Iodine Nutritional Status and Related Factors among Chinese School-Age Children in Three Different Areas: A Cross-Sectional Study.

We evaluated the iodine nutritional status and related factors among school-age children based on the 2016 National Nutrition and Health Surveillance of Children and Lactating Women; 3808 children from Hebei, Guangxi, and Zhejiang province were included in the study. Urinary iodine concentration (UIC), thyroid-stimulating hormone (TSH), body mass index (BMI), vitamin A (VA), and vitamin D (VD) were measured. The abnormal rate of UIC and TSH were assessed. Relationships between UIC/TSH and the possible factors were analyzed. The overall median UIC was 185.14 µg/L, and the median UIC of children aged 8-10 was 164.60 µg/L. Prevalence of iodine deficiency and excess was 13.84% and 14.36%, respectively, and 12.87% of children showed TSH excess. UIC, as well as the abnormal rates of iodine deficiency (ID) and TSH, were significantly different among the three provinces. The median UICs and excess rates increased with age, reaching 211.45 µg/L and 21.35% at age of 14~, while TSH showed the opposite trend. Overweight children tended to have lower UIC and higher TSH. Higher UIC and TSH were found in VA sufficient group (p < 0.01). Further, the VD deficient group had a higher TSH compared to the sufficient group (p < 0.01). Moreover, UI and TSH distribution was obviously different among different vitamin A/D status (p < 0.05). Although the median UIC of school-age children was optimal, there were pockets of inadequate and excessive UI in the three provinces. Compared to the national IDD monitoring results in 2014, the iodine nutritional status of children was greatly improved. Considerations of region, age, BMI, VA, or VD are needed in the future iodine evaluation and surveillance.

Orthostatic proteinuria: an overestimated phenomenon?

BACKGROUND: Although orthostatic proteinuria (OP) is the most common cause of childhood proteinuria, excluding transient proteinuria, data regarding prevalence and long-term prognosis are limited. We aimed to determine prevalence of OP in healthy schoolchildren evaluating relationships with age, gender and body mass index, and determine follow-up. METHODS: A total of 1701 healthy children aged 6-15 years were selected using a population-based, stratified, cluster-sampling method; and random urine samples were taken. For proteinuria ≥ 1+ in first urine samples, second and third random samples were taken at least 2 weeks apart to exclude transient proteinuria. For continuing proteinuria after third samples, first morning urine samples were collected. Cases where proteinuria was not detected in first morning urine samples were diagnosed as OP. RESULTS: Sixty-four of 1701 children (3.7%) had proteinuria on first random urine samples. After second and third urine samples, proteinuria persisted in only 16 (0.94%). OP was detected in 11 (0.65%). Prevalence of OP tended to decrease with increasing BMI, though not statistically significant. All 7 cases with OP who were re-evaluated later, had no proteinuria 3 years after diagnosis. CONCLUSIONS: Prevalence of OP in our study was lower than the literature. At least three random urine samples should be taken to exclude transient proteinuria in an asymptomatic child/adolescent before making a diagnosis of OP using first morning urine samples. OP is a benign condition and resolves spontaneously in most cases. Underweight children had a tendency for OP compared with overweight and obese children; however, further studies with larger number of patients are needed.

Exposure of Portuguese children to the novel non-phthalate plasticizer di-(iso-nonyl)-cyclohexane-1,2-dicarboxylate (DINCH).

Di-(iso-nonyl)-cyclohexane-1,2-dicarboxylate (DINCH) is used as substitute for high molecular weight phthalate plasticizers such as di-(2-ethylhexyl) phthalate (DEHP) and di-(iso-nonyl) phthalate (DINP). Due to a rapid substitution process we have to assume omnipresent and increasing DINCH exposures. The aim of this study was to evaluate DINCH exposure in 112 children (4-18years old) from Portugal, divided in two groups: 1) normal-/underweight following the usual diet; and 2) obese/overweight but under strict nutritional guidance. First morning urine samples were collected during the years 2014 and 2015. Oxidized DINCH metabolites (OH-MINCH, oxo-MINCH, cx-MINCH) were analyzed after enzymatic hydrolysis via on-line HPLC-MS/MS with isotope dilution quantification. We detected DINCH metabolites in all analyzed samples. Urinary median (95th percentile) concentrations were 2.14µg/L (15.91) for OH-MINCH, followed by 1.10µg/L (7.54) for oxo-MINCH and 1.08µg/L (7.33) for cx-MINCH. We observed no significant differences between the two child-groups; only after creatinine adjustment, we found higher metabolite concentrations in the younger compared to the older children. Median (95th percentile) daily DINCH intakes were in the range of 0.37 to 0.76 (2.52 to 5.61) µg/kg body weight/day depending on calculation model and subpopulation. Body weight related daily intakes were somewhat higher in Group 1 compared to Group 2, irrespective of the calculation model. However, in terms of absolute amounts (µg/day), DINCH intakes were higher in Group 2 compared to Group 1. In regard to age, we calculated higher intakes for the younger children compared to older children, but only with the creatinine-based model. This new data for southern European, Portuguese children adds information to the scarce knowledge on DINCH, confirming omnipresent exposure and suggesting higher exposures in children than adults. Significant sources and routes of exposure have yet to be unveiled. For now, all calculated daily intakes are far below established health benchmark levels (TDI, RfD). However, rapidly increasing exposures have to be expected over the next years.

Daily intake of bisphenol A and triclosan and their association with anthropometric data, thyroid hormones and weight loss in overweight and obese individuals.

Bisphenol A (BPA) and triclosan (TCS) were determined in urine of Belgian overweight and obese (n=151) and lean (n=43) individuals. After the first urine collection (0M), obese patients started a diet program or have undergone bariatric surgery. Hereafter, three additional urine samples from obese patients were collected after 3 (3M), 6 (6M) and 12 (12M) months. Both compounds were detected in >99% of the samples. BPA had median concentrations of 1.7 and 1.2ng/mL in obese and lean groups, respectively, while TCS had median concentrations of 1.5 and 0.9ng/mL in the obese and lean groups, respectively. The obese group had higher urinary concentrations (ng/mL) of BPA (p<0.5), while no significant differences were found for TCS between the obese and lean groups. No time trends between the different collection moments were observed. The BPA concentrations in the obese group were negatively associated with age, while no gender difference or relationship with body mass index was observed. For TCS, no relationships with gender, BMI, or age were found. The temporal variability of BPA and TCS was assessed with calculation of the intraclass correlation coefficient, Spearman rank correlation coefficients, and surrogate category analysis. We observed evidence that single spot urine samples might be predictive of exposure over a longer period of time. Dietary intakes of BPA and TCS did not differ significantly among the time points considered after obese individuals started losing weight (6 and 12months). Multiple linear regression analyses after adjusting for age and weight loss revealed negative associations between urinary TCS and serum FT4 in the 0M and 3M female obese individuals and positive associations between urinary BPA and serum TSH in the lean group.

The body composition and excretory burden of lean, obese, and severely obese individuals has implications for the assessment of chronic kidney disease.

Obesity could affect associations between creatinine generation, estimated body surface area, and excretory burden, with effects on chronic kidney disease assessment. We therefore examined the impact of obesity on the performances of estimated glomerular filtration rate (eGFR), the urine albumin:creatinine ratio (ACR), and excretory burden in 3611 participants of the Chronic Renal Insufficiency Cohort. Urine creatinine excretion significantly increased with body mass index (BMI) (34 and 31% greater at 40 kg/m(2) or more versus the normal of 18.5-25 kg/m(2)) in men and women, respectively, such that patients with a normal BMI and an ACR of 30 mg/g had the same 24-h albuminuria as severely obese patients with ACR 23 mg/g. The bias of eGFR (referenced to body surface area-indexed iothalamate (i-)GFR) had a U-shaped relationship to obesity in men but progressively increased in women. Nevertheless, obesity-associated body surface area increases were accompanied by a greater absolute (non-indexed) iGFR for a given eGFR, particularly in men. Two men with eGFRs of 45 ml/min per 1.73 m(2), height 1.76 m, and BMI 22 or 45 kg/m(2) had absolute iGFRs of 46 and 62 ml/min, respectively. The excretory burden, assessed as urine urea nitrogen and estimated dietary phosphorus, sodium, and potassium intakes, also increased in obesity. However, obese men had lower odds of anemia, hyperkalemia, and hyperphosphatemia. Thus, for a given ACR and eGFR, obese individuals have greater albuminuria, absolute GFR, and excretory burden. This has implications for chronic kidney disease management, screening, and research.

Fasting-induced reductions in cardiovascular and metabolic variables occur sooner in obese versus lean mice.

It is not uncommon for laboratory animals to be fasted prior to experimentation. Fasting evokes marked reductions in heart rate (HR), blood pressure (BP), heat production and oxygen consumption (VO(2)) in rodents. Mice with diet-induced obesity exhibit elevated HR and BP, and lower VO(2) and heat production in the fed condition versus their lean counterparts. It is unknown whether body composition alters the tempo of response to fasting. We tested the hypothesis that cardiovascular and metabolic responses to fasting are delayed in obese versus lean male C57BL/6J mice. In the fed condition, mice that consumed high-fat (HF, 45% fat) chow for 98 ± 5 days had elevated (P < 0.05) body fat percentage (DEXA), serum leptin (ELISA), HR and BP (72-h biotelemetry), and lower (P < 0.05) heat production and VO(2) (72-h metabolic chamber) versus animals that consumed standard chow (CON, 10% fat; n = 16 per group). HR, BP, VO(2), heat production and serum leptin decreased (all P < 0.05) in response to a 16-h fast (16:00-08:00 h) in both groups. Although the overall fold changes in cardiovascular and metabolic parameters were similar in magnitude among animals, fasting-induced reductions in cardiovascular and metabolic variables occurred ∼4 and ∼7 h earlier (P < 0.05), respectively, in HF versus CON mice. These findings indicate that while metabolic and cardiovascular stress evoked by a 16-h fast at 22°C is not different between HF and CON mice, fasting-induced responses occur sooner in obese animals.

Estimating aminoglycoside clearance and creatinine clearance in underweight patients.

PURPOSE: An adjustment factor (AF) was developed and evaluated to determine the best method for estimating aminoglycoside clearance (CL(amino)) and creatinine clearance (CL(cr)) in underweight patients. METHODS: This study was a retrospective, multicenter, chart analysis of aminoglycoside pharmacokinetic data obtained between January 2000 and August 2006 at the University of Southern California University Hospital and Cedars-Sinai Medical Center. Adult patients were included in this study if they had received inpatient aminoglycoside therapy, were at least 60 inches tall, and were at least 10% below their ideal body weight (IBW). CL(cr) and CL(amino) were estimated and compared to actual CL(amino) using the Cockcroft-Gault equation with actual serum creatinine (SCr) (CG(SCr)), Cockcroft-Gault equation with SCr rounded to 1 mg/dL (CG(rnd)), and Cockcroft-Gault equation multiplied by an AF (CG(AF)). Results An AF of 0.69 was determined from 52 patients and tested in 53 separate patients. The CG(AF) method was more precise and less biased than the CG(SCr) equation; the CG(rnd) equation was less biased than the CG(SCr) equation; the CG(AF) method was more precise and less biased than the CG(rnd) equation, but this difference was not statistically significant. In underweight patients with an SCr concentration of > or = 1 mg/dL, the CG(AF) method had less bias compared with the CG(SCr) equation. CONCLUSION: Both the CG(rnd) and CG(AF) methods of predicting CL(amino) in underweight patients were superior to the CG(SCr) equation. The CG(AF) method was more accurate in patients exhibiting greater differences between IBW and actual body weight.

Regulation of angiotensin II type I receptor (AT1R) protein levels in the obese Zucker rat kidney and urine.

Increased renal expression of the angiotensin II, type-1 receptor (AT1R) has been associated with increased blood pressure (BP) and progression of renal disease. We tested whether common medications used to treat hypertension and the metabolic syndrome alter renal AT1R; and whether urine AT1R can be used as a reasonable noninvasive marker of renal levels in the obese Zucker rat, a model for human metabolic syndrome. Immunoblotting revealed that renal and urinary levels of AT1R were significantly higher in obese versus lean rats and correlated (R = 0.62, p < 0.05). Chronic treatment with BP lowering, candesartan, an AT1R antagonist, increased renal levels of AT1R in both lean (282% of lean controls) and obese (178% of obese controls) rats, but decreased urine AT1R levels in obese rats (72% of obese controls). Similarly, chronic treatment with rosiglitazone (RGZ), a peroxisome proliferator activated receptor (subtype gamma) agonist, significantly decreased urine (43% of obese controls) but not renal AT1R (105%) in obese rats. Blood pressure, measured by radiotelemetry, was significantly correlated in untreated and RGZ-treated rats to renal AT1R (R = 0.57, p = 0.0035). Finally, high- (4%) and medium- (0.4%) NaCl diets increased excretion of AT1R in obese rats to approximately 400% of low- (0.04%) NaCl diet. This effect was markedly blunted in lean rats. Overall, we demonstrate increased renal AT1R levels in obese rats. Urine AT1R correlated with renal levels only in the untreated state. Relative salt-sensitivity of AT1R excretion in obese, relative to lean rats, may have implications for both BP and renal disease in the metabolic syndrome.

Urinary beta2-microglobulin as a possible sensitive marker for renal injury caused by tenofovir disoproxil fumarate.

Tenofovir disoproxil fumarate (TDF) is renally excreted by a combination of glomerular filtration and active tubular secretion, and its renal safety profiles have been reported based on a limited increase of serum creatinine (sCr) levels. However, renal tubular function has not previously been well monitored. We measured sCr and urinary beta2-microglobulin (U-beta2MG) levels cross-sectionally in 70 patients treated with TDF [TDF+] and 90 patients on other antiretroviral therapy who had never been exposed to TDF [TDF-]. The mean U-beta2MG was significantly higher in TDF+ patients than that in TDF- patients (p < 0.0001), though no statistical difference was detected in their creatinine clearance estimated by using the Cockcroft-Gault equation. Multivariate analysis showed that coadministration of boosted lopinavir (LPV) and patients' body weight were associated with U-beta 2MG levels in TDF+ patients. U-beta2MG levels were significantly higher in those who also received boosted LPV [TDF+LPV+] (p = 0.0007), and abnormally high levels were noted in 67.7% of them. Furthermore, in the TDF+LPV+ group, U-beta2MG levels showed significant negative correlation with patients' body weight (p = 0.0029) and abnormal U-beta2MG was observed in all six patients with body weight less than 55 kg. In four patients, a rapid fall in U-beta2MG occurred after cessation of TDF. Relative to sCr, U-beta2MG could be a more sensitive marker of renal tubular injury caused by TDF. Boosted LPV co-administration and low body weight may be risk factors for TDF-induced renal tubular dysfunction, probably because these factors are associated with an increase in TDF concentration.

Sex and body-type interactions in the regulation of renal sodium transporter levels, urinary excretion, and activity in lean and obese Zucker rats.

BACKGROUND: Female humans and rodents are relatively protected against the development of hypertension and renal disease. Whether this protection is modified during insulin resistance and obesity, however, is not known. OBJECTIVE: Because renal sodium reabsorption has a central role in determining blood pressure, we hypothesized that lean female rats would bave reduced renal expression, activity, and urinary excretion of 8 major sodium transporters/channels. METHODS: Lean and obese, male and female Zucker rats (n = 4-8 per group) were fed progressively higher levels of dietary NaCl over a period of 54 days. Urinary excretion of renal sodium transport proteins was determined for 3 different dietary levels (0.04%, 0.4%, and 4%) of NaCl. With the high-NaCl diet, natriuretic responses to benzamil, furosemide, and thiazide were used as in vivo markers for activity of the epithelial sodium channel (ENaC), the bumetanide-sensitive Na-K-2C1 cotransporter (NKCC2), and the thiazide-sensitive NaCl cotransporter (NCC), respectively. RESULTS: Female rats (of both body types) had lower plasma renin activity and insulin levels than their male counterparts. Likewise, immunoblotting revealed female rats had increased whole kidney abundance of NCC and of the alpha, beta, and gamma subunits of ENaC, as well as decreased abundance of the type 3 sodium hydrogen exchanger (NHE3), type 2 sodium phosphate cotransporter (NaPi-2), and alpha-1 sodium-potassium-adenosine triphosphatase (Na-K-ATPase), compared with males. Obese rats had reduced levels of NKCC2, NHE3, and gamma-ENaC, but higher levels of NaPi-2 and NCC. Urine excretion of sodium transporters in lean female rats was nearly undetectable, whereas obese rats of both sexes excreted markedly more NKCC2 and NCC, which agreed with greater natriuretic responses to thiazide and furosemide. CONCLUSIONS: Obese female rats are similar to lean female rats with regard to the sex-distinct pattern of renal sodium transporters. However, obese female rats are more like obese male rats with regard to increased natriuretic response tofurosemide and thiazide, and to urine excretion of several transporters including NCC. Our results suggest that, with obesity, there is some loss of the protective female advantage.

Urinary albumin excretion in lean, overweight and obese glucose tolerant individuals: its relationship with dyslipidaemia, hyperinsulinaemia and blood pressure.

The presence of microalbuminuria has become an important tool for therapeutic intervention. In this study we investigated whether the dysmetabolic syndrome of obesity was associated with or could occur in the absence of microalbuminuria. The study was conducted in 71 clinically healthy, glucose tolerant Hispanics (age: 43 +/- 1.4 years, body mass index (BMI): 28.7 +/- 0.6 kg/m(2), systolic blood pressure (SBP): 117 +/- 2 mm Hg, diastolic blood pressure (DBP): 77 +/- 1.3 mm Hg, urinary albumin excretion: 10.2 +/- 0.6 mg/24 h). Subjects were classified as lean (BMI <25), overweight (BMI >25 <30) and obese (BMI >30 kg/m(2)). Greater BMI was associated with higher body weight, waist-to-hip ratio (WHR), BP, fasting insulin, triglyceride, post glucose load insulin and glucose, and lower high-density lipoprotein (HDL) cholesterol levels. However, no significant differences in the urinary albumin excretion (mg/24 h) were found between lean (9.0 +/- 0.9; median: 9.1), overweight (11.3 +/- 1.2; median: 10.5) and obese (11.1 +/- 1.2; median: 9.7) subjects. In addition, microalbuminuria (urinary albumin excretion >30 mg/24 h) was not found in any of the study subjects. For all subjects combined, as well as for each of the groups separately, the urinary albumin excretion was unrelated to the BMI, WHR, body weight, triglyceride, cholesterol (total, LDL or HDL), fasting or post-load glucose and insulin plasma concentrations. Neither in females nor in males, abdominal fat accumulation was associated with an increase in the urinary albumin excretion. However, in the obese groups, urinary albumin excretion was strongly related to the level of SBP (r(2): 0.67; P < 0.0001) and DBP (r(2): 0.55; P < 0.0001). In summary, obesity, hyperinsulinaemia and dyslipidaemia per se are not determinants of increased albumin excretion. However, in the obese subjects, the BP, particularly the SBP, was a strong determinant of the level of albumin in the urine. Microalbuminuria may occur later in the course of the dysmetabolic syndrome, due to worsening of hypertension and development of hyperglycaemia.