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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hypercoagulable state in patients with diabetes mellitus, glomerular diseases and pregnancy induced hypertension was studied by using new methods. The research items included platelet function, coagulation, anti-coagulation system, fibrinolysis and TEG examination. The results showed that there was a hypercoagulable state in patients with diabetes mellitus, pregnancy induced hypertension and glomerular diseases, especially in those with uremia and nephrotic syndrome.
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PMID:[Clinical research of hypercoagulation in patients with diabetes mellitus, glomerular diseases and pregnancy induced hypertension]. 228 69

We describe an 8-year-old boy who was diagnosed as having diabetes mellitus at the age of 3 months. During the follow-up the diabetes was uncontrolled, and he presented nephrotic syndrome with renal function impairment, a renal biopsy showing a membranous nephropathy. Subsequently he had episodes of anemia and dyspnea, due to alveolar hemorrhage, and he also developed Fanconi's syndrome. A later renal biopsy showed membranous glomerulonephritis and interstitial nephritis. The presence of antitubular basement membrane antibodies was noted but antialveolar basement membrane antibodies were not detected. We do not believe that this unusual clinical picture was a coincidence, and we speculate about a possible explanation.
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PMID:Membranous nephropathy, antitubular basement membrane antibodies and alveolar hemorrhage in a diabetic child. 228 22

A 59-year-old woman, one of 5 cases with familial type III hyperlipoproteinemia reported at our clinic to date, had nephrotic syndrome and diabetes mellitus, but had neither coronary atherosclerosis nor xanthoma. A renal biopsy specimen revealed a massive cluster of foam cells containing apolipoprotein B and E in the mesangial region of the kidney. A restricted diet intake combined with lipid-lowering drugs such as cholestyramine, clinofibrate, and bezafibrate, in addition to methylprednisolone was not very effective in lowering serum triglyceride and cholesterol levels within physiological ranges. Therefore, plasmapheresis, using a dextran sulfate-cellulose column, was performed. Repeated plasmapheresis resulted in a marked decrease in both serum total cholesterol and triglyceride. A second renal biopsy specimen performed 2 years later revealed a marked reduction in foam cells with concurrent improvement in her nephrotic syndrome and glucose intolerance. These results suggest that familial type III hyperlipoproteinemia may be responsible for glomerular lipidosis resulting in nephrotic syndrome. They also indicate that plasmapheresis using a dextran sulfate-cellulose column is very effective in the removal of abnormal lipoproteins such as beta-very low density lipoprotein and intermediate density lipoprotein in a case of familial type III hyperlipoproteinemia.
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PMID:Effects of plasmapheresis on familial type III hyperlipoproteinemia associated with glomerular lipidosis, nephrotic syndrome and diabetes mellitus. 231 Apr 24

A 47-year-old Arab male presented with a nephrotic syndrome and renal failure. Proliferative retinopathy was documented on fundoscopy. There was no history of symptomatic hyperglycemia, and biochemically, there was impaired glucose tolerance. This patient had classical microangiopathic complications that are closely related to the severity and duration of diabetes mellitus in the absence of overt hyperglycemia.
Diabetes Res Clin Pract 1990 Mar
PMID:Classical microangiopathic diabetic complications in the absence of overt diabetes mellitus. 234 Jul 96

The case of a 58-year-old man with nephrotic syndrome and characteristic pathologic renal lesions of KW disease is presented. No evidence of diabetes was found by oral or intravenous glucose tolerance tests. The possibilities of light-chain disease, membranoproliferative form of glomerulonephritis, and amyloidosis were excluded by histochemistry and immunofluorescent microscopy.
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PMID:Occurrence of intercapillary nodular glomerulosclerosis in the absence of glucose intolerance. 240 11

In an insulin dependent diabetic who was hyperglycaemic and ketotic despite 3,000 u of insulin injected subcutaneously in 2 divided doses daily, 50 u of intravenous insulin infused over 24 hr restored normal glucose homeostasis. A combination of insulin (800 u) and aprotinin (10,000 u) given twice daily also produced adequate glucose homeostasis for a period of 12 months. The patient then developed local hypertrophy of subcutaneous tissue at the injection site and her diabetic control deteriorated. Non-selective proteinuria followed and she developed nephrotic syndrome. Renal biopsy revealed a membraneous glomerulonephritis with subepithelial immune complexes, appearances consistent with a drug-induced glomerulonephritis. Withdrawal of aprotinin led to a gradual remission of nephrotic syndrome and proteinuria over several months. During this period, her diabetes was well controlled with continuous subcutaneous infusion of insulin at a dose of 500 u/24 hr. This case report demonstrates: the effective use of aprotinin for prolonged periods in insulin dependent diabetics with abnormal absorption of subcutaneously injected insulin; aprotinin induced lipohypertrophy which was not observed when insulin was injected alone; aprotinin-associated glomerulonephritis and nephrotic syndrome; the effective use of CSII--at higher insulin doses--in such patients with subcutaneous malabsorption of insulin.
Diabetes Res 1985 Jul
PMID:Aprotinin induced lipohypertrophy and glomerulonephritis in an insulin dependent diabetic. 241 74

Careful ultrastructural studies of the rat model of nephrotic syndrome induced by puromycin aminonucleoside have demonstrated morphological features which are only seen in proteinuric glomeruli fixed without interruption of the blood pressure. These consist of balloon-like swellings bounded by attenuated epithelial cell cytoplasm, with an area of bare basement membrane at the base. A theory of the mechanism of proteinuria was proposed on the basis of these findings. To test the proposed wide validity of that theory, we improved the method of surface fixation and performed similar studies in sequential manner, using chronic serum sickness glomerulonephritis in the rat as a model of proteinuria. Glomeruli were studied by light microscopy, transmission and scanning electron microscopy. The findings were correlated with the level of proteinuria in the 24 h preceding death and with the duration of serum sickness. Epithelial cell 'balloons' are also demonstrated in this model, correlating with the presence of proteinuria, but with slightly different configurations from those seen in puromycin nephrosis. Surface fixation revealed similar balloons in two other models of proteinuria: a graft versus host induced model of systemic lupus erythematosus in the mouse, and chronic streptozotocin-induced diabetes in the rat. A lengthy search failed to find bare basement membranes in any of these models of proteinuria. We conclude, therefore, that the mechanism of proteinuria proposed in puromycin nephrosis does not apply in these models, and we suggest an alternative mechanism by which the 'balloons' may develop, as a further manifestation of the epithelial cell dysfunction which causes foot process effacement.
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PMID:A morphological study of experimental proteinuria using a novel form of surface fixation. 264 11

Hyperlipidemia and hypertension, two major risk factors for accelerated atherosclerosis, undoubtedly contribute to the excessive cardiovascular morbidity and mortality experienced by renal transplant recipients. The present survey of posttransplant hyperlipidemia in 500 cyclosporine-treated patients documented a 37.6% incidence of hypercholesterolemia, which occurred within 6 months posttransplant in 82% of patients. An etiologic relation to corticosteroid therapy was suggested by the strong correlation between prednisone doses and cholesterol levels, by the reduced cholesterol levels in patients undergoing steroid withdrawal, and by the reduction in hypercholesterolemia to 13% by 3 years posttransplant when steroid doses were less than 10 mg daily. Hypertriglyceridemia, which was present in 14.7% of the patients, was more severe under CsA-prednisone compared with azathioprine-prednisone therapy. Hypertriglyceridemia, which occurred later in the posttransplant course than hypercholesterolemia, strongly correlated with an excessive percent relative weight and elevated serum creatinine but not with steroid or CsA doses. Increasing age, diabetes mellitus, beta-blockers and nephrotic syndrome contribute to posttransplant hyperlipidemia in the CsA-Pred era as they did in the azathioprine era of immunosuppression.
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PMID:Lipid abnormalities in cyclosporine-prednisone-treated renal transplant recipients. 266 33

Probucol is a lipid-regulating agent structurally dissimilar to other known agents, with a unique pharmacodynamic and clinical profile. It is effective in the treatment of primary Type IIa and IIb hyperlipoproteinaemias, including polygenic (non-familial) hypercholesterolaemia and both heterozygous and homozygous forms of familial hypercholesterolaemia, with reductions in plasma total cholesterol and low density lipoprotein (LDL)-cholesterol levels of about 10 to 20% being attained. Marked effects on cutaneous and tendinous xanthomas have been observed, with significant regression often apparent after 2 or 3 months' therapy. Preliminary trials also indicate efficacy in hyperlipoproteinaemia secondary to nephrotic syndrome and diabetes mellitus. The mechanism of the reduction in LDL-cholesterol levels is yet to be fully elucidated, but it is thought that the decrease results from enhanced catabolism, and there is preliminary evidence of an independent antioxidant effect. In contrast with all other known lipid-lowering agents, probucol also effects a consistent reduction in serum high density lipoprotein (HDL)-cholesterol levels, of around 20 to 30%; the clinical significance of this observation is unclear, although some preliminary investigations suggest a beneficial effect in enhancing reverse cholesterol transport. The influence of probucol treatment on cardiovascular morbidity and mortality remains to be fully investigated; a large trial quantifying the potential effect of probucol against the development of atherosclerotic lesions is currently in progress. Adverse effects of probucol are generally mild, seldom requiring treatment withdrawal, with gastrointestinal effects such as diarrhoea predominating. However, indications of an increased frequency of ventricular arrhythmias and sudden death in association with QT interval prolongation in some animals have prompted some concern. Although there is evidence of a degree of QT prolongation in a number of trials in humans, the nature and clinical significance of this effect requires clarification, as no increased incidence of cardiac arrhythmias is apparent. Thus, probucol appears to be of benefit in primary and secondary hyperlipoproteinaemia of Types IIa and IIb, and particularly in homozygous familial hypercholesterolaemia, with marked effects on xanthomas, and a generally favourable adverse effect profile. There is no evidence to date causally relating occasional QT interval prolongation in patients to any incidence of arrhythmias or sudden death. Pharmacodynamic investigations are likely to clarify further the place of probucol in therapy, particularly with respect to its distinctive lowering of plasma HDL-cholesterol levels.
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PMID:Probucol. A reappraisal of its pharmacological properties and therapeutic use in hypercholesterolaemia. 266 36

An elevated serum cholesterol level is a well known major risk factor for developing atherosclerosis in general, and for coronary heart disease in particular. There are many lipid lowering agents currently available. We used gemfibrozil in twenty hyperlipidemic cases who failed to response to diet control for three months. They were thirteen males and seven females with their ages ranging from thirty to eighty-one year-old. They included ten diabetes, one nephrotic syndrome and nine pure hyperlipidemic patients. All cases received gemfibrozil 600mg twice daily for 4-12 weeks. Gemfibrozil caused an increase in HDL cholesterol. The reductions in serum level of total cholesterol, total cholesterol/HDL cholesterol, and triglyceride were found. Only one case developed mild gastrointestinal side effect. There was no other major side effects.
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PMID:[Gemfibrozil in the treatment of hyperlipidemia]. 276 68


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