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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autopsy findings in a 39-year-old male gorilla included aortic dissection, internal rupture of the aortic arch with axial direction of the tear, external rupture of the ascending aorta, cardiac tamponade, myocardial hypertrophy, cystic and basophilic degeneration of the aortic media, marked obesity, severe degenerative joint disease, focal glomerulonephritis, and widespread hemosiderosis.
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PMID:Aortic dissection in a gorilla. 374 87

Experimental evidence suggests a role for obesity in the formation and progression of some glomerular lesions, but data for human glomerulonephritis are lacking. In a cohort of 162 incident patients with biopsy-proven immunoglobulin A (IgA) nephropathy, we assessed whether the presence of an elevated body mass index (BMI >/= 25 kg/m(2)) at the time of the first renal biopsy (RB1) correlated with clinical data at RB1 (24-hour proteinuria, arterial hypertension, and renal function), pathological data (global optical score [GOS] with detailed pathological indices), and clinical progression to both arterial hypertension and chronic renal failure (CRF). In both univariate and multivariate analyses, the presence of an elevated BMI at RB1 was significantly associated with the severity of pathological renal lesions (GOS and vascular, tubular, and interstitial indices). Hypertension-free survival was significantly less in overweight patients (P: < 0.0001) compared with those with normal weight. In a Cox regression analysis for hypertension-free survival including 24-hour proteinuria greater than 1 g, GOS, and metabolic parameters, only elevated BMI and GOS were independent factors for the development of arterial hypertension. CRF-free survival was also significantly less in patients with an excessive BMI. In a multivariate Cox regression analysis for CRF-free survival, hypertension, GOS, and BMI at RB1 were independent risk factors for CRF. In IgA nephropathy, excessive body weight and/or BMI are underestimated predictive factors for the development of arterial hypertension and, ultimately, CRF.
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PMID:Excessive body weight as a new independent risk factor for clinical and pathological progression in primary IgA nephritis. 1127 71

The insulin resistance syndrome (syndrome X, metabolic syndrome) has become the major health problem of our times. Associated obesity, dyslipidemia, atherosclerosis, hypertension, and type 2 diabetes conspire to shorten life spans, while hyperandrogenism with polycystic ovarian syndrome affect the quality of life and fertility of increasing numbers of women. Whereas a growing number of single genetic diseases affecting satiety or energy metabolism have been found to produce the clinical phenotype, strong familial occurrences, especially in racially prone groups such as those from the Indian subcontinent, or individuals of African, Hispanic, and American Indian descents, together with emerging genetic findings, are revealing the polygenetic nature of the syndrome. However, the strong lifestyle factors of excessive carbohydrate and fat consumption and lack of exercise are important keys to the phenotypic expression of the syndrome. The natural history includes small for gestational age birth weight, excessive weight gains during childhood, premature pubarche, an allergic diathesis, acanthosis nigricans, striae compounded by gynecomastia, hypertriglyceridemia, hepatic steatosis, premature atherosclerosis, hypertension, polycystic ovarian syndrome, and focal glomerulonephritis appearing increasingly through adolescence into adulthood. Type 2 diabetes, which develops because of an inherent and/or an acquired failure of an insulin compensatory response, is increasingly seen from early puberty onward, as is atheromatous disease leading to coronary heart disease and stroke. A predisposition to certain cancers and Alzheimer's disease is also now recognized. The looming tragedy from growing numbers of individuals affected by obesity/insulin resistance syndrome requires urgent public health approaches directed at their early identification and intervention during childhood. Such measures include educating the public on the topic, limiting the consumption of sucrose-containing drinks and foods with high carbohydrate and fat contents, and promoting exercise programs in our nation's homes and schools.
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PMID:Insulin resistance syndrome in children. 1518 Oct 20

There has been a major increase in obesity among children over the past twenty years. Obesity is associated with glomerular hyperperfusion and hyperfiltration from physiological (mal)adaptation resulting from afferent arteriolar vasodilatation. The renal injury from hyperfiltration in obesity is further exacerbated by concomitant presence of dyslipidemia, hyperglycemia and/or insulin resistance, inflammation and hypertension. The renal injury clinically manifests as microalbuminuria, proteinuria and/or poor renal function, and is histologically characterized by glomerulomegaly, mesangial expansion and/or sclerosis, which has been termed "obesity related glomerulopathy". Obesity portends a poor prognosis in subjects with chronic kidney diseases, IgA nephropathy and nephrectomy. Obese individuals on dialysis and renal transplant have mixed outcomes. The purpose of this review is to highlight the nondiabetic consequences of obesity on kidney for the pediatric nephrology community as we begin to address the obesity epidemic in children.
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PMID:Nondiabetic consequences of obesity on kidney. 1649 17

The obesity epidemic has reached nephrology in the form of increasing numbers of patients with chronic kidney disease (CKD) caused by obesity-related metabolic disorders, IgA nephropathy, stone disease, and a unique glomerulopathy now known as obesity-related glomerulopathy (ORG). Obesity has been identified as an independent risk factor for CKD, and patients with central adiposity or high waist-to-hip ratios appear to have the highest risk. The metabolic syndrome is a risk factor for albuminuria and CKD, and studies now show that the risk of CKD increases with increased numbers of components of the metabolic syndrome. Obesity is not just a bystander or accelerator of other kidney diseases, but has unique histopathologic characteristics that can cause progressive kidney disease. ORG may accompany and worsen IgA nephropathy, urate nephropathy, and possibly even diabetic nephropathy. The origins of obesity-related kidney disease can be traced to insufficient glomerular complement from birth, and low birth weight may be an important precursor to obesity and its many comorbidities. Intervention strategies may need to target prenatal care through the elderly to combat this problematic epidemic.
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PMID:Epidemiology of obesity and chronic kidney disease. 1704 19

We reported a case of a 38-year-old woman with both massive proteinuria and severe obesity. We diagnosed her as metabolic syndrome from her waist size of over 90 cm around her umbilicus, hyperlipidemia (high TG level) and hypertension. The urinary protein was more than 3.5 g/day and body mass index was 38.7 at admission. The renal biopsy specimen revealed IgA nephropathy. According to Clinical guidelines of IgA nephropathy 2nd version, Committee of IgA Nephropathy-the Special Study Group on Progressive Glomerular Disease, the Ministry of Health, Labor and Welfare of Japan-, her prognosis belonged to a rather poor group. We planed to administer steroid treatment first, however considering the adverse effects of steroid therapy, such as hyperlipidemia and diabetes mellitus, we tried to decrease her body weight as much as possible, and then treated her with both angiotensin converting enzyme inhibitor and anti-platelet drug. After her body mass index (body weight) was approximately 30.1 % (30 kg) less than that on admission, a parallel reduction of urinary protein was observed, and the final level was approximately 0.18 g/day. Decline in the body weight, diet and exercise were the chief measures that reduced the urinary protein without corticosteroid therapy.
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PMID:[An IgA nephropathy case with highly reduced urinary protein concomitant with reduced obesity]. 1712 85

The pathological role of obesity has rarely been studied in primary glomerular diseases. The purpose of this study is to examine the clinicopathological influence of obesity in IgA nephropathy (IgAN). 74 patients with IgA nephropathy in our institution from October 2000 to January 2004 were retrospectively divided into two groups according to body mass index (BMI): the non-obese group (group N) with BMI < 25 kg/m(2), and the obese group (group O) with BMI > or = 25 kg/m(2). There were 50 patients in group N and 24 patients in group O. Clinical analysis showed no significant difference between these two groups in blood pressure, serum cholesterol, creatinine clearances or grade of hematuria. However, urinary protein excretion and serum creatinine were significantly greater in group O than in group N. Although semiquantitative analysis of light-microscopical findings showed no significant differences in the severity of mesangial proliferation, matrix expansion, glomerulosclerosis or crescent formation, image analysis showed that total glomerular area and tuft area were significantly larger in group O. In addition, ultrastructural study revealed significantly higher glomerular basement membrane thickness in group O. 62 patients (46 patients, group N; 16 patients, group O) were followed in our institution for one year. Urinary protein was significantly decreased only in patients who received steroid in both groups. Although administration of ACE inhibitor or ARB tended to decrease urinary protein in group O, the change was not statistically significant. Our findings indicate that obesity may accelerate the increase of proteinuria in IgAN through ultrastructural modification of the glomerular basement membrane.
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PMID:Clinicopathological influence of obesity in IgA nephropathy: comparative study of 74 patients. 1749 42

Amylin (islet amyloid peptide) plays a critical role in islet amyloidosis and in the development of beta-cell dysfunction in patients with diabetes; however, the involvement of amylin in renal amyloidosis has not been studied. For this reason, we surveyed 149 patients with biopsy-proven diabetic nephropathy (DN). The results were compared to 95 renal disease control patients, which included membranoproliferative glomerulonephritis, light-chain deposition, IgA nephropathy, and obesity-related glomerulopathy (ORG). Seventy-two of the 149 patients with DN showed amylin deposition in their renal tissue. Amylin was mainly distributed in the expanded mesangial area, Kimmelstiel-Wilson nodules, Bowman's capsule, and in blood vessels. The frequencies of mesangial proliferation, glomerular nodule lesions, and glomerular sclerosis were higher in DN patients with amylin deposits. Furthermore, the tubular interstitial lesions were more severe in these patients. Of the 95 disease-control patients, four with ORG were positive for renal amylin deposits. Our study has found renal amylin deposition in patients with DN and that the deposition was associated with disease severity. We suggest that strict metabolic control and reversing insulin resistance in patients with diabetes may blunt the process of amylin deposition in the kidney and possibly protect renal function in these patients.
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PMID:Amylin deposition in the kidney of patients with diabetic nephropathy. 1749 60

Elevated serum uric acid level is associated with obesity, insulin resistance, diabetes, nephropathy, and hypertension. Epidemiologic studies suggest that serum uric acid levels are heritable. We sought to identify chromosomal regions harboring quantitative trait loci that influence serum uric acid in Mexican Americans using data from 644 participants in the San Antonio Family Heart Study. Serum uric acid was found to exhibit significant heritability (0.42) in this population (P = 2 x 10(-7)) after accounting for covariate effects. In addition, genetic correlations between serum uric acid and other cardiovascular risk factors, such as body mass index, waist circumference, systolic BP, and pulse pressure, were identified, suggesting that the genes associated with uric acid level are also associated with these phenotypes. Multipoint linkage analysis identified quantitative trait loci with measurable effects on serum uric acid variability. The highest multipoint logarithm of odds score of 3.3 was found at 133 cM on chromosome 6q22-23, a region that also contains genes that seem to influence familial IgA nephropathy, obesity, BP, insulin resistance, and type 2 diabetes. Given the relationship between uric acid level and these conditions, future studies should investigate potential candidate susceptibility genes found in this region.
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PMID:Genome scan for determinants of serum uric acid variability. 1797 10

This report describes the case of a 57-year-old man who underwent a repeated renal biopsy 25 years after the first biopsy in which the diagnosis of IgA nephropathy was made. Although the patient exhibited gradually increasing proteinuria and a slowly progressive renal impairment, the histological findings of the repeat biopsy revealed no evidence of either glomerular inflammatory changes or IgA deposition. Instead, a marked decrease in the glomerular density and hypertrophy of the remnant glomeruli were noted. Almost a complete disappearance of urinary protein excretion by a calorie-restricted diet indicated that the patient's obesity and its related factors may have contributed to the present nephropathic development.
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PMID:Obesity-related nephropathy associated with a history of IgA nephropathy. 1882 22


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