, adiposity and, as result of anorexia, protein malnutrition in PD patients. It has been suggested that replacement of a glucose-based by an amino acids-based PD fluid (AA-PDF) for one exchange per day might improve the nutritional status and lipid profile. Due to the uptake of methionine from the dialysate, however, exposure to AA-PDF might aggravate hyperhomocysteinaemia, a frequently occurring risk factor for atherosclerosis in uraemic patients.


METHODS
We studied the impact of a once daily exchange with 1.1% AA-PDF instead of glucose-based PD fluid for 2 months on plasma methionine and total homocysteine (tHcy) levels, lipid profile, butyrylcholinesterase (BChE) and body fat mass of seven stable PD patients. Results are expressed as mean+/-SEM.


RESULTS
Methionine levels did not increase significantly during therapy, but tHcy levels increased substantially from 60+/-12 to 84+/-19 micromol/l after 1 month (P=0.039), and to 85+/-22 micromol/l after 2 months of AA-PDF treatment. Serum triglyceride concentration decreased from 3.0+/-0.4 mmol/l at entry to 2.6+/-0.5 mmol/l (at 1 month, P=0.041 vs baseline). Serum BChE also decreased from 6.9+/-0.4 U/ml at entry to 6.3+/-0.4 U/ml after 2 months (P=0.014). Total cholesterol concentration and cholesterol fractions did not change. The reduced exposure to glucose-based PD fluid for 2 months resulted in a 0.5 kg reduction in fat mass which was due mainly to a reduction in fat mass of the trunk region (0.3 kg, P=0.031).


CONCLUSIONS
It is concluded that methionine-containing AA-PDF induces an increase in the plasma tHcy level. This might, potentially, offset the beneficial effects of an improved serum lipid profile and reduced fat mass on the risk of cardiovascular disease in PD patients. Lowering the methionine content of the fluid, therefore, may be required to overcome this adverse effect.
Brulez
H F
HF
Department of Nephrology, Academisch Ziekenhuis Vrije Universiteit, Amsterdam, The Netherlands.
van Guldener
C
C
Donker
A J
AJ
ter Wee
P M
PM
D000273:Adipose Tissue / Q000033:anatomy & histology* / Q000187:drug effects; D000328:Adult; D000596:Amino Acids / Q000494:pharmacology*; D000704:Analysis of Variance; D002784:Cholesterol / Q000097:blood*; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D015243:Cholesterol, VLDL / Q000097:blood; D003404:Creatinine / Q000097:blood; D015314:Dialysis Solutions / Q000737:chemistry*; D005260:Female; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D009929:Organ Size; D010530:Peritoneal Dialysis; D014280:Triglycerides / Q000097:blood*; D014511:Uremia / Q000097:blood / Q000628:therapy*
D000596:Amino Acids; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D015243:Cholesterol, VLDL; D015314:Dialysis Solutions; D014280:Triglycerides; D006710:Homocysteine; D002784:Cholesterol; D003404:Creatinine