Nonfasting Non–High-Density Lipoprotein Cholesterol Is Adequate
for Lipid Management in Hemodialysis Patients
Simon Desmeules, MD, Jean-François Arcand-Bossé, MD, Jean Bergeron, MD,
Pierre Douville, MD, and Mohsen Agharazii, MD
● Background: Guidelines for the management of dyslipidemia in patients with chronic kidney disease are based
on results from the fasting lipid profile, which can be difficult to obtain from patients on an afternoon or night
dialysis schedule. The present study tests the hypothesis that nonfasting non– high-density lipoprotein (HDL)
cholesterol (total cholesterol–HDL cholesterol) results are similar to fasting non-HDL results as a basis for the
management of dyslipidemia in hemodialysis patients. Methods: Forty-eight long-term hemodialysis patients with a
mean age of 63.6 years (42% with diabetes, 54% administered statins) participated in this study. For the lipid profile,
blood samples were drawn after a 12-hour overnight fast (fasting) and again in a nonfasting state before the
subsequent hemodialysis session. Data were analyzed by using paired t-test and regression analysis. Results:
Non-HDL cholesterol values were nearly identical regardless of whether the patient was fasting (r
2
0.995). Only 2
patients (4%) had a nonfasting triglyceride (TG) level greater than 500 mg/dL (>5.6 mmol/L), which would have
required confirmation after an overnight fast. Non-HDL values had the greatest level of correlation (absolute relative
difference, 5.7%). When comparing the subgroup of patients with a TG level less than 200 mg/dL (<2.3 mmol/L),
nonfasting non-HDL cholesterol values identified 3 additional patients compared with fasting calculated low-
density lipoprotein cholesterol for whom lipid-lowering therapy would have been introduced according to current
guidelines. Conclusion: In our study, non-HDL cholesterol levels were equivalent whether evaluated in the fasting
or nonfasting state. We recommend that nonfasting non-HDL cholesterol level be used for the management of
dyslipidemia in hemodialysis patients without imposing a 12-hour fast period. Am J Kidney Dis 45:1067-1072.
© 2005 by the National Kidney Foundation, Inc.
INDEX WORDS: Hemodialysis (HD); lipid profile; nonfasting; fasting; dyslipidemia; non– high-density lipoprotein
(HDL) cholesterol.
T
HE CARDIOVASCULAR mortality rate is
20 times greater in patients with chronic
kidney disease than in the general population.
1
In
an attempt to reduce the burden of cardiovascu-
lar disease in patients with chronic kidney dis-
ease, aggressive management of cardiovascular
risk factors has been proposed. Qualitative and
quantitative modifications of the uremic lipid
profile may be responsible in part for the inverse
relation observed between total cholesterol (TC)
level and mortality in the end-stage renal disease
population.
2
Hemodialysis patients usually have
“normal” TC and low-density lipoprotein (LDL)
cholesterol levels, whereas they have a tendency
toward lower high-density lipoprotein (HDL)
cholesterol and higher triglyceride (TG) levels.
3
This lipid profile is described as atherogenic
dyslipidemia in the general population.
Recently, guidelines for the management of
patients with dyslipidemia and chronic kidney
disease have been published.
4
Algorithms are
based on results from the fasting lipid profile,
which can be more difficult to obtain from pa-
tients with diabetes and patients with an after-
noon or night dialysis schedule. Apolipoprotein
B100 (ApoB) concentrations are not affected by
meals; however, these measurements are expen-
sive and not readily available in most clinical
centers.
Non-HDL cholesterol represents the sum of
LDL, intermediate-density lipoprotein (IDL), and
very LDL cholesterol levels and correlates highly
with ApoB level. Therefore, it has been sug-
gested that non-HDL cholesterol level may be a
better marker of “atherogenic cholesterol” than
LDL cholesterol level.
5
Non-HDL cholesterol
can be calculated easily by subtracting HDL
from TC (non-HDL = TC – HDL). In the general
population, non-HDL cholesterol level is at least
as powerful a predictor of cardiovascular disease
From the Services of Nephrology and Biochemistry, De-
partment of Medicine, Centre Hospitalier Universitaire de
Québec-Hôtel-Dieu de Québec, 11, Côte du Palais, Québec,
Canada.
Received December 28, 2004; accepted in revised form
March 8, 2005.
Originally published online as doi:10.1053/j.ajkd.2005.03.002
on April 19, 2005.
Address reprint requests to Simon Desmeules, MD, Ser-
vice of Nephrology, CHUQ-Hôtel-Dieu de Québec, 11, Côte
du Palais, Quebec City, QC G1R 2J6, Canada. E-mail:
simon.desmeules@mail.chuq.qc.ca
© 2005 by the National Kidney Foundation, Inc.
0272-6386/05/4506-0012$30.00/0
doi:10.1053/j.ajkd.2005.03.002
American Journal of Kidney Diseases, Vol 45, No 6 (June), 2005: pp 1067-1072 1067