Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0730345 (microalbuminuria)
 4,018 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present the results of a population based study designed to estimate the prevalence of diabetic retinopathy in a series of 284 type 2 diabetics residing in low income areas of Mexico City. These patients were identified in a survey performed between February 1990 and October 1992 (The Mexico City Diabetes Study). We located 214 (75.35%) of the original 284 patients and invited them to attend a clinic where they were interviewed and had a complete ophthalmologic examination. All participants had, in addition to the retinal examination by a certified ophthalmologist, seven fields stereo fundus photographs taken with a Topcon 50X retinal camera. Photos were taken using ASA 100 Kodak film and processed in their laboratory. All photographs were read and graded for quality and level of diabetic retinopathy (DR) in the Reading Center of the Department of Ophthalmology of the University of Wisconsin. A total of 37 (43.5%) men and 69 (53.5%) women had no evidence of DR. In 16 (18.8%) men and 21 (16.3%) women there was background DR. In 25 (29.4%) men and 30 (23.3%) women there was preproliferative DR. In 5 (5.9%) men and in 7 (5.4%) women there was proliferative DR. Macular edema was diagnosed in 7 (8.2%) men and 6 (4.7%) women, of these in 3 (3.5%) men and in 5 (3.9%) women the macular edema was central. This complication is associated with duration of diabetes, chronic poor metabolic control and microalbuminuria. A very significant proportion of cases with sight threatening DR remains undiagnosed and untreated. Consequently there is a significant number of cases developing into blindness that could have been prevented.
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PMID:Diabetic retinopathy in Mexico. Prevalence and clinical characteristics. 780 88

Normalbuminuric patients who have long-standing IDDM have a wide range of renal structure, from within normal limits to advanced lesions that overlap those of patients who have high levels of MA and border on those seen in patients who have overt DN. Patients who have low-level MA have reduced glomerular structure similar to that of patients who have NA. Low GFR, hypertension, or both can occur in patients who have NA or low-level MA and are associated with more advanced lesions. Patients who have MA and AER greater than 45 mg/24 hr have more advanced lesions than do patients with NA or low-level MA, but similar lesions are present in these patients whether AER is greater than or less than 100 mg/24 hr. Increasing AER in NA and MA patients who have long-standing IDDM is associated with GBM and mesangial expansion. A structural basis for MA cannot currently be deduced from studies of glomerular epithelial cell fine structure, capillary wall charge site analysis, or immunohistochemical studies of renal ECM composition. Hemodynamic adaptations to mesangial expansion and reduced filtration surface and, perhaps, hydraulic conductivity may accelerate glomerular damage, as expressed by increasing AER. Microalbuminuria derives its clinical utility in IDDM, as it identifies a population of patients at statistically increased risk of progression to overt DN by acting as a marker of already well-established DN lesions. Although MA is currently the best of the widely used indicators of DN risk, it is not precise. Therapies that reduce MA may ultimately slow or prevent progression toward ESRD, but this finding requires confirmation by demonstrating that a given treatment strategy can preserve GFR.
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PMID:Glomerular changes in normo- and microalbuminuric patients with long-standing insulin-dependent diabetes mellitus. 892 36

A cross-sectional study was conducted among 517 patients with diabetes mellitus at all health centres in Melaka Tengah District to examine whether these patients and their associated cardiovascular risk factors were managed according to current guidelines. All patients had Type 2 diabetes mellitus with mean age of 57.9 +/- 10.5 years and the mean duration of diabetes was 7.2 +/- 6.0 years. The glycaemic control was poor with 53.6% of the patients having HbAlc above 8% (mean = 8.5%) and 24% of them had microalbuminuria. Among these patients with poor glycaemic control, about 47.6% of them were on monotherapy. Three hundred and fifty (67.7%) patients had hypertension but only 11 (3.1%) achieved target blood pressure of less than 130/80 mmHg. Only 18.3% of the diabetics with hypertension were prescribed angiotensin converting enzyme inhibitors and 0.3% with angiotensin receptor blockers. Nearly two-third of them had low-density lipoprotein cholesterol greater than 2.6 mmol/l (mean = 3.4 mmol/l) but only 6.8% were prescribed lipid-lowering agents. Aspirin was prescribed to 8.2% of diabetics aged above 40 years. Sixteen percent of the patients smoked, 53% did not do any exercise, and the mean BMI was 26.8 kg/mn. The management of diabetes mellitus and its associated cardiovascular risk factors was suboptimal on the basis of current clinical guidelines. A greater effort in educating doctors in the health centres about these management and adherence to the guidelines is important in reducing patients' risk of cardiovascular disease and its associated morbidity and mortality.
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PMID:Management of type 2 diabetes mellitus: is it in accordance with the guidelines? 1651 8

NCX 4016, 2-(acetyloxy)benzoic acid 3-[(nitrooxy)methyl]phenyl ester, is a new molecule in which a nitric oxide (NO)-releasing moiety is covalently linked to aspirin. After enzymatic metabolism, NCX 4016 releases both components. In vitro and in some animal models, these components exert their pharmacologic effects simultaneously. Nitric oxide (NO) is a small gaseous molecule that exerts several activities which may prevent atherothrombotic disorders. Moreover, it displays a protective activity on the gastric mucosa. NCX 4016 has been shown to inhibit platelet activation in vitro more effectively than aspirin, to inhibit smooth muscle cell proliferation, to exert an endothelial cell protective activity and to suppress the function of several inflammatory cells potentially involved in atherothrombosis. In animal models, NCX 4016 protected from platelet thromboembolism, prevented restenosis in atherosclerosis-prone animals, protected the heart from ischemia/reperfusion injury, and induced neoangiogenesis in critically ischemic limbs. Moreover, it displayed little or no gastric toxicity and appeared to protect stomach from noxious stimuli, including aspirin. NCX 4016 has been evaluated in healthy volunteers and found to inhibit platelet cyclo-oxygenase-1 (COX-1) similarly to or slightly less than aspirin, to raise the circulating levels of NO-degradation products, and to have little or no gastric toxicity in short term studies. In particular, in phase II studies, NCX 4016 had favorable effects on effort-induced endothelial dysfunction in intermittent claudication and on platelet-activation parameters elicited by short-term hyperglycemia in type II diabetics. In patients with type II diabetes the effects of NCX 4016 on microalbuminuria and on some hemodynamic parameters were promising. The pharmacokinetics of in vivo aspirin- and NO- released by NCX 4016, as well as the bioavailability of the two molecules, were not yet adequately studied. Also, the long-term tolerability of NCX 4016, as well as its possible effectiveness in preventing ischemic cardiovascular events and progression of atherosclerosis, should be explored.
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PMID:Pharmacologic profile and therapeutic potential of NCX 4016, a nitric oxide-releasing aspirin, for cardiovascular disorders. 1696 26

Because diabetes mellitus was not being adequately treated according to guidelines in an academic general medicine clinic, 2 of the authors (W.S.A. and A.H.G.) instituted an educational program to see if we could improve the appropriate management of diabetes mellitus in the academic general medicine clinic. Following this educational program, we investigated the appropriate management of 196 unselected patients with diabetes mellitus, mean age 61 years, who were followed up for at least 1 year in an academic general medicine clinic. The blood pressure was reduced to <130/80 mm Hg in 161 of 196 diabetics (82%). The hemoglobin A1c was reduced to <7.0% in 134 of 196 diabetics (68%). Angiotensin-converting enzyme inhibitors or angiotensin receptor blockers were used to treat 50 of 51 diabetics (98%) with coronary artery disease (CAD), ischemic stroke, or peripheral arterial disease; 33 of 35 diabetics (94%) with a glomerular filtration rate <60 mL/min/1.73 m; 54 of 57 diabetics (94%) with microalbuminuria, and 21 of 22 diabetics (96%) with electrocardiographic left ventricular hypertrophy. Aspirin was used to treat 50 of 51 diabetics (98%) with CAD, ischemic stroke, or peripheral arterial disease. beta-Blockers were used to treat 36 of 39 diabetics (92%) with CAD. Statins were used to treat 168 of 196 diabetics (86%). Smoking cessation counseling was documented in 39 of 53 smokers (74%). Of 196 diabetics, 196 (100%) had a neurological examination, 129 (66%) were referred to an ophthalmologist for an eye examination, and 125 (64%) were referred to a podiatrist for foot care. These data show that an educational program on the appropriate management of diabetes mellitus improved the management of diabetes mellitus in an academic general medicine clinic.
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PMID:Prevalence of appropriate management of diabetes mellitus in an academic general medicine clinic. 1926 67

Diabetic nephropathy (DN) is one of the major microvascular diseases and most common in diabetic patient, finally results in kidney failure. The main features of DN are basement membrane thickening, microalbuminuria, proteinuria, glomerular, mesangial hypertrophy and ECM protein accumulation. Recent discoveries have been shown that numerous pathways are activated during the development of DN in Diabetes mellitus. The small non-coding miRNA plays an important role in regulating the pathway which is involved in DN. In our study we consolidate different pathways which regulated by miRNAs in molecular signaling which results in causing DN. We embedded entire pathway in the form of regulatory network and we could able to understand that some of the miRNAs like miR-29 family, miR-377 and miR-25 would be able to control DN.
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PMID:Molecular signaling cascade of miRNAs in causing Diabetes Nephropathy. 2375 89

Diabetic nephropathy, a major complication of diabetes mellitus (DM), is increasing worldwide and the large majority of patients have type 2 DM. Microalbuminuria has been used as a diagnostic marker of diabetic nephropathy. But owing to its insufficient sensitivity and specificity, other biomarkers are being sought. In addition, the pathophysiology of diabetic nephropathy is not fully understood and declines in renal function occur even without microalbuminuria. In this study, we investigated urinary proteins from three study groups (controls, and type 2 diabetic subjects with or without microalbuminuria). Non-targeted label-free Nano-LC QTOF analysis was conducted to discover underlying mechanisms and protein networks, and targeted label-free Nano-LC QTOF with SWATH was performed to qualify discovered protein candidates. Twenty-eight proteins were identified as candidates and functionally analyzed via String DB, gene ontology and pathway analysis. Four predictive mechanisms were analyzed: i) response to stimulus, ii) platelet activation, signaling and aggregation, iii) ECM-receptor interaction, and iv) angiogenesis. These mechanisms can provoke kidney dysfunction in type 2 diabetic patients via endothelial cell damage and glomerulus structural alteration. Based on these analyses, three proteins (kininogen-1, basement membrane-specific heparan sulfate proteoglycan core protein, and roundabout homolog 4) were proposed for further study as potential biomarkers. Our findings provide insights that may improve methods for both prevention and diagnosis of diabetic nephropathy.
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PMID:Roles of kininogen-1, basement membrane specific heparan sulfate proteoglycan core protein, and roundabout homolog 4 as potential urinary protein biomarkers in diabetic nephropathy. 3266 74