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

Diabetic nephropathy is the most important complication of diabetes, because it is a major cause of morbidity and mortality for diabetic subjects. Since not all subjects with diabetes are at risk of developing this complication, we conducted a study to determine if heredity might be a possible risk factor for diabetic nephropathy in non-insulin dependent diabetes. Twenty-one factors including inheritance of nephropathy and hypertension were investigated in 109 individuals with NIDDM: 50 patients without proteinuria (Group I), 20 patients with intermittent proteinuria (Group II), and 39 patients with continuous proteinuria (Group III) matched for age and duration of diabetes. Of those patients, 55 patients with inheritance of diabetes were also divided into three groups: 29 patients without proteinuria (Group I), 9 patients with intermittent proteinuria (Group II), and 17 patients with continuous proteinuria (Group III). Individuals in Groups II and III has significantly higher frequency of inheritance of diabetic nephropathy than those in Group I, and also individuals with inheritance of diabetic nephropathy had significantly higher frequency of diabetic nephropathy than those without it. Frequency of hypertension, retinopathy and body mass index in the past were significantly higher in subjects in Groups II or Group III than in those in Group I. There were no significant differences between subjects in Groups II and III. These findings suggest that susceptibility to diabetic nephropathy in NIDDM may be hereditary, although hypertension and obesity may also be important risk factors for diabetic nephropathy.
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PMID:[The possibility of hereditary factors in the susceptibility to diabetic nephropathy in NIDDM]. 163 29

Exogenous obesity is characterized hemodynamically by expanded intravascular (plasma) volume associated with an increased cardiopulmonary volume and cardiac output. In contrast, essential hypertension is related to an increased total peripheral resistance that is more or less uniformly distributed throughout the component organ circulations associated with a contracted plasma volume in proportion to the height of arterial pressure. Thus, both cardiac output and total peripheral resistance are elevated in obesity hypertension, and both impose a load on the left ventricle, resulting in both a volume and a pressure overload left ventricular hypertrophy. Although renal vascular resistance is not as increased as it is in lean hypertensive patients, these patients are subjected to hyperfiltration and proteinuria. Additionally, these hemodynamic alterations coexist with carbohydrate intolerance, hyperinsulinemia, hyperlipidemia, and hyperuricemia. With weight reduction and associated pressure reduction, the hemodynamic and metabolic changes reverse toward normal. However, should this not be achievable, the angiotensin converting enzyme inhibitors and calcium antagonists provide rational physiological approaches to drug therapy. With these agents pressure reduction is achieved through a fall in vascular resistance without intravascular volume expansion, and this is associated with reduced left ventricular mass and preserved cardiac and renal function, and without exacerbation of preexisting metabolic perturbations. Hence, these two classes of antihypertensive agents may provide a rational and physiological means for reversing the pathophysiological alterations of hypertensive disease in those obese patients in whom weight control is not possible.
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PMID:Obesity hypertension. Converting enzyme inhibitors and calcium antagonists. 173 Apr 48

We report a case of Klinefelter's syndrome who developed a decrease of serum gonadotropin levels, particularly LH, after CyA treatment for complicated focal glomerulosclerosis (FGS). A 38-year-old man suffering from general malaise and pretibial edema was diagnosed FGS by renal biopsy in October 1988, and was referred to our hospital for further evaluation and treatment for FGS in December 1988. He was not married, and closer anamnesis revealed that he had had impaired seminal ejaculation from the age of 30. The physical examination showed 37% obesity, scanty body hair, pretibial edema and small bilateral testes (3.0 x 1.5cm). Laboratory findings included marked proteinuria (5.3g/day) and mild renal dysfunction (serum creatinine 1.3mg/dl, glomerular filtration rate 57.2ml/min). Endocrinologically, high basal levels of LH and FSH (133.6mIU/ml and 93.7mIU/ml, respectively) and the hyperresponses of LH and FSH to LH-RH stimulation were found, but the other pituitary hormone levels, thyroid and adrenal status, were in the normal range. In testicular biopsy, nodularly proliferated Leydig cells and no seminal tubules could be seen. The chromosome analysis showed 47,XXY karyotype, which confirmed the diagnosis of Klinefelter's syndrome in this patient. From 9 January 1989, CyA (6mg/Kg.day) was orally administered for 4 weeks in order to treat for FGS. After CyA administration, basal levels of LH and FSH remarkably decreased, particularly LH, and their decrease lasted for at least 6 weeks after cessation of CyA (final levels; LH 28.2mIU/ml, FSH 69.8mIU/ml). On the other hand, serum testosterone level was low normal or slightly under normal, and no apparent changes could be seen during CyA treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cyclosporine A (CyA)-induced decrease of serum gonadotropin levels in a case of Klinefelter's syndrome. 190 51

It has been recently suggested that focal glomerulosclerosis (FGS) is analogous to atherosclerosis. Obese Zucker (OZ) rats spontaneously develop hyperlipidemia, proteinuria and FGS. To evaluate the role of the monocyte (MO) and its derivatives in the pathogenesis of the lesion, 30 OZ rats and 15 lean littermates (LZ) were followed for up to 240 days of age. At 75, 120 and 240 days of age, groups of 10 OZ and 5 LZ were assessed with respect to serum total and free cholesterol (TC and FC), triglyceride, lipoprotein electrophoresis, renal histology, histochemistry and immunohistochemistry. All serum lipids were raised at 75 days in OZ rats and increased progressively at 120 and 240 days. The early lesions of FGS were first demonstrated in OZ at 120 days with more advanced lesions at 240 days. FGS was seen in LZ only at 240 days when their serum lipids were raised. Intraglomerular MO infiltration was significantly higher in OZ than in LZ at all time periods (p less than 0.01) and greater in glomeruli with FGS lesions than in those without (p less than 0.01 and 120 days and p less than 0.05 at 240 days). Staining for ED1 and Ia antigens with monoclonal antibodies demonstrated increasing numbers of intraglomerular ED1+ and Ia+ cells with increasing age and extent of FGS. The findings suggest a role for intraglomerular macrophages in the pathogenesis of FGS in OZ.
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PMID:Monocytes and macrophages in focal glomerulosclerosis in Zucker rats. 194 26

The euglobulin fibrinolytic activity was measured in 56 non-insulin-dependent diabetics and 118 age-matched healthy controls before and after venous occlusion for 5 min at 100 mmHg of the left antecubital vein. In the basal state, fibrinolytic activity was impaired in diabetics compared with controls (93.1 +/- 6.7 vs 101.6 +/- 0.9 BAU) (P less than 0.05) and plasma fibrinogen level was increased but this did not reach statistical significance (467.3 +/- 264.1 vs 359.2 +/- 200.2 mg/dl). In diabetics, stimulated fibrinolysis following venous occlusion was depressed compared with controls (110.6 +/- 3.9 vs 121.6 +/- 1.9 BAU) (P less than 0.05). No relation of fibrinolytic activity to age, duration of diabetes, obesity, serum triglyceride, HbA1c, or 24 h proteinuria was demonstrated. In the diabetic retinopathy group, the fibrinolytic activity was lower than in the non-retinopathy group. Diabetics with long-standing diabetes (10 years or more) who remained free from retinopathy had significantly increased fibrinolytic activity than the diabetics with short-standing diabetes (less than 10 years) who have developed retinopathy (P less than 0.05). These findings imply a poor fibrinolytic activity, not in all diabetics, but only in those with retinopathy, and this may play a role in the development of diabetic retinopathy.
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PMID:Euglobulin fibrinolytic activity in NIDDM patients. 195 78

Although hypoalbuminemia is a fundamental characteristic of nephrotic syndrome (NS), there are many patients with massive proteinuria that do not develop hypoalbuminemia. We have studied the clinical and biochemical characteristics of 19 patients with persistent massive proteinuria (greater than 5 g/d) and normal serum albumin (group I) in comparison with 16 patients with similar proteinuria excretion, but persistent hypoalbuminemia (group II). Most of group I patients had diagnoses suggesting glomerular hyperfiltration (focal glomerulosclerosis [FGS] associated with vesicoureteral reflux [VUR], reduction of renal mass, proteinuria associated with obesity, sclerotic phase of idiopathic crescentic glomerulonephritis [GN] in contrast with those of group II, in which membranous GN was the most frequent diagnosis. We prospectively investigated differences in the antiproteinuric effect of captopril, an antiotensin-converting enzyme inhibitor (ACEI); after 6 months of treatment, proteinuria decreased clearly in group I (7.1 +/- 1.7 to 3.7 +/- 1.7 g/d; P less than 0.001), whereas no significant changes were observed in group II (8.1 +/- 2.4 to 8.8 +/- 4 g/d). Serum creatinine (Scr) remained stable during captopril treatment in group I, whereas three patients in group II showed a worsening of renal function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nephrotic proteinuria without hypoalbuminemia: clinical characteristics and response to angiotensin-converting enzyme inhibition. 199 78

An obese patient with nephrotic syndrome was admitted to the hospital because of increasing edema in the legs. With 25 kg weight loss, proteinuria decreased from 15 g to 5 g/day. Renal biopsy revealed mesangial glomerulopathy. The serum IgE level was highly elevated, and the radioallergosorbent test (RAST) was strongly positive for many kinds of allergens. No significant change in proteinuria, compared with the highly right atrial pressure period, was observed after normalization in the right atrial pressure. In spite of a decrease in body weight (27 kg) (113 to 86 kg) in 140 days, no significant change in proteinuria was observed. After additional therapy with an anti-allergic drug, proteinuria was completely abolished. These results suggest that a combination of weight loss and treatment with an anti-allergic drug is very important therapy for massive obesity with nephrotic syndrome. Since RAST was strongly positive for many kinds of allergens, the pathophysiology in this nephrotic syndrome may be, at least partially, related to the immunologic abnormalities.
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PMID:Improvement of nephrotic syndrome in a massively obese patient after weight loss and treatment with an anti-allergic drug. 209 99

Young female obese (cp/cp) and lean littermates (?/+) of the recently developed congenic strain, SHR/NIH-corpulent (SHR/N-cp), were fed for 6.5 months isocaloric diets containing 54 percent carbohydrate as either sucrose or starch. Glycemic, lipidemic and renal parameters were determined after 1, 3 and 6 months. Systolic blood pressure and plasma corticosterone levels were determined after 3 months. After 6.5 months rats were killed for histological examination. Obese rats were hyperglycemic following an oral glucose challenge (1 hour response greater than 11.1 mmol/l) (200 mg/dl), hyperinsulinemic, hypertriglyceridemic, and developed proteinuria and mild hypertension. Feeding sucrose, as compared to starch, further increased serum glucose, insulin and triglyceride levels and urinary protein excretion in obese rats and serum triglyceride levels in lean rats. An amelioration of glucose intolerance was observed in sucrose-fed obese rats by 6 months. In contrast to serum insulin levels, serum triglyceride levels increased with age in obese rats. Obese rats exhibited hypertrophy of the kidney and adrenal cortex with abnormal histology. The study demonstrates that obese female SHR/N-cp rats exhibit some of the metabolic and histopathological changes associated with NIDDM in humans and that feeding sucrose, as the source of dietary carbohydrate, further magnifies the expression of diabetes in this model.
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PMID:Influence of genetic obesity, dietary carbohydrate and age on parameters of glucose tolerance and kidney and adrenal gland histology in female SHR/N-corpulent rats. 217 55

With respect to the great number of diabetics in our population and the development of renal insufficiency as a fatal complication at diabetic patients (15-25% of chronic haemodialysis patients suffer from diabetes mellitus) we examined diabetics of a rural district. We registered a total of 1164 diabetics: 690 of them showed normal renal function while 405 patients had serum creatinine in threshold values and 69 patients' serum creatinines exceeded 120 mumol/l. The age of onset and the duration of diabetes mellitus, its type and the metabolic control, furthermore symptoms of proteinuria, hypertension, obesity and retinopathy were registered in relation to renal function. The duration of diabetes, the metabolic control, proteinuria turned out to be prognostically important factors.
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PMID:[Diabetes mellitus and development of kidney insufficiency]. 226 Mar 64

Prevalence of vascular complications in newly diagnosed untreated diabetic patients with obesity was studied over a period of 18 years. A total of 742 patients including 241 subjects with obesity (BMI greater than 25) were analyzed. Obese patients showed higher serum cholesterol and triglyceride and lower HDL-cholesterol levels than non-obese patients. Average prevalence of obesity is shown to be 32.5% with higher prevalence in women (37.8%) than in men (28.3%, P less than 0.01). No definite change is found in yearly prevalence throughout the observation period. Ischemic ECG findings and hypertension were observed more frequently in obese (35.8% and 34.9%, respectively) than in non-obese (25.2%, P less than 0.02; 24.5%, P less than 0.01, respectively) subjects, while diabetic retinopathy was less in obese patients (P less than 0.05). The prevalence of proteinuria was almost the same in obese and non-obese groups. These results coincide with the general concept that obesity may be responsible for the development of macroangiopathy in diabetes mellitus.
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PMID:Prevalence of vascular complications in untreated diabetics with obesity during an 18 year period. 228 41


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