Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During pregnancy women with Type 1 diabetes do not differ from normal women with respect to pregnancy-associated changes in serum lipid levels. However influence of diabetic nephropathy on lipoprotein metabolism in pregnancy has not been described previously. Changes in lipids were compared during and after pregnancy in 10 Type 1 diabetic women without macroproteinuria as well as in 5 diabetic women with macroproteinuria due to diabetic nephropathy. In the pregnant women with macroproteinuria, compared to the diabetic women without macroproteinuria, we observed both significantly higher total and percent increases in serum levels of total cholesterol (97% versus 48%) and of LDL-cholesterol (137% versus 50%), which had risen progressively throughout gestation. The percent increases in serum triglycerides (115% versus 128%) were similar in both patient groups. Metabolic control was improved during pregnancy in both groups of women. Renal function remained normal throughout pregnancy in the diabetic women without nephropathy and worsened during pregnancy in the proteinuric women. The mean protein excretion showed a physiological rise from 0.107 +/- 0.040 g 24 h-1 before pregnancy to 0.336 +/- 0.234 g 24 h-1 in the third trimester in the nonproteinuric women, and an increase from 2.2 +/- 1.0 to 7.1 +/- 1.7 g 24 h-1 during the same period in the women with macroproteinuria. Therefore, it is concluded that the greater increase in serum lipid levels during pregnancy in the women with pre-existing diabetic nephropathy can mainly be explained by the concomitant increase in proteinuria associated with development of the nephrotic syndrome in these patients.
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PMID:Increases in serum lipids during pregnancy in type 1 diabetic women with nephropathy. 803 24

In order to clarify the abnormalities of the coagulation and fibrinolysis system in patients with various renal diseases, we produced a new monoclonal antibody for FDP (fibrin/fibrinogen degradation product) D-dimer (D-D E72). We also established a new highly sensitive method of enzyme-linked immunosorbent assay (ELISA) for urinary FDP D-dimer using this monoclonal antibody. The urine from 110, patients with various renal diseases was investigated for the FDP D-dimer. The results are summarized as follows: 1) Urinary FDP D-dimer in normal subjects was 0.69 +/- 0.60 ng/ml. 2) The level of urinary FDP D-dimer in patients with primary nephrotic syndrome and in patients with chronic renal failure was significantly higher than that of normal subjects, whereas the urinary FDP D-dimer levels in patients with diabetes mellitus were higher than those of normal subjects. 3) In the CGN and NS groups there was a tendency for an increase in the level of urinary FDP D-dimer in more active forms of the disease. 4) A significant correlation between urinary FDP D-dimer and urinary protein in the CGN and NS groups was demonstrated. 5) In all of the renal diseases investigated in this study, the ratio of urinary FDP D-dimer to total FDP was less than 4%.
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PMID:[Significance of urinary fibrin/fibrinogen degradation product (FDP) D-dimer measured by highly sensitive ELISA method with a new monoclonal antibody (D-D E72) in various renal diseases]. 807 18

A 35-year-old Japanese woman with nephrotic syndrome due to mesangial proliferative glomerulonephritis was treated with steroid hormone for 5 years and suddenly developed uveitis in the left eye. She had many cells in the anterior chamber, fine granular keratitic precipitates on the posterior surface of the cornea and retinal edema around the optic disc. Diabetes mellitus had been diagnosed, but it was considered to be steroid diabetes mellitus. This patient showed depressed spontaneous blastogenesis. Since nephrotic syndrome is occasionally associated with an immune-mediated process, uveitis in this case might be related to an immunity disorder.
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PMID:Uveitis in nephrotic syndrome. 809 86

Large-scale and systemic epidemiological, pathological and experimental studies emphasized and documented the childhood origin of atherosclerosis. There is increasing consensus that lipid levels in children to a large extent determine the rate of coronary artery disease (CAD) in the adult population. Minimal sudanophilic intimal deposits, and the presence of intracellular and extracellular lipid, and a slight increase in interstitial ground substance in 3 years of age or older patients are found. In the Bogalusa Hearth Study aortic fatty streaks were strongly related the antemortem levels of both total cholesterol and low-density lipoprotein cholesterol (LDL-C) independent of race, sex, and age, and were negatively correlated with the ratio of high-density lipoprotein (HDL-C) to low-density plus very-low-density lipoprotein cholesterol (LDL-C+VLDL-C). The potential for primary prevention is real and the strongest piece of evidence for its is the remarkable trend in CHD mortality rates in recent times, rapidly downward in many western countries. A number of factors influence plasma levels of lipid and lipoproteins in newborn, in infants, in children and adolescents and their relevance as possible predictors of adult coronary artery disease. They are certain inherited disorders of dyslipoproteinemia (familial hypercholesterolemia, familial combined hyperlipidemia, hyperapobetalipoproteinemia, and hypoalphalipoproteinemia) and secondary causes of hyperlipidemia (congenital biliary atresia, glycogen storage diseases, hypothyroidism, diabetes mellitus and nephrotic syndrome, etc).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Atherosclerosis and juvenile dyslipidemias]. 818 5

It is not certain whether the life expectancy of patients with membranous nephropathy is shorter than that of an age-matched healthy population. Forty-one patients (21 males, 20 females) aged between 16 and 70 years (average age: 33.3 years) were followed for 20 years. The patients were divided into two groups: group I (n = 18), consisting of patients in whom nephrotic syndrome persisted for more than two years or until death, and group II (n = 23), consisting of patients except for group I. The non-survival criteria are death or renal death. Twelve patients (29.3%) died during the study period. Eight patients belonged to group I and 4 to group II. The causes of death in group I patients were end-stage renal failure in 3 cases, ischemic heart disease in 1 case, subarachnoid hemorrhage in 1 case, malignancy in 2 cases, suicide in 1 case, and those in the group II patients were pneumonia, malignancy, cerebral softening, and diabetes mellitus, respectively. Eight patients who died in group I had a significantly longer difference between their actual life span (ALS) and life expectancy (LE) and a significantly smaller ratio of ALS to LE than the patients who died in group II (ALS-LE: -29.9 +/- 4.5 years in group I vs. -9.0 +/- 6.8 years in group II, p < 0.05, ALS x 100/LE: 22.5 +/- 8.0% in group I vs. 80.9 +/- 25.2% in group II, p < 0.05). In group I, the ratio of observed to expected death was 4.76 (95% confidence interval, 2.05 to 9.37) and significantly higher than that of the control population. In group II, however, the ratio was 1.09 (95% confidence interval, 0.30 to 2.80), and the difference from the control population was not statistically significant. These results suggest that longstanding nephrotic syndrome is associated with a shortened life expectancy in patients with membranous nephropathy.
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PMID:[Shortening of life expectancy in patients with membranous nephropathy--based on 20 years follow up study]. 826 5

Hypercoagulability is a condition where as a result of certain pathological changes in the blood inadequate cumulation of thrombocytes or fibrin occurs which finally can lead to arterial or venous thrombosis, depending on vascular wall damage. In the submitted review the authors analyze the most important inborn and acquired causes of hypercoagulation states. As to inborn causes, deficiens of natural anticoagulation proteins (antithrombin III, protein C, protein S) are most important as well as dysfibrinogenaemia, impaired fibrinolysis associated with deficiency of natural activators of fibrinolysis or increased activity of their inhibitors and homocystinuria. The most frequent acquired causes of hypercoagulation states are the presence of anticardiolipin antibodies ("lupus anticoagulans"), pregnancy, the use of oral contraceptives, malignity, nephrotic syndrome, postoperative conditions, diabetes mellitus and some other diseases.
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PMID:[Hypercoagulation states]. 828 11

The effect of prostaglandin E1 (PGE1) on the renin-aldosterone system was investigated in hospitalized patients with non-insulin-dependent diabetes mellitus presenting with continuous proteinuria but without nephrotic syndrome. Of the 20 patients studied, 10 had continuous positive proteinuria > or = 200 mg/day and 10 had continuous positive proteinuria < 200 mg/day. Prostaglandin E1 (40 micrograms in 100 ml normal saline) was infused intravenously over 2 h twice daily for 4 weeks. Plasma renin activity (PRA) and the plasma aldosterone concentration (PAC) were determined by radioimmunoassay at 0 and 120 min after a frusemide injection given before the start of PGE1 treatment and during administration of PGE1 in week 4. The patients who had proteinuria < 200 mg/day showed significant decreases in the PRA0 and the ratio of PRA120:PRA0 and a decrease in the PAC120 during prostaglandin PGE1 administration. When the results for the two patient groups were combined, both the PAC120 and the PRA120 were found to be significantly lowered during administration of PGE1. The results indicate that PGE1 may be valuable in the treatment of diabetic nephropathy, since the compound inhibited the increased reactivity of the renin-aldosterone system in patients with non-insulin-dependent diabetes mellitus.
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PMID:Effect of prostaglandin E1 on the renin-aldosterone system in patients with diabetic nephropathy. 829 55

Arterial hypertension is a dominant pathogenetic factor for glomerulosclerosis. Nevertheless metabolic factors such as hyper- or dyslipoproteinemia may significantly modify and accelerate the process of glomerular scarring. Hyperlipidemia and lipoprotein abnormalities are often encountered in patients with nephrotic syndrome and chronic renal disease. Although the significance of lipid deposition in renal tissue and the role of lipoproteins in the pathogenesis of renal disease in man has not yet been clearly defined, experimental and clinical data indicate a damaging effect of disturbed lipid metabolism on the kidney. In humans glomerular lipid deposition is observed in several genetic diseases, including lecithin-cholesterol acyltransferase activity deficiency. Studies on animals with reduced renal mass, diabetes mellitus or arterial hypertension have shown that hypercholesterolemia increases the incidence of glomerulosclerosis. Especially the interaction of arterial hypertension and dyslipoproteinemia leads to a rapid and pronounced development of glomerulosclerosis. As most of these studies have been performed in the rat, which has a different lipoprotein profile than man, these results should be carefully interpreted with regard to their relevance for humans. In vitro cell culture studies on human glomerular cells have provided insight into the possible cellular mechanisms of lipid-induced glomerular damage. Apoprotein E containing lipoproteins that are pathologically elevated in many renal diseases are avidly taken up by human glomerular cells. Mesangial cells seem to play a central role in the initiation of glomerulosclerosis by proliferation and production of excess extracellular matrix. Lipoproteins are able to stimulate DNA synthesis in these cells and increase the synthesis of mitogens and matrix proteins. The pathogenetic role of modified, oxidized lipoproteins has not yet been elucidated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Arterial hypertension and hyperlipidemia as determinants of glomerulosclerosis. 830 44

314 patients, aged 65 years or older, were biopsied because of a history of renal disease. In 203 patients, glomerular disease was diagnosed with one fourth having systemic disease and the remaining primary glomerulonephritis. 90 patients had tubulointerstitial disease, and 21 patients showed prominent vascular pathology. In a comparison with patients of younger age groups, it appeared that amyloidosis, membranous nephropathy, vasculitis and diabetes had a significantly higher incidence in the elderly. Main glomerular syndromes such as nephrotic syndrome and rapidly progressive glomerulonephritis imply to be managed appropriately. Glomerulosclerosis was found in high frequency, either as an isolated feature or associated with other lesions. Glomerulosclerosis seemed to be ischemic in origin and seems to represent a distinct entity as a cause of pathology in the elderly.
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PMID:Renal biopsy in the elderly. 832 38

Forty-two patients with the nephrotic syndrome were grouped according to the absence or presence of renal failure and/or diabetes mellitus. All patients had a similar degree of hypoalbuminemia and urinary protein losses. A lipid and apoprotein pattern was generated in serum and ultracentrifugally isolated lipoproteins. Low-density lipoprotein composition was essentially normal in uremic patients while in the other patients with the nephrotic syndrome, a considerable lipid enrichment was noted. The very-low-density lipoprotein content in lipids was uniformly increased in nephrotic patients irrespective of the presence of complications. High-density lipoprotein cholesterol and serum apolipoprotein A I and E concentration was significantly reduced in uremic patients with respect to normal subjects and to the other groups considered. Serum apolipoprotein A II and B levels were also decreased in uremics. All patients had increased serum apoprotein C II and C III concentration. We conclude that diabetes mellitus does not affect the pattern of hyperlipoproteinemia of nephrotic syndrome while the characteristic lipoprotein and apoprotein pattern of uremia is present irrespective of nephrosis in uremic, nondiabetic patients.
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PMID:Pattern of hyperlipoproteinemia in human nephrotic syndrome: influence of renal failure and diabetes mellitus. 836 82


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