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 26,365 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A retrospective study was done in 66 children (0.21% of all admitted children) below the age of 18 years with persistent hypertension diagnosed at the Department of Pediatrics, Faculty of Medicine Siriraj Hospital from Jan 1999 to Dec 2003. Male to female ratio was 1.4:1 with 54.5% aged between 6-12 years old and 9.1% aged less than 1 year. Hypertension was found to be severe (BP more than the 99th percentile for age, sex and height) in 79.1% but most (78.6%) of the patients did not have symptoms related to hypertension. Chronic headaches were found in 10%, hypertensive encephalopathy in 8.6%, epistaxis in 1.4% and visual disturbance in 1.4%. The most common cause of hypertension was renal parenchymal diseases (62.7%) mainly lupus nephritis (26.9%), idiopathic nephrotic syndrome (16.4%) and chronic renal failure (16.4%). Other causes of hypertension included renovascular diseases (7.5%), drug-induced (7.5%), essential (7.5%), tumors (4.5%), coarctation of aorta (3.0%), bronchopulmonary dysplasia (3.0%), and pheochromocytoma (1.5%). Obesity and overweight (body mass index, BMI more than 25) was found in only 10 patients (15.1%). The proportion of children with BMI more than 25 was not different between essential and secondary hypertension (p = 0.15). Left ventricular hypertrophy was noted in 7.5%, hypertensive retinopathy in 3.0%, and hypertensive encephalopathy in 9.0%. One-third of the patients had normal BP within 1 month and another 47.0% had normal BP within 6 months of diagnosis. One-fifth of the patients also needed surgical intervention for specific underlying diseases. The authors suggest that since a large number of children with hypertension have secondary hypertension, intensive investigation and prompt management should be done in all. Obesity and overweight is not reliable in the differentiation between primary and secondary hypertension. Short term outcome of hypertension is good with medications and surgery in selected cases but long term outcome is still unknown.
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PMID:Persistent hypertension in Thai children: etiologies and outcome. 1704 51

Chronic kidney disease coexists with metabolic syndrome and this relationship may be apparent before overt manifestations of cardiovascular disease. To investigate early stages of the natural history of associations between renal function and metabolic syndrome, we phenotyped 1572 young (mean age=18.4 years), apparently healthy men for metabolic risk factors and estimated their creatinine clearance based on the Cockcroft-Gault equation. High metabolic risk (clustering of at least three metabolic risk factors) was revealed in 8.7% (137) of the subjects and was associated with a 6.9-fold increase in the odds of glomerular hyperfiltration (95% confidence interval (CI): 3.9-11.5) when compared to reference (from none to two metabolic risk factors). Overweight, elevated blood pressure, and low high-density lipoprotein (HDL) cholesterol increased the multivariate-adjusted odds ratio of glomerular hyperfiltration to 6.6 (95% CI: 3.8-11.6), 1.8 (95% CI: 1.0-3.0), and 2.5 (95% CI: 1.5-4.3), respectively. Systolic and diastolic blood pressures clustered together with leptin in the factor analysis and this blood pressure-adiposity component correlated with estimated creatinine clearance (r=0.329, P<0.0001) and explained on its own 10.2% of the variance in the estimated renal function. Our data reveal the silent epidemics of metabolic risk among young, apparently healthy men. Furthermore, the results indicate that high metabolic risk is associated with glomerular hyperfiltration before overt manifestations of cardiovascular disease.
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PMID:Glomerular hyperfiltration: a new marker of metabolic risk. 1763 26

This report describes the prevalence and characteristics of people with a family history of ESRD in a first-degree relative (FH-ESRD). This is a cross-sectional study of individuals in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) cohort, a population-based sample of US residents who are 45 yr and older. FH-ESRD was ascertained at baseline among 12,030 participants of the cohort, and multivariate logistic regression was used to identify characteristics that were independently associated with FH-ESRD. FH-ESRD was reported by 9.5% of participants. Individual characteristics that were independently associated with FH-ESRD included black race (odds ratio [OR] 2.14; 95% confidence interval [CI] 1.82 to 2.53); female gender (OR 1.28; 95% CI 1.08 to 1.51); a history of diabetes (OR 1.22; 95% CI 1.02 to 1.47); a 1-SD change in the log of the C-reactive protein level (OR 1.10; 95% CI 1.01 to 1.19); and World Health Organization body mass index weight categories normal (OR 2.11; 95% CI 0.66 to 6.79), overweight (OR 2.64; 95% CI 0.82 to 8.42), and obese (OR 3.48; 95% CI 1.09 to 11.1) compared with underweight. Black but not white individuals with FH-ESRD were more likely to have an estimated GFR <60 ml/min per 1.73 m(2). There is a high prevalence of FH-ESRD among US adults, and the prevalence of FH-ESRD was higher among lack individuals. Individuals with a positive family history were more likely to have diabetes and to be obese. If confirmed, then these findings suggest that individuals with FH-ESRD may benefit from interventions to improve the detection and treatment of chronic kidney disease risk factors such as diabetes and obesity.
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PMID:Prevalence and characteristics of a family history of end-stage renal disease among adults in the United States population: Reasons for Geographic and Racial Differences in Stroke (REGARDS) renal cohort study. 1734 25

The prevalence of obesity worldwide has increased dramatically. Besides, an approximately two-fold higher rate of increase in mean BMI among the incident ESRD has been reported in the US population from 1995-2002. Chronic kidney disease (CKD) prevalence increases from 2.9% among adults with an ideal BMI to 4.5% among obese adults. The development of CKD is usually the culminating result of the interaction of multiple risk factors. Obesity represents one example of a multitoxicity state and given the background of genetic susceptibility and/or reduced nephron number, overweight may initiate renal remodeling and/or accelerate kidney failure. Obesity may be the number one preventable risk factor for CKD. Weight loss has indeed been shown to improve glomerular hemodynamics and reduce urine albumin excretion. Thus, obese patients with CKD should be counseled on the benefits of weight loss.
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PMID:Obesity and kidney disease. 1840 77

With one billion people overweight worldwide, the need to identify risk factors and treatments for obesity is urgent. The present study determined whether rats genetically prone to diet-induced obesity (DIO) show preexisting differences in meal microstructure and are sensitive to central anorectic effects of corticotropin-releasing factor type 2 (CRF(2)) receptor stimulation. Male, selectively bred DIO rats and their diet resistant (DR) counterparts (n = 9/genotype) were weaned onto low-fat chow and compared as young adults for spontaneous or intracerebroventricular urocortin 2 administration-induced (0, 0.3, 1, 3 microg) differences in ingestion. DIO rats were hyperphagic selectively at the dark cycle onset, showing shorter latencies to initiate feeding, faster returns to eating following meal completion, and a lower satiety ratio than DR rats. At other times, DIO rats had briefer postmeal intervals, but ate smaller and briefer meals, resulting in normal intake. DIO rats also ate faster than DR rats. Urocortin 2 was less potent in DIO rats, ineffective at the 0.3 microg dose, but produced CRF(2) antagonist-reversible anorexia at higher doses. Though heavier, chow-maintained DIO rats were proportionately as or more lean than DR rats. Thus, DIO rats showed signs of a preexisting, heritable deficit in the maintenance of postmeal satiety and a reduced sensitivity to anorectic CRF(2) agonist stimulation. The meal patterns of DIO rats temporally resemble human 'snacking' behaviour, which predicts adult obesity. Because central CRF(2) stimulation retains full anorectic efficacy at higher doses in the DIO model, manipulating this neuropeptidergic system might yield new therapeutic approaches for diet-induced obesity.
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PMID:Feeding microstructure in diet-induced obesity susceptible versus resistant rats: central effects of urocortin 2. 1762 84

The number of patients with chronic kidney disease-CKD is still growing. Overweight and obesity present also an important problem of world public health. However, there are not many data showing possible association between obesity and incresing risk of development of renal failure recently it has been demonstrated that in obese patients secondary focal segmental glomerulosclerosis and glomerular hypertrophy appear more frequently. The aim of this study was to estimate glomerular filtration rate-GFR in patients with normal serum creatinine concentration undergoing primary angioplasty according to body mass index. The study included 1413 patients udergoing primary angioplasty for acute myocardial infarction. The following parameters were assessed: age, gender, family history of cardiovascular disease, risk factors of cardiovascular disease (hypertension, diabetes mellitus, obesity etc.), previous myocardial infarction, pre-existing heart failure, treatment given, localization of infarct, coronary stenting, serum creatinine before angioplasty, cholesterol, LDL, HDL, triglycerides, glucose, blood pressure. Of a total of 1413 patients, 1337 (94.62%, 943 M, 394 F) had correct serum creatinine concentration (below 1.5 mg/dl for men, below 1.2 mg/dl for women). Glomerular filtration rate was calculated from serum creatinine levels by using the simplified Modification of Diet in Renal Disease Study formula--MDRD, Cockcroft-Gault equation and Jeliffe formula. An average value of GFR in study group was 79.94 +/- 24.51 ml/min (Cockcroft-Gault equation), 73.02 +/- 21.96 ml/min (Cockcroft-Gault adjusted to weight), 90.37 +/- 25.1 ml/min (MDRD equation) and 77.67 +/- 21.65 ml/min (Jeliffe formula). A significant lower serum creatinine levels and GFR (assessed by 3 formulas and Cockcroft-Gault using adjusted weight) were observed in women group. In the whole study group (with normal serum creatinine levels) substantial correlation was found between age and serum creatinine concentration (r = 0.13, p > 0.001), GFR (MDRD, r = -0.37, p < 0.001, Cockcroft-Gault, r = -0.62, p < 0.001, adjusted to weight r = -0.64, p < 0.001, Jeliffe r = -0.61, p < 0.001) and also between BMI and GFR (MDRD r = 0.28, p < 0.001, Cockcroft-Gault, r = 0.31, p < 0.001, adjusted to weight r = 0.08, p < 0.001, Jeliffe r = 0.341, p < 0.001), but not with serum creatinine concentration (r = 0.03, p = 0.3). In patients with normal serum creatinine levels percentage of patients with GFR below 60 ml/min ranges from 4.79% up to 30.74%. In patients with higher BMI, higher GFR may be partially caused by glomerular hyperfiltration. Overweight or obesity are significant, but potentially changeable risk factors for development of chronic renal failure. However, chronic kidney disease is one of the complications of obesity.
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PMID:[Obesity as a risk factor of chronic kidney disease in patients undergoing primary angioplasty]. 1841 92

TREATMENT OF ARTERIAL HYPERTENSION - Blood pressure (BP) should be regularly measured in all patients with CKD (Strength of Recommendation C). - BP control and proteinuria reduction delay progression of CKD (Strength of Recommendation A) and reduce cardiovascular risk (Strength of Recommendation C). Thus, control of both factors should be the treatment objective. - The BP target in patients with CKD should be < 130/80 mmHg, and 125/75 mmHg if proteinuria is > 1 g/24 hours (Strength of Recommendation A). - Lifestyle changes should be made: low-sodium diet (less than 100 mEq/day of sodium or 2.4 g/day of salt); weight reduction if patient is overweight (body mass index 20-25 kg/m2); regular aerobic physical exercise and moderate alcohol intake for BP control and prevention of cardiovascular risk (Strength of Recommendation A). - The choice of the antihypertensive drug in patients with CKD depends on the etiology of CKD, cardiovascular risk, or presence of clinical or subclinical cardiovascular disease (Strength of Recommendation A). - Two or more antihypertensive drugs are usually required to control blood pressure in patients with CKD (Strength of Recommendation B), and will frequently include a diuretic, which in stages 4-5 should be a loop diuretic (Strength of Recommendation B). - Renin-angiotensin-aldosterone system (RAAS) inhibitors are first choice drugs in patients with diabetic nephropathy, patients with non-diabetic nephropathy with a protein/creatinine ratio higher than 200 mg/g, and patients with heart failure (Strength of Recommendation A). The combination of ACEIs and ARBs is indicated for reducing proteinuria that remains high despite treatment with a RAAS inhibitor, provided potassium levels do not exceed 5.5 mEq/L (Strength of Recommendation B). - When RAAS blockers are started or their dose is changed in patients with advanced CKD, kidney function and serum potassium levels should be monitored at least after 1-2 weeks. DIAGNOSIS AND TREATMENT OF DYSLIPIDEMIA - A complete evaluation of the lipid profile including total cholesterol, LDL-C, HDL-C, and triglycerides should be performed in any patient with CKD at baseline and at least annually (Strength of Recommendation B). - In patients with stage 4-5 CKD and LDL-C >or= 100 mg/dL, treatment to decrease levels to < 100 mg/dL should be considered because of their high CV risk. This reduction is recommended in secondary prevention and in primary prevention in diabetic patients. Lipid-lowering treatment is recommended in all other patients, although no evidence showing its benefits is available yet (Strength of Recommendation C). - In patients with stage 4-5 CKD and triglyceride levels >or= 500 mg/dL which are not corrected by treating the underlying cases, treatment with triglyceride-lowering drugs may be considered to reduce the risk of pancreatitis. However, treatment with fibrates should be used with caution, and these drugs should not be associated to statins due to the risk of rhabdomyolysis (Strength of Recommendation C). There is little experience on the efficacy and safety of omega-3 fatty acids for the treatment of hypertriglyceridemia in patients with grade 4-5 CRF, but they may be considered a possibly safer alternative to fibrates (Strength of Recommendation C). SMOKING - Smoking is a cardiovascular risk factor and a risk factor for progression of kidney disease in patients with CRF (Strength of Recommendation B). - Use of active measures to achieve smoking cessation is recommended in patients with CRF (Strength of Recommendation C). HOMOCYSTEINE - Hyperhomocysteinemia has been postulated as a cardiovascular risk factor in the general population and in kidney patients, but the available evidence is not consistent. - There is no evidence that vitamin therapy decreases cardiovascular risk in patients with CRF, and recommendation of routine vitamin measurement and start of vitamin therapy to reduce cardiovascular risk in these patients is therefore questionable (Strength of Recommendation B). LEFT VENTRICULAR HYPERTROPHY - Left ventricular hypertrophy (LVH) is a cardiovascular risk factor in patients with CRF (Strength of Recommendation B). - It is advisable to perform an echocardiogram at baseline and every 12-24 months and to consider treatments allowing for LVH regression (Strength of Recommendation C). The approach to LVH should be early and multifactorial because its reversibility is limited once established (Strength of Recommendation C). - RAAS blockade with ACEIs or ARBs partially reverts LVH in patients with CRF (Strength of Recommendation B). ANTI-PLATELET AGGREGATION - Because of the high cardiovascular risk in patients with CKD, anti-platelet aggregant therapy, especially low-dose aspirin, would be indicated in patients with type 2 diabetes as primary prevention, and in all patients with CKD as secondary prevention. There is however no evidence of the benefits of anti-platelet aggregant therapy in primary prevention in patients with CKD, particularly in stages 4-5; indication for treatment in this situation should therefore be individualised because of its greater risk of bleeding. - Adequate good blood pressure control should previously be achieved to minimise the risk of haemorrhagic stroke (Strength of Recommendation C).
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PMID:[Arterial hypertension and dyslipidemia in patients with chronic kidney disease (CKD). Anti-platelet aggregation. Goal oriented treatment]. 1901 37

Obesity is highly prevalent in African Americans and is associated with increased risk of End-Stage Renal Disease (ESRD) and death. It is not known if the effect of obesity is similar among blacks and whites. The aim of this study is to examine racial differences in the association of obesity with ESRD and survival in elderly patients (age >65). Data were obtained for 74,167 Medicare patients with acute myocardial infarction (AMI) between February 1994 and July 1995. BMI was calculated as weight (kg) divided by height (m(2)). We evaluated the association of BMI class with ESRD incidence and death using multivariable Cox proportional hazards models, testing for race-BMI interactions. Compared to whites, African Americans had higher BMI (26.9 vs. 26.0, P < 0.0001) and estimated glomerular filtration rate (72.4 ml/min/1.73 m(2) vs. 66.6 ml/min/1.73 m(2), P < 0.0001). Crude ESRD rates increased with increasing obesity among whites but not among blacks. However, after adjusting for age, sex, and other comorbidities, obesity was not associated with increased ESRD rate among blacks or whites and the interaction between race and BMI was not significant. Furthermore, for both races, patients classified as overweight, class 1 obese, or class 2 obese had similar, significantly better survival abilities compared to normal weight patients and the race BMI interaction was not significant. In conclusion, obesity does not increase risk of ESRD among black or white elderly subjects with cardiovascular disease (CVD). However, both obese blacks and whites, in this population, experience a survival benefit. Further studies need to explore this obesity paradox.
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PMID:Obesity, end-stage renal disease, and survival in an elderly cohort with cardiovascular disease. 1932 42

The aim of this study was to analyse whether Physical Activity Index (PAI), Physical Fitness, Screen Time (watching TV and computer use), Socio-economic Status and Commuting to School made a significant contribution to longitudinal changes in Body Mass Index (BMI) in youth. This longitudinal study was carried out over a period of 3 years with 345 students (147 boys) who were between 11 and 16 years old at the beginning of the study. Students were invited to perform tests from FITNESSGRAM Battery for Curl-Ups, Push-Ups, Back-Saver Sit and Reach, and 20 m Shuttle-Run (CRF). Fitness tests were categorized in "Healthy Zone" (HZ) and "Under Healthy Zone" (UHZ), PAI in "less active" and "active"; Socio-economic Status, in low, middle and high education level, and Commuting in active and passive. BMI was corrected for age and gender meaning that we subtracted the age-and-sex-specific cut points for overweight. Corrected body mass index was used as dependent variable in a Linear Mixed Model. The main result was the strong positive and independent association of individuals with CRF performances UHZ with corrected body mass index. In conclusion, the results of this longitudinal study showed markedly an important relationship of lower fitness levels with the risk of being overweight/obese, in particular CRF and abdominal strength.
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PMID:A 3-year longitudinal analysis of changes in Body Mass Index. 2002 39

There is now solid knowledge for associating overweight and obesity with CKD. The risk for ESRD is progressively higher at increasing body mass index (BMI) levels and in extremely obese individuals such risk is 5 times higher than that in persons with normal body mass. Visceral fat, insulin resistance and inflammation are nicely inter-correlated in cross sectional studies in CKD patients but it is still untested whether the association between waist circumference or waist-hip ratio and CKD underlies a causal connection. Notwithstanding knowledge on the quantitative relationship between risk factors implicated in kidney damage is still limited, evidence derived from clinical series in patients with various renal diseases (IgA nephropathy, renal agenesia or post-nephrectomy) supports the hypothesis that obesity is an important factor in the progression and perhaps even in the initiation of CKD. Hyperfiltration is commonly found in obese persons. Due to high sympathetic activity, high levels of angiotensin II and hyperinsulinemia, obese persons display enhanced sodium reabsorption in the proximal tubule and are unable to rapidly increase sodium excretion. Enhanced proximal salt reabsorption determines a reduced delivery of sodium to the macula densa and therefore promotes afferent vasodilatation and enhanced renin synthesis. As a result of high local angiotensin II levels, the efferent arteriole is constricted in the obese. Glomerulomegaly and focal glomerulosclerosis represent the anatomical counterparts of glomerular hyperfiltration-hypertension. Hyperfiltration apart, evidence is emerging that inflammatory cytokines produced by fat cells trigger inflammation in the kidney and that this mechanism contributes to reduce renal function in the obese.
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PMID:Overweight, obesity and metabolic alterations in chronic kidney disease. 2008 47


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