Yu Eguchi

Validation of the Friedewald Equation for Evaluation of Plasma LDL-Cholesterol

In most clinical laboratories, low density lipoprotein (LDL) cholesterol is usually estimated indirectly with the Friedewald equation or directly with the N-geneous assay. We assessed LDL-cholesterol values obtained by both methods to find an appropriate fasting period and to assess the influence of the energy content of the last meal. Blood samples were taken from 28 healthy volunteers who had consumed a standard meal (107 g of carbohydrate, 658 kcal) followed by a fasting period of 12 and 18 h, or a high-energy meal (190 g of carbohydrate, 1011 kcal) with a fasting period of 12 h. Prolongation of the fasting period from 12 h to 18 h decreased glucose level, but did not decrease triacylglycerol, total cholesterol, or high density lipoprotein (HDL) cholesterol. LDL-cholesterol levels measured with the N-geneous assay did not change (94.0 ± 21.5 to 96.3 ± 19.1 mg/dl). LDL-cholesterol levels calculated with the Friedewald equation were also similar after fasting periods of 12 h (98.5 ± 21.4 mg/dl) and 18 h (99.7 ± 20.2 mg/dl). The high-energy meal did not change the level of LDL-cholesterol measured with the N-geneous assay (96.1 ± 21.2 mg/dl), or the glucose, triacylglycerol, total cholesterol, or HDL-cholesterol level, but LDL-cholesterol levels evaluated from the Friedewald equation (92.6 ± 20.3 mg/dl) became significantly lower. A fasting time longer than 12 h is not necessary to obtain reasonable blood lipid levels. The Friedewald equation gave higher LDL-cholesterol levels than N-geneous assay in young Japanese females who had eaten a low-energy meal, and lower values when they had eaten a high-energy meal. Thus, it may be necessary to pay attention to energy of nigh meal prior to blood withdrawal.

Relationship between chronic kidney disease and sleep blood pressure in patients with sleep apnea syndrome

Chronic kidney disease (CKD) is common disease in patients with sleep apnea syndrome (SAS), which is considered to be responsible for secondary and nocturnal hypertension. In this study, we assessed blood pressure (BP) changes in SAS patients with CKD. Of 460 Japanese outpatients with suspected SAS who underwent ambulatory BP monitoring within 3 months of overnight polysomnography, 198 patients (172 males and 26 females) who were not receiving treatment with antihypertensives or nitroglycerin were enrolled. The estimated glomerular filtration rate (eGFR) was calculated, and the patients were stratified into the high (H; eGFR⩾60 ml min−1 per 1.73 m2) or the low (L; eGFR<60 ml min−1 per 1.73 m2) group. The patients in the L group were significantly older than those in the H group (P<0.001), and body mass index was significantly smaller in the L group than in the H group (P=0.025). The rate of patients treated with statin (P=0.030) and the levels of both triglyceride (P=0.006) and creatinine (P<0.001) differed significantly between the two groups. The sleep data, 24-h BP, awake BP and morning BP showed no significant differences between the two groups. However, sleep systolic and diastolic BPs were significantly higher in the L group (122.5±16.7 mm Hg and 81.1±12.2 mm Hg, respectively) than in the H group (117.1±11.8 mm Hg, P=0.033; and 76.1±9.5 mm Hg, P=0.012, respectively). SAS patients with CKD had elevated sleep BP. This result suggests that appropriate treatments for both SAS and CKD prevent sleep BP elevation, which is considered a risk factor for the onset risk of a cardiovascular event.