UMLS:C0033687 - FACTA Search

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Query: UMLS:C0033687 (proteinuria)
24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Microalbuminuria is defined in principle as abnormally increased albumin excretion below the level that is characteristic for proteinuria. In diabetes, microalbuminuria is defined as having an excretion rate of 20 to 200 micrograms/min. This level of albuminuria predicts overt renal disease in both non-insulin-dependent diabetes mellitus and insulin-dependent diabetes mellitus patients, and it is also associated with increased mortality. In nondiabetic individuals, the albumin excretion rate is not normally distributed with a skewed upper distribution. Excretion rate is lower during daytime, even during rest, than overnight. The median values in several studies for daytime and overnight albumin excretion rates are approximately 4 and 3 micrograms/min, respectively, with the upper 90th percentile approximately 15 and 10 micrograms/min, respectively. Microalbuminuria in population studies is significantly, but weakly, correlated to blood pressure, triglycerides, and low high-density lipoprotein cholesterol, as well as plasma glucose and obesity. These parameters are elements of the so-called metabolic syndrome. New studies in insulin-dependent diabetes mellitus on the transition from normo- to microalbuminuria show that high normal excretion rate and poor metabolic control are associated with progression. In non-insulin-dependent diabetes mellitus, microalbuminuria is quite common (20% to 25% of patients) in both newly diagnosed patients and patients with established diabetes. In many studies, a prevalence of approximately 20% is found, and again microalbuminuria is associated with components of the metabolic syndrome, which includes poor metabolic control and blood pressure elevation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Epidemiology of microalbuminuria in diabetes and in the background population. 792 49

Impairment of renal function, severe proteinuria and arterial hypertension are the strongest clinical predictors of an unfavorable outcome in IgA nephropathy (IgAN). Glomerulosclerosis and interstitial fibrosis are the most reliable histologic prognostic markers. Metabolic syndrome and insulin resistance probably affect the clinical course of the disease. Among the known gene polymorphism it seems that there is a link between the ACE gene D allele and the progression of IgAN. Elevated blood pressure should be actively treated. The target blood pressure is 130/80 mmHg or less and the goal should also be to reduce proteinuria. Several large-scale trials are currently testing corticosteroids and other drugs in the treatment of IgAN.
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PMID:Clinical course and treatment of IgA nephropathy. 1178 99

It has been previously shown that 2-hydroxyestradiol (2-OHE) attenuates the development of renal disease in genetic nephropathy associated with obesity and the metabolic syndrome. The purpose of this study was to test the hypothesis that 2-OHE, irrespective of its effects on metabolic status and/or obesity, exerts direct renoprotective effects in vivo. First, the effects of increasing doses of 2-OHE on mesangial cell growth, proliferation, and collagen synthesis in isolated rat glomerular mesangial cells were evaluated in vitro. Second, the effects of 12-wk administration of 2-OHE (10 micro g/h per kg) on renal function and structure in chronic puromycin aminonucleoside (PAN)-induced nephropathy in rats were evaluated in vivo. 2-OHE concentration-dependently (0.001 to 1 micro mol/L; P < 0.001) inhibited serum (2.5%)-induced cell growth ((3)H-thymidine incorporation), collagen synthesis ((3)H-proline incorporation), and cell proliferation (cell number). Importantly, the inhibitory effects of 2-OHE (0.1 micro mol/L) were not blocked by ICI182780 (50 micro mol/L), an estrogen receptor antagonist. In vivo, chronic administration of PAN (75 mg/kg + 5 x 20 mg/kg) over 12 wk induced severe chronic renal disease. Chronic treatment with 2-OHE significantly (P < 0.05) attenuated PAN-induced decrease in glomerular filtration, reduced proteinuria, and the elevated BP, and it had no effect on PAN-induced increase in plasma cholesterol and triglycerides levels. 2-OHE had no effects on plasma testosterone levels in male nephropathic animals. Immunohistochemical staining for collagen IV and proliferating cell nuclear antigen (PCNA) in glomeruli and transforming growth factor-beta (TGF-beta) in renal tubular cells were significantly higher in PAN nephropatic rats versus control animals with intact kidneys. PAN also markedly increased glomerular and interstitial macrophage infiltration (ED1(+) cells). 2-OHE had no effects on renal tubular cell TGF-beta, but it significantly reduced glomerular PCNA and collagen IV and glomerular and interstitial macrophage infiltration. In summary, this study provides the first evidence that 2-OHE exerts direct renoprotective effects in vivo. These effects are mediated by estrogen receptor-independent mechanisms and are due, at least in part, to the inhibition of some of the key proliferative mechanisms involved in glomerular remodeling and sclerosis.
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PMID:2-Hydroxyestradiol attenuates renal disease in chronic puromycin aminonucleoside nephropathy. 1239 44

Patients with hypertension (78 men, 113 women aged 20-73 years) were stratified according to risk of development of cardiovascular complications. In low and moderate risk patients (n=31) with borderline hypertension, dyslipidemia and pronounced obesity mainly non-drug measures were employed directed at lowering of excess body mass. Medium risk patients (n=25) with isolated hypertension group were treated with angiotensin converting enzyme inhibitors and phenylalkylamine calcium antagonists. High risk patients (n=55) with metabolic syndrome received same antihypertensive drugs as medium risk patients. In very high risk patients (n=79) with diabetes, excessive body mass, dyslipidemia and proteinuria complex therapy consisting of antihypertensive and hypoglycemic drugs and non-drug interventions was used. This risk stratification based management of patients with hypertension on turned out to be highly effective and resulted not only in normalization of blood pressure but also in improvement of carbohydrate and lipid metabolism, lowering of resistance to insulin and excessive body mass, and improvement of renal function.
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PMID:[Stratification of patients with hypertension and selection of antihypertensive therapy]. 1249 81

Diabetic nephropathy has become the single largest cause of end-stage renal disease (ESRD) worldwide. Until recently, it was thought that once a patient developed overt proteinuria, diabetic nephropathy was irreversible and inevitably progressed to ESRD. However, the reversal of lesions caused by diabetic nephropathy (e.g., glomerular basement membrane thickening and mesangial matrix increase) has been demonstrated in a series of patients who underwent a pancreas transplantation 10 years prior to the reversal. Remission of nephrotic range proteinuria has also been reported in some patients with type 1 diabetes from the Collaborative Study Group during a median follow-up of 3 years of angiotensin-converting enzyme (ACE) inhibitor administration; no deterioration of renal function was observed in these patients. Remission and regression in nephropathy of type 1 diabetes patients have also been reported when blood pressure was controlled aggressively. Recent clinical trials have demonstrated that angiotensin II receptor blocker (ARB) preserved renal function and slowed the progression of nephropathy to ESRD in patients with type 2 diabetes. Since many patients with type 2 diabetes manifest with a metabolic syndrome, multifactorial intensive treatment is necessary; such treatment includes behavior modifications, dietary intervention, exercise, and smoking cessation. In this population, pharmacological therapy targeting hyperglycemia, hypertension (including ARB/ACE inhibitor), and hyperlipidemia in cases of type 2 diabetes is also necessary.
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PMID:Remission and regression of diabetic nephropathy. 1292 17

The prevalence of chronic kidney disease (CKD) is on the rise in all ethnic groups. This is because of the increased prevalence of obesity, diabetes mellitus, the metabolic syndrome, and the inadequate control of elevated blood pressure and other cardiovascular-renal risk factors, especially in ethnic minority populations. The implications of the aforementioned trends in risk factor prevalence and control are profound. Moreover, these trends negatively impact patient quality of life and place an enormous financial burden on the health care system for the provision of care to patients with CKD, end-stage renal disease (ESRD), and/or cardiovascular disease (CVD). Thus, it is of utmost importance to devise strategies that prevent kidney disease and delay progressive loss of kidney function in persons with CKD. Proven strategies include pharmacological interventions that lower blood pressure to less than target levels (<130/80 mm Hg), attainment of optimal glycemic control (Hb A1c <7%), and reducing urinary protein excretion. It is also possible, although yet unproven, that correction of anemia and aggressive treatment of dyslipidemia may forestall the loss of kidney function. In general, ethnic minorities are underrepresented in most large trials. Recently, a few outcome clinical trials in blacks have reinforced the lessons of kidney function preservation already learned in nonblack populations. That is, the reversible risk factors for CKD appear to be virtually identical and, at least in nondiabetic CKD, pharmacological targeting of the renin-angiotensin-aldosterone system (RAAS) with angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers preserves kidney function better than non-RAAS blood pressure-lowering regimens, especially when significant proteinuria exists. Although more CKD studies in ethnic minorities are needed, until they become available, the best available evidence from the existing clinical trial database should be applied to minorities with CKD-even when specific data are not available for a specific racial or ethnic group. Why this approach? First, there are no known unique risk factors for kidney disease in any ethnic group. Second, poor control of reversible risk factors for CKD is universal, particularly in blacks and other ethnic minorities. Thus, it is logical to predict that more efficient use of strategies proven to forestall loss of kidney function will reduce the excess of CKD and ESRD in ethnic minorities relative to non-minority populations. However, medical-based strategies alone are probably not enough. The global epidemic of obesity will fuel the growing population of persons, especially among ethnic minorities, with diabetes, the main cause of CKD, ESRD, and CVD. The obesity and diabetes epidemics are unlikely to abate without innovative and ultimately effective public health approaches.
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PMID:Pharmacological strategies for kidney function preservation: are there differences by ethnicity? 1473 May 36

Cardiovascular disease is a major cause of mortality in individuals with diabetes. Many factors, including hypertension, contribute to the high prevalence of CVD in this population. Hypertension occurs approximately twice as frequently in patients with diabetes compared with patients without diabetes. Conversely, recent data suggest that hypertensive persons are more likely to develop diabetes than normotensive persons. In addition, up to 75% of CVD in patients with diabetes may be attributed to hypertension, leading to recommendations for more aggressive blood pressure control (ie, < 130/85 mm Hg) in persons with coexistent diabetes and hypertension. Increasing obesity further contributes to both diabetes and hypertension and significantly increases CVD morbidity and mortality. Other important risk factors for CVD in these patients include atherosclerosis, dyslipidemia, microalbuminuria, endothelial dysfunction, platelet hyperaggregability, coagulation abnormalities, and diabetic cardiomyopathy. The current knowledge regarding these risk factors has been reviewed, placing special emphasis on the metabolic syndrome, hypertension, microalbuminuria, and the role of obesity in these disorders. Although not discussed in detail, it is acknowledged that both hygienic measures (weight loss and aerobic exercise) and treatment strategies that include aspirin, statins, INS sensitizers, and antihypertensive agents that reduce renin-angiotensin-aldosterone system activity have been shown to reduce inflammation, coagulation abnormalities, endothelial function, proteinuria, and in some cases reduce CVD and renal disease progression. Additional therapeutic agents are currently being developed specifically to improve INS sensitivity and other CVD risk factors that are components of the cardiometabolic syndrome.
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PMID:Insulin and insulin resistance: impact on blood pressure and cardiovascular disease. 1487 Oct 51

To determine whether the clustered features of the metabolic syndrome precede the 7 year incidence of cardiovascular disease (CVD) and type 2 diabetes, we examined 6182 Japanese male office workers aged 35-59 years without any history of CVD. The 5588 subjects without type 2 diabetes also constituted the nondiabetic cohort, and were re-examined over seven successive years. Components of the metabolic syndrome included glycemic disorder (type 2 diabetes for the risk of CVD and impaired fasting glucose for the risk of type 2 diabetes), systemic obesity, hypertension, dyslipidemia, proteinuria, and elevated white blood cell (WBC) count. After controlling for age, family history of diabetes, alcohol intake, and cigarette smoking, the multivariate-adjusted relative risk of incidence of CVD compared with absence of components was 3.18, 3.48, 12.55, and 14.15 (P for trend <0.001), for the presence of 1,2,3, and > or =4 components, respectively. The corresponding relative risks of incidence of type 2 diabetes were 1.92, 4.36, 6.44, and 15.08 (P for trend <0.001). In both non-smokers and current smokers, the multivariate-adjusted relative risks of incidence of CVD and type 2 diabetes increased as the number of components increased (P for trend <0.001 for all). Our findings indicate that clustered features of the metabolic syndrome are closely associated with development of CVD and type 2 diabetes in middle-aged Japanese.
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PMID:Components of the metabolic syndrome as predictors of cardiovascular disease and type 2 diabetes in middle-aged Japanese men. 1503 28

The 5-year incidence of coronary artery disease (CAD) and progression to overt proteinuria was investigated in patients with type 2 diabetes mellitus who had microalbuminuria with (MA+R group, n=93) or without (MA-R group, n=138) diabetic retinopathy. The rate of progression to overt proteinuria was higher in the MA+R group than in the MA-R group. The MA-R group had more components of metabolic syndrome than the MA+R and normoalbuminuric (NA, n=205) groups. The MA-R group had a higher 5-year incidence of CAD than the NA group. The incidence of CAD tended to be higher in the MA-R group than in the MA+R group, but statistical significance was not reached. The present study shows that patients with diabetic retinopathy and microalbuminuria represent a group with incipient diabetic nephropathy having higher risk for progression to overt proteinuria. On the other hand, patients with microalbuminuria and no retinopathy may represent a group with characteristics of metabolic syndrome.
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PMID:Incidence of overt proteinuria and coronary artery disease in patients with type 2 diabetes mellitus: the role of microalbuminuria and retinopathy. 1522 28

Zucker diabetic fat (ZDF) rats with the metabolic syndrome and hyperlipidemia develop focal and segmental sclerosis. The role of oxidative and nitrosative stress in the nephropathy in ZDF was studied. Renal histology, function, and immunohistologic and biochemical parameters of oxidative and nitrosative stress were evaluated at 8 and 22 wk of age in ZDF and Zucker lean (ZL) rats and after chronic treatment with ebselen, an antioxidant and peroxinitrite scavenger. At 8 wk, ZDF rats showed hyperglycemia, no proteinuria or nephropathy, but higher levels of dihydrobiopterin and 3-nitrotyrosine (3-NT)-modified proteins compared with age-matched ZL rats. At 22 wk, ZDF rats developed focal and segmental sclerosis, proteinuria, decreased creatinine clearance, and renal tissue levels of glutathione and tetrahydrobiopterin with further elevation in dihydrobiopterin and 3-NT-modified proteins, in contrast to age-matched ZL rats. Renal immunohistologic expression of lipid peroxidation products and 3-NT-modified proteins also increased in 22-wk-old ZDF but not in ZL rats. Chronic ebselen treatment of ZDF rats restored renal tissue levels of glutathione and tetrahydrobiopterin; prevented significant accumulation of dihydrobiopterin, lipid peroxidation products, and 3-NT-modified proteins; and ameliorated focal and segmental sclerosis, proteinuria, and fall in creatinine clearance without affecting mean BP, body weight, and blood glucose, compared with the untreated ZDF rats. Chronic ebselen therapy also ameliorated vasculopathy with lipid deposits and tubulointerstitial scarring, inflammation, and upregulated alpha-smooth muscle actin expression. These findings suggest that ZDF rats develop a progressive nephropathy with glomerular, vascular, and tubulointerstitial pathology. Oxidative and nitrosative stress predates the nephropathy, which is improved by peroxinitrite scavenger ebselen, and thus considered its cause and not consequence.
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PMID:Nephropathy in Zucker diabetic fat rat is associated with oxidative and nitrosative stress: prevention by chronic therapy with a peroxynitrite scavenger ebselen. 1533 88

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