Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Serum osteocalcin and alkaline phosphatase levels, as indexes of bone formation, and urinary calcium and hydroxyproline excretions relative to creatinine, as indexes of bone resorption, were measured in 10 obese women before and after two months of hypocaloric diet. In basal condition, serum osteocalcin, but not alkaline phosphatase levels, were higher in obese than in controls (7 +/- 0.4 vs 5.3 +/- 0.2 ng/ml). Urinary calcium/creatinine and hydroxyproline/creatinine ratios were also significantly higher than those in normals (0.37 +/- 0.05 vs 0.2 +/- 0.01 and 0.035 +/- 0.004 vs 0.02 +/- 0.002, respectively). After weight loss, serum osteocalcin significantly increased (9.5 +/- 0.5 ng/ml), while urinary calcium/creatinine and hydroxyproline/creatinine ratios fell to the normal values (0.23 +/- 0.03 and 0.026 +/- 0.001). In conclusion, it appears that obesity, at least in young women, is associated with a high bone turnover, which seems to be reversible with weight loss.
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PMID:[Assessment of bone resorption/neoformation indexes in obese women before and after weight loss]. 209 52

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

The aim of this study was to investigate the relation between exposure to carbon disulfide, as measured by personal air sampling, and the excretion of 2-thiothiazolidine-4-carboxylic acid (TTCA) in urine. The subjects of investigation were 29 workers involved in the production of viscose rayon fibers. The average exposure level was 12.6 mg/m3 (range less than 1-66). The present Dutch occupational exposure limit ("MAC-value") is 60 mg/m3. After logarithmic transformation of the data, the following linear regression equation was found: log (TTCA) = 0.84 log (CS2) - 1.10, wherein TTCA is expressed as mmol/mol creatinine and CS2 as mg/m3. The correlation coefficient was 0.95. Neither the hepatic drug-metabolizing capacity (antipyrine clearance) nor the degree of obesity (Quetelet index) influenced the relationship significantly. On basis of the equation it was possible to establish tentative biological limit values corresponding to the respective occupational exposure limit values. The calculated biological limit value of 0.77 mg/g creatinine (= 0.57 mmol/mol creatinine) corresponds, with 95% confidence, to time-weighted average of air concentration lower than the TLV level of 30 mg/m3.
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PMID:Biological monitoring of carbon disulfide. 230 13

Effects of the diuretic drug furosemide were examined in obese animals to evaluate the hypothesis that organ damage by reactive drug metabolites may be potentiated by this disease. Obese overfed Sprague-Dawley rats that were treated ip with 450 mg/kg furosemide on the basis of total body mass suffered a 58% mortality rate over 24 h. This contrasted with 0% mortality in animals of normal body mass. On the basis of median histopathology scores, organ necrosis was judged to be greater in the liver (2+) and kidneys (1+) of obese rats than in the liver (1+) and kidneys (less than 1+) of normal controls (p less than 0.05). Obese animals demonstrated a fourfold rise in fat mass over controls. The low solubility of furosemide in lipid makes it probable that aggravated drug toxicity in obese rats dosed to total body mass resulted in part from elevated furosemide concentrations in lean body mass. In a subsequent study designed to minimize this possibility, furosemide was administered on the basis of fat-free body mass to equalize initial drug exposure in obese and control rats. Even with this downward dosage adjustment, obese animals suffered increased hepatic necrosis (median score of 2+ versus 0 in treated controls), greater impairment of renal function (plasma creatinine concentration of 2.41 mg/dl versus 0.96 mg/dl in treated controls), and more extensive enzymuria (enzyme excretion 175-300% more elevated than in treated controls). In conclusion, obese rats appear to be at increased risk of furosemide-induced liver and kidney injury due to at least two factors: (1) increased exposure of target organs in lean body mass to furosemide when the dosing of this poorly lipophilic drug was based on total body mass, and (2) increased susceptibility of target organs in lean body mass to furosemide injury when dosing was adjusted downward to reflect fat-free body mass and to equalize initial drug exposure.
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PMID:Obesity as a risk factor in drug-induced organ injury. III. Increased liver and kidney injury by furosemide in the obese overfed rat. 246 6

Hypertension in the obese may be related to hyperinsulinaemia. To investigate this relationship further, we infused somatostatin (250 micrograms/h in 100 ml saline) or saline, single-blind and in a random order, for 10 h in seven obese hyperinsulinaemic hypertensive patients and in seven normo-insulinaemic hypertensive controls. Every 2 h, blood pressure, plasma insulin, glucose, sodium, potassium, renin, cortisol and aldosterone concentrations and the urinary sodium:creatinine ratio were determined. Two hours after the somatostatin infusion was started, mean arterial blood pressure was significantly reduced in the obese hyperinsulinaemic patients (from 128 +/- 11 to 114 +/- 11 mmHg, P less than 0.05) but not in the controls and this reduction persisted throughout the study. The somatostatin infusion reduced plasma insulin and increased plasma glucose similarly in both groups. Plasma sodium, potassium, renin, cortisol and aldosterone concentrations and the urinary sodium:creatinine ratio were unchanged after the somatostatin infusion. These results suggest that hyperinsulinaemia could help sustain the blood pressure rise in obesity.
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PMID:Reduction of blood pressure in obese hyperinsulinaemic hypertensive patients during somatostatin infusion. 257 63

Rates of elevated urinary albumin concentration, defined as microalbuminuria (30-299 micrograms/ml) and macroalbuminuria (greater than or equal to 300 micrograms/ml), were determined on random morning urine specimens in the population of Nauru, which has a high prevalence of non-insulin-dependent diabetes mellitus. The prevalence of elevated urinary albumin levels in the total Nauruan population was very high: 26 and 30% of men and women, respectively, had microalbuminuria, whereas 13% of both sexes had macroalbuminuria. Of the subjects with macroalbuminuria, 66% had diabetes. The prevalence increased with worsening glucose tolerance; 26% of subjects with normal glucose tolerance had either micro- or macroalbuminuria, increasing to 43% of subjects with impaired glucose tolerance, 63% of newly diagnosed diabetic subjects, and 75% of previously diagnosed diabetic subjects. Associations between elevated urinary albumin concentration and putative risk factors were assessed for both the total population (n = 1184) and the diabetic subgroup alone (n = 318). Fasting plasma glucose and hypertension were the most important independent correlates for the whole population, whereas plasma creatinine was also important in diabetic subjects. Age at onset and duration of diabetes were not found to be significantly associated with elevated albumin concentration. In subjects with normal glucose tolerance, hypertension and hyperuricemia were the most important associated factors. These results suggest that blood glucose, blood pressure, and possibly obesity and plasma uric acid are important modifiable risk factors for both micro- and macroalbuminuria in this population.
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PMID:Prevalence and risk factors for micro- and macroalbuminuria in diabetic subjects and entire population of Nauru. 258 79

The predictive value of the Cockcroft-Gault equation in patients with Cushing's syndrome was evaluated in 23 patients. Patients were subdivided based on total body weight into two groups, obese and nonobese. Estimated creatinine clearance (EClcr) values were obtained by the Cockcroft-Gault method using ideal body weight (IBW) and total body weight (TBW). These values were then compared with a 24-hour measured creatinine clearance (MClcr). EClcr values based on TBW consistently overestimated measured values in all patients (p less than 0.05). In obese patients with Cushing's syndrome IBW predictions were not statistically different. However, linear regression analysis revealed a poor correlation (r = 0.32). Daily creatinine production rates (Ucr) were calculated and contrasted with an appropriate historical control for obese and nonobese subjects. Nonobese patients revealed a marked reduction in total Ucr compared with normal-weight controls (p less than 0.05). Obese patients also showed a reduction in Ucr when compared with a normal obese control population (p less than 0.05). Difficulty in predicting creatinine clearance in patients with Cushing's syndrome appears to be related to alterations in Ucr. These data suggest that the pathophysiologic changes that accompany Cushing's syndrome are sufficient to alter Ucr and may limit the usefulness of existing methods to predict creatinine clearance and renal function in these patients.
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PMID:Estimation of creatinine clearance in patients with Cushing's syndrome. 260 51

We examined hyperuricemia in patients with coronary heart disease. In 85 patients with coronary sclerosis confirmed by coronary angiography, the serum urate level (6.08 +/- 1.60 mg/dL) was not different from that in subjects with normal coronary arteries (6.47 +/- 1.69 mg/dL). The incidence of hyperuricemia in patients with coronary sclerosis was 26%, and was significantly correlated with diuretics, obesity and hypertriglyceridemia, but not with hypertension or hypercholesterolemia. To elucidate the mechanism of urate metabolism in coronary sclerosis, we separated coronary sclerosis patients without complicating factors into hyperuricemics and normouricemics, and studied urate metabolism in comparison with subjects with normal coronary arteries. We found that normouricemics with coronary sclerosis had decreases in the filtered urate load and urate clearance with a normal urate-creatinine clearance ratio. Hyperuricemics with coronary sclerosis had decreases in urate clearance and urate-creatinine clearance ratios, but the filtered urate load was similar to that in normouricemics. It is suggested that in coronary sclerosis patients, normouricemics had a low glomerular filtration of urate with normal tubular urate transport, whereas hyperuricemics had enhanced tubular reabsorption of urate without any difference of urate filtration from normouricemics.
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PMID:Differences in urate metabolism between normouricemia and hyperuricemia in coronary heart disease in man. 262 19

For alterations in serum creatinine to reflect changes in GFR, urine creatinine excretion must remain constant. Although serum creatinine is often used to monitor chronic changes in allograft GFR, creatinine excretion has not been systematically investigated in renal transplant recipients. In the present study, creatinine excretion was examined in 100 patients who survived at least 12 months with functioning renal allografts. Overall, there was a progressive decline in creatinine excretion from 1420 +/- 410 mg/24 hr at 3 months to 1240 +/- 394 mg/24 hr at last follow-up, 89 +/- 35 months after transplantation (mean +/- SD). The decline in creatinine excretion was greatest in those who subsequently returned to dialysis (-27.4 +/- 20.2%, P less than .05) compared with those who died (-6.9 +/- 24.1%), or survived with functioning allografts (-3.7 +/- 18.1%). Multivariate analysis demonstrated that age, sex, body weight, obesity, diabetes, and cumulative average daily corticosteroid dose (factors that affect muscle mass) all influenced creatinine excretion. However, early post-transplant clinical parameters failed to predict patients who subsequently had declines in creatinine excretion. Thus, it was not possible to predict patients in whom chronic changes in allograft function would be underestimated by changes in serum creatinine. Although clinically relevant functional alterations can be detected by changes in serum creatinine, additional measures of GFR should be used to complement the serum creatinine and monitor chronic changes in allograft function after renal transplantation.
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PMID:Creatinine excretion after renal transplantation. 267 99


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