Effect of Nutrition Education on the Vegetable Intake of Residents in Okinawa.

Background: Increasing vegetable intake is recommended for promoting health in communities. This study investigated the effects of nutrition education on vegetable intake and the factors associated with changes in vegetable intake among residents of Okinawa. Methods and Results: Subjects (n=1,345; mean [±SD] age 56.8±14.6 years; 40.5% male) were recruited from among local residents participating in the Yui Kenko Project. Subjects completed the brief-type self-administered diet history questionnaire (BDHQ) and questionnaires on socioeconomic demographics and social capital. Subjects were divided into 2 groups according to residential area, namely south Okinawa (n=679), where local health promotion activities have been undertaken since the early 2000s, and central Okinawa (n=666). Survey results were fed back to each subject, and health lectures were then conducted at local community centers. After 1 year, the BDHQ was repeated to investigate changes in vegetable and nutritional parameters. After the intervention, residents of south Okinawa increased their crude and energy-adjusted vegetable intake (P<0.05), whereas residents of central Okinawa showed decreased vegetable intake (P<0.05). Univariable and multivariable regression models indicated that, in south Okinawa, participation in local health promotion activities and agreement with general trust were positively correlated with changes in energy-adjusted vegetable intake, whereas in central Okinawa no correlations were observed. Conclusions: The status of social capital should be taken into account when implementing initiatives to increase vegetable intake in communities.

Effects of xanthine oxidase inhibitors on renal function and blood pressure in hypertensive patients with hyperuricemia.

Hyperuricemia may promote the progression of hypertension and renal dysfunction. However, the effects of hyperuricemia treatment on blood pressure and renal function in adult hypertensive patients with hyperuricemia remain unclear. A total of 137 hypertensive patients with hyperuricemia (96 men and 41 women; mean age of 67 years) who recently started taking xanthine oxidase inhibitors (allopurinol or febuxostat) as outpatients were recruited. Serum uric acid level, estimated glomerular filtration rate (eGFR, ml min(-1) per 1.73 m(2)) and blood pressure (mm Hg) were retrospectively compared immediately before and shortly after starting treatment with xanthine oxidase inhibitors. The mean blood pressure and the eGFR immediately before starting treatment were 128/71 mm Hg and 44.6 ml min(-1) per 1.73 m(2), respectively. Although the eGFR decreased from 46.6 to 44.6 ml min(-1) per 1.73 m(2) before starting treatment with xanthine oxidase inhibitors, it increased to 46.2 ml min(-1) per 1.73 m(2) (P=0.001, compared with immediately before treatment) without any significant changes in blood pressure after the administration of xanthine oxidase inhibitors. Multiple regression analysis revealed that the increase in eGFR after starting xanthine oxidase inhibitor treatment positively correlated with the changes in systolic blood pressure and negatively correlated with the changes in uric acid levels and the use of renin-angiotensin system inhibitors. These results suggest that xanthine oxidase inhibitors may delay the progression of renal dysfunction in adult hypertensive patients with hyperuricemia.

Interrelationship between brachial artery function and renal small artery sclerosis in chronic kidney disease.

Chronic kidney disease (CKD), characterized by senile inflammation, is a risk factor for cardiovascular disease. Conduit artery function and small artery structure relate to cardiovascular disease. We examined the correlations, determinants and interrelationships of arterial indices in association with CKD in a cross-sectional study of 139 patients (60% male; mean age 44 years) with CKD (stages 3-5, 39%) who underwent a renal biopsy. Conduit artery function and small artery sclerosis were assessed by brachial artery flow-mediated dilatation (FMD) and semiquantitative evaluation of small artery intimal thickening (SA-IT), respectively. The estimated glomerular filtration rate correlated with FMD (r=0.31, P=0.0002) and inversely correlated with SA-IT (r=-0.54, P<0.0001). Multiple regression analysis showed that FMD was inversely correlated with SA-IT and vice versa. In addition, high-sensitivity C-reactive protein (hs-CRP) was significantly correlated with SA-IT, but not FMD. Multiple logistic analysis revealed that higher hs-CRP concomitant with decreased FMD was further associated with the risk of severe SA-IT compared with their individual effects. These findings suggest that both conduit artery and small artery disease develop with mutual interaction in parallel with decreased kidney function. Coexistence of inflammation and conduit artery dysfunction may be closely related to renal small artery sclerosis in patients with CKD.

Hypertriglyceridemia accompanied by increased serum complement component 3 and proteinuria in non-nephrotic chronic kidney disease.

BACKGROUND: Hypertriglyceridemia (hTG) is a risk factor for progression of chronic kidney disease (CKD); however, it remains unknown whether the adipocytokine complement component 3 (C3) is involved in the association between hTG and CKD. METHODS: The study included 138 patients (54 % male) with non-nephrotic (serum albumin ≥3 g/dl) CKD who had undergone a renal biopsy and did not have hypocomplementemic disease. Renal arteriolopathy was assessed semi-quantitatively. We examined the cross-sectional associations between proteinuria and hTG with or without a higher serum C3 level (hC3), defined as equal or above the median value. RESULTS: The mean (SD) age of the patients was 42 (±17) years and urine protein was 1.2 (±1.2) g/gCr. Patients with hTG had a significantly higher urine protein than those without hTG. Subgroup analysis showed that the hTG+/hC3+ group had higher grade arteriolopathy and urine protein levels. Multiple logistic regression analysis adjusted for age, sex, and diabetes mellitus showed that hC3+ alone was associated significantly with higher levels of urine protein [odds ratio (OR), 2.98; 95 % confidence interval (CI) 1.19-7.46, p = 0.02]; however, hTG alone showed no such association. hTG+/hC3+ was a significant factor when hTG-/hC3- was used as the reference (adjusted OR 5.32; 95 % CI 1.40-20.17, p = 0.01), with this OR being decreased by adjustment for arteriolopathy. CONCLUSIONS: hTG accompanied by hC3 was associated with proteinuria in non-nephrotic CKD. Arteriolopathy may influence this association. A prospective study is needed to determine the predictive value of this association in CKD progression.

An association between uric acid levels and renal arteriolopathy in chronic kidney disease: a biopsy-based study.

Uric acid (UA) can induce renal arteriolopathy in animal models. Whether there is an association between UA and renal arteriolopathy in patients with chronic kidney disease (CKD) is unknown. Here, we examined the cross-sectional association of serum UA levels with renal arteriolar hyalinosis and wall thickening. Arteriolar parameters were assessed by semiquantitative grading (max: grade 3) of arterioles in 167 patients with CKD (mean age, 42.4 years; 86 men and 81 women) who underwent renal biopsy. The mean serum UA level was 6.4 mg dl(-1). We observed hyalinosis in 94 patients (56%) and wall thickening in 119 patients (71%). As the UA level tertile increased, the proportion of higher-grade (grade 2 and 3) hyalinosis and wall thickening increased (hyalinosis, P<0.0001 and wall thickening, P=0.0002, for trend). Multiple logistic analysis adjusted for age ≥40 years, sex, hypertension status, diabetes mellitus status and estimated glomerular filtration rate <60 ml min(-1) per 1.73 m(2) showed that hyperuricemia (UA ≥7 mg dl(-1)) was significantly associated with a higher risk of hyalinosis (adjusted odds ratio: 3.13; 95% confidence interval: 1.23-7.94; P=0.02) and higher-grade (equal to or higher than the mean value) wall thickening (adjusted odds ratio: 2.66; 95% confidence interval: 1.11-6.38; P=0.03). Hence, these results suggest that hyperuricemia may be related to renal arteriolar damage in patients with CKD.

Beneficial effect of switching from a combination of angiotensin II receptor blockers other than losartan and thiazides to a fixed dose of losartan/hydrochlorothiazide on uric acid metabolism in hypertensive patients.

Among the angiotensin II receptor blockers (ARBs), losartan (LOS) has uricosuric action. The clinical benefits of LOS compared with those of other ARBs may be apparent when it is combined with diuretics, which have an unfavorable influence on serum uric acid (SUA). The effects of switching from combinations of ARBs other than LOS and thiazides to a fixed-dose combination comprising 50 mg LOS and 12.5 mg hydrochlorothiazide on blood pressure (BP), SUA, percent fractional excretion of UA (FEUA), and urine pH were assessed in 57 hypertensive outpatients. A significant reduction in BP was observed after 6 months (P < .01). The switching therapy significantly decreased SUA level (6.0 ± 1.3 vs. 5.7 ± 1.3 mg/dL, P < .01), which was accompanied by increases in FEUA (P < .01) and urine pH (P < .01). The change in SUA was negatively correlated with the changes in FEUA (P < .004) and estimated glomerular filtration rate (P < .05). The change in FEUA was positively correlated with the changes in urine pH (P < .05) but not with BP or estimated glomerular filtration rate. In a separate group of patients treated with ARBs other than LOS (n = 82), a significant BP reduction was observed, but no change in SUA or FEUA was observed. In conclusion, switching therapy decreased SUA level, which was accompanied by an increase in FEUA. This result may depend on the balance between LOS-induced inhibitory action of urate transporter 1 and hydrochlorothiazide-induced plasma volume reduction. The increase in urine pH plays a role in UA urinary excretion.

Impaired heart rate baroreflex in older rats: role of endogenous angiotensin-(1-7) at the nucleus tractus solitarii.

Age-related baroreflex reductions in function may originate from central neural dysregulation as well as vascular structural/functional changes. We determined the role of 2 angiotensin (Ang) peptides at the nucleus tractus solitarii in age-related baroreflex impairment. Baroreflex sensitivity control of heart rate in response to increases in blood pressure was tested in younger (3 to 5 months) and older (16 to 20 months) anesthetized male Sprague-Dawley rats before and after bilateral solitary tract injections of the Ang II type 1 (AT1) receptor antagonist candesartan (24 pmol) or the Ang-(1-7) antagonist (D-Ala7)-Ang-(1-7) (144 fmol or 24 pmol). Basal reflex sensitivity of older rats was significantly lower than younger rats. In younger rats, the reflex was facilitated by bilateral candesartan injections and attenuated by bilateral (D-Ala7)-Ang-(1-7) injections. In older rats, the reflex was facilitated by AT1 blockade; however, (D-Ala7)-Ang-(1-7) injected into the solitary tract nucleus had no effect. Neprilysin mRNA in the medulla was lower in older rats compared with younger rats, whereas angiotensin-converting enzyme (ACE), ACE2, and mas receptor mRNA levels of older rats did not differ from values of younger rats. Thus, opposing actions of endogenous Ang II and Ang-(1-7) in the solitary tract nucleus contribute to baroreflex function in response to increases in mean arterial pressure of younger rats. The attenuated counterbalancing effect of Ang-(1-7) on baroreflex function is lost in older rats, which may be attributable to diminished production of the peptide from neprilysin.