The present study evaluated the reliability of equations using spot urine (SU) samples in the estimation of 24-hour urine sodium excretion (24-HUNa). Equations estimating 24-HUNa from SU samples were derived from first-morning SU of 101 participants (52.4 ± 11.1 years, range 24–70 years). Equations developed by us and other investigators were validated with SU samples from a separate group of participants (n = 224, 51.0 ± 10.9 years, range 24–70 years). Linear, quadratic, and cubic equations were derived from first-morning SU samples because these samples had a sodium/creatinine ratio having the highest correlation coefficient for 24-HUNa/creatinine ratio (r = 0.728, p < 0.001). In the validation group, the estimated 24-HUNa showed significant correlations with measured 24-HUNa values. The estimated 24-HUNa by the linear, quadratic, and cubic equations developed from our study were not significantly different from measured 24-HUNa, while estimated 24-HUNa by previously developed equations were significantly different from measured 24-HUNa values. The limits of agreement between measured and estimated 24-HUNa by six equations exceeded 100 mmol/24-hour in the Bland-Altman analysis. All equations showed a tendency of under- or over-estimation of 24-HUNa, depending on the level of measured 24-HUNa. Estimation of 24-HUNa from single SU by equations as tested in the present study was found to be inadequate for the estimation of an individual’s 24-HUNa.
Background and ObjectivesWe estimated the prevalence of hypertension and hypertension subtypes in a large semi-urban city in Korea, using 24-hour ambulatory blood pressure monitoring (ABPM) in a randomly selected sample population.Subjects and MethodsA random sample (aged 20-65 years) from a city with an adult population of approximately 600000 was selected by using a list-assisted random digit dialing method. The 24-hour ABPM and conventional blood pressure measurement (CBPM) of these individuals were obtained.ResultsAmong the 496 participants, valid 24-hour ABPM and CBPM were obtained from 462 (93%) individuals. The estimated prevalence of hypertension in Goyang was 17.54% by CBPM and 32.70% by 24-hour ABPM (p<0.01). In the age stratified analysis, both CBPM and 24-hour ABPM showed increased prevalence of hypertension with age. The estimated prevalence of masked hypertension was 16.22% and that of white-coat hypertension was 1.08%. Men had a higher prevalence of masked hypertension than women (20.79% vs. 11.86%, p=0.0295). The estimated prevalence of masked hypertension was 17.5%, 20.58%, 24.34%, and 13.29% in the age categories of 30s, 40s, 50s, and 60s, respectively. The estimated prevalence of masked uncontrolled hypertension was 26.79% in patients with hypertension who were taking antihypertensive medications.ConclusionThe estimated prevalence of hypertension by 24-hour ABPM was higher than that by CBPM, revealing high prevalence of masked hypertension. The high prevalence of masked hypertension supports the adoption of ABPM in the national population survey and clinical practice to improve public health and reduce health care costs.
The authors developed an equation to estimate 24-hour urine sodium (24HUNa) using the average of three spot urine (SU) samples (morning-first, morning, and evening) from 74 individuals and validated this equation using the average of three SU samples (morning-first, daytime, and evening) from 174 additional individuals. Compared with previously published equations using a single SU sample, the currently developed equation using the average of three SU samples showed much lower bias from measured 24HUNa (À2.9 vs >10 mmol/ 24 h). The intraclass and concordance correlation coefficients of the proposed equation using the average of three SU samples were 0.909 and 0.832, respectively. The limits of agreement were À64.1-58.3 mmol/24 h and approximately 100 mmol/24 h for the currently developed and previously published equations, respectively. All equations showed a tendency to overestimate or underestimate 24HUNa in a manner dependent on the level of 24HUNa but irrespective of the number of SU samples considered. Nonetheless, among the currently tested equations, our equation using the average of three SU samples provided the best estimation of 24HUNa at a population level.
Kidney fibrosis has been accepted to be a common pathological outcome of chronic kidney disease (CKD). We aimed to examine serum levels and tissue expression of chemokine (C-C motif) ligand 8 (CCL8) in patients with CKD and to investigate their association with kidney fibrosis in CKD model. Serum levels and tissue expression of CCL8 significantly increased with advancing CKD stage, proteinuria level, and pathologic deterioration. In Western blot analysis of primary cultured human tubular epithelial cells after induction of fibrosis with rTGF-β, CCL8 was upregulated by rTGF-β treatment and the simultaneous treatment with anti-CCL8 mAb mitigated the rTGF-β-induced an increase in fibronectin and a decrease E-cadherin and BCL-2 protein levels. The antiapoptotic effect of the anti-CCL8 mAb was also demonstrated by Annexin V/propidium iodide staining assay. In qRT-PCR analysis, mRNA expression levels of the markers for fibrosis and apoptosis showed similar expression patterns to those observed by western blotting. The immunohistochemical analysis revealed CCL8 and fibrosis- and apoptosis-related markers significantly increased in the unilateral ureteral obstruction model, which agrees with our in vitro findings. In conclusion, CCL8 pathway is associated with increased risk of kidney fibrosis and that CCL8 blockade can ameliorate kidney fibrosis and apoptosis.
The present study evaluated the response of blood pressure (BP) by dietary sodium in sodium resistant (SR) subjects. One hundred one subjects (mean age, 46.0 yr; 31 hypertensives) were admitted and given low sodium-dietary approaches to stop hypertension (DASH) diet (LSD, 100 mM NaCl/day) for 7 days and high sodium-DASH diet (HSD, 300 mM NaCl/day) for the following 7 days. On the last day of each diet, 24 hr ambulatory BP was measured. Morning systolic BP (SBP) and diastolic BP (DBP) were elevated after HSD in all subjects (P < 0.01), but daytime SBP and DBP were not changed (P > 0.05). In hypertensive subjects, morning DBP elevation was greater than daytime DBP elevation (P = 0.036), although both DBPs were significantly elevated after HSD. The augmented elevation of morning DBP in hypertensive subjects was contributed by the absolute elevation of morning DBP (P = 0.032) and relative elevation to daytime DBP (P = 0.005) in sodium resistant (SR) subjects, but not by sodium sensitive subjects. Although there was no absolute elevation, SR subjects with normotension showed a relative elevation of morning SBP compared to daytime SBP change after HSD (P = 0.009). The present study demonstrates an absolute and relative elevation of morning BP in SR subjects by HSD.
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