Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalences of risk factors and angiopathy were studied in 260 diabetic patients, 100 females and 160 males, 35-54 years old, in Uppsala. The prevalence, in females and males separately, of hypertension (WHO-criteria) was 46-34%, of hypercholesterolaemia (greater than or equal to 6.7 mmol.l-1) 32-29%, and of obesity (relative BMI greater than or equal to 120%) 25-20%. Those smoking greater than 15 cigarettes/day were 11-20%. Mean HbA1 was 10.6-10.5%. The prevalence of angina pectoris was 11-6%, of possible infarction 4-6%, and of major ECG abnormalities 6-4%. Large vessel (cardiovascular) disease was independently related to HbA1 (strongly), hypertension, cholesterol, age and familial NIDDM. The prevalence of severe retinopathy (blindness, new vessels or large hemorrhage) was 0% with 7-13 years of diabetes duration, and 26% with greater than or equal to 14 years of duration. The prevalence of severe proteinuria was 4% with 7-13 years of diabetes duration, and 15% with greater than or equal to 14 years of duration. Small vessel (retinopathy and nephropathy) disease was independently related to diabetes duration (strongly), HbA1 and hypertension. The data were discussed related to data from the London, Berlin and Tokyo centres of the WHO Multinational Study of Vascular Disease in Diabetics, using the same study protocol in the present study.
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PMID:Prevalences of risk factors and angiopathy in diabetic patients in Uppsala. 152 37

Concentrations of urinary albumin and the albumin:creatinine ratio were measured in early-morning urine specimens from 5670 people older than 40 years who participated in a health screening survey of a local workforce. Sex-specific reference intervals were determined in a subgroup of 3597 people after excluding 2073 individuals with Albustix-positive proteinuria; diabetes mellitus; bacteriuria; current hypertension; body mass index greater than or equal to 30 kg/m2; or serum triglyceride greater than or equal to 2.5 mmol/L. The 97.5 percentile concentration for urinary albumin was 28 mg/L in men and 29 mg/L in women; for the albumin:creatinine ratio this was 2.3 g/mol in men and 2.8 g/mol in women. In the study population, the degree of albuminuria showed piecewise log-linear relationships with diastolic blood pressure (P = 0.0001) and body mass index (P = 0.0001), log-linear relationships with hypertriglyceridemia (P = 0.0001) and hypercholesterolemia (P = 0.0001), and a negative piecewise linear relationship with high-density lipoprotein (HDL) cholesterol (P = 0.0461).
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PMID:Albuminuria in people at least 40 years old: effect of obesity, hypertension, and hyperlipidemia. 152 18

A matched case-control study was performed to assess the prevalence of pathological proteinuria (greater than 50 mg/l) 18-34 years after onset of insulin-dependent diabetes mellitus (IDDM), in relation to intensive insulin therapy. Three groups of patients were studied greater than or equal to 18 years after onset of IDDM. In patients of group A and group B, intervention took place greater than or equal to 8 years after onset of IDDM: group A changed from traditional insulin therapy to continuous subcutaneous insulin infusion (CSII), and patients of group B changed from traditional insulin treatment (less than 3 injections/day) to multiple daily insulin injection therapy. Patients of group C continued traditional insulin therapy without intervention. The prevalence of pathological proteinuria was 3/21, 5/21, and 15/21 in group A, B, and C, respectively; 22.0 (95% confidence interval: 19.5 to 24.5) years, 22.1 (19.9 to 24.3) years, and 22.6 (20.2 to 25.0) years after onset of IDDM in group A, B, and C. The prevalence of pathological proteinuria differed significantly between group A and B vs. group C (x2 = 16.2, p less than 0.001; odds ratio 15 (3.2 to 70.3)). Glycosylated haemoglobin was 7.5 (6.9 to 8.1)% in group A, 7.6 (6.3 to 8.3)% in group B, and 8.9 (8.2 to 9.6)% in group C. In group A and B, 4/21 patients had hypertension, compared to 11/21 patients in group C. In group B, 1/21 patients had serum-creatinine greater than 130 mumol/l.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathological proteinuria in patients with insulin-dependent diabetes mellitus: relation to intensive insulin therapy. 152 68

A review of the putative risk factors associated with the development of coronary heart disease in diabetes is presented. Emphasis is given to the effect of nephropathy (persistent proteinuria) and hypertension on cardiovascular mortality in IDDM. Risk factors associated with CHD in NIDDM are also reviewed. Finally, possible reasons to explain the increased incidence of CHD associated with proteinuria in IDDM patients, including lipoprotein abnormalities, increased fibrinogen levels, increased platelet adhesiveness, and altered hemostatic variables, are discussed.
Diabetes 1992 Oct
PMID:Risk factors for coronary heart disease in diabetes mellitus. 152 26

Patients with the clinical diagnosis of ischemic heart disease who were found to be free of significant coronary artery atherosclerotic disease (n = 150) underwent coronary vasodilator reserve testing, 2-dimensional echocardiography, and dipyridamole limited-stress thallium testing. After exclusions (predominantly for technically poor coronary artery Doppler signals or suboptimal echocardiography), 100 patients formed the study population. The purpose was to characterize typical cardiac and coronary artery findings in hypertensive patients with severe left ventricular (LV) hypertrophy (n = 15) and to investigate the evidence for myocardial ischemia unrelated to coronary atherosclerosis in early and advanced hypertensive heart disease. Normotensive and hypertensive control groups without LV hypertrophy (n = 12 and 34, respectively) were used for comparison. Severe LV hypertrophy was defined as LV mass index greater than or equal to 50% above established gender specific norms using 2-dimensional-directed M-mode echocardiography and the cube equation corrected to agree with necropsy estimates of mass. Clinical characteristics more often associated with severe LV hypertrophy were black race (67%), diabetes mellitus (33%), proteinuria (47%) and elevated creatinine (1.5 +/- 0.9 mg/dl). Baseline electrocardiograms and dipyridamole limited-stress thallium scans were highly likely to be abnormal (94 and 73%, respectively). Both eccentric and concentric cardiac hypertrophies were found in the severe group. Ejection fraction was significantly lower (0.51 vs 0.68, p = 0.002) and basal coronary flow velocity higher (12.0 vs 5.0 cm/s, p = 0.0004) among these patients when compared with normotensive control patients. Coronary flow reserve did not differ between control groups but was significantly depressed in patients with severe LV hypertrophy (2.5 vs 3.9, p = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Morphologic, hemodynamic and coronary perfusion characteristics in severe left ventricular hypertrophy secondary to systemic hypertension and evidence for nonatherosclerotic myocardial ischemia. 153 Sep 94

The angiotensin converting enzyme (ACE) inhibitors are a group of effective drugs with a unique mechanism of action. These drugs have proven to be useful for hypertension and congestive heart failure. Early clinical trials of captopril used doses that are now known to be inappropriately high, and dose-related adverse effects were observed frequently. The recognition that lower doses are effective has reduced the incidence of adverse reactions and resulted in improved patient tolerance. When patients are properly selected and correctable risk factors are removed, serious side effects are uncommon. Unfortunately, the early reputation of nephrotoxicity persists, as does the belief that significant blood dyscrasias, endocrine effects and rash are serious risks for the average patient. After wide use of captopril, enalapril and lisinopril, and investigational trials of nearly a dozen newer agents, a sufficiency of clinical observation, experimental evidence and accurate postmarketing recording of events is accumulating to allow insight into the major toxicities with regard to more intelligent patient selection, more rational dosing and proper identification of risk factors. The most common adverse reactions are cough and skin rash. It appears that the agents are generally not cross-reactive with regard to skin rash, although it is not clear whether this effect is drug-specific or class-specific with regard to cough. Statistically but not clinically significant lowering of haemoglobin and hematocrit is common; these effects are inconsequential in most patients. Neutropenia, once thought to be prevalent, now appears to be so only in patients with autoimmune or collagen-vascular disease; the majority of patients outside these groups are at low risk. Hyperkalaemia is a frequent occurrence. This should not be surprising in view of the effect of the ACE inhibitors on plasma aldosterone. When dietary potassium intake is regulated and sources of altered potassium excretion are identified, hyperkalaemia is seldom a serious problem. Identification of sodium and water deficits allows correction before the drugs are started, and the frequency of hypotension and hyperkalaemia caused by the drugs is quite low if these factors are properly managed. An unexpected finding emerging in recent years is the dry cough associated with ACE inhibitor therapy. Its mechanism is not definitely known. Nonsteroidal anti-inflammatory drugs may control this symptom in some patients. The frequent observation of proteinuria in patients taking ACE inhibitors has gained notice and sometimes caused undue alarm. It is difficult to separate disease effects in diabetes and hypertension from true drug effects.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Adverse effects of angiotensin converting enzyme (ACE) inhibitors. An update. 153 95

Levels of cardiovascular risk factors were determined in 75 patients with Type 2 diabetes mellitus. The patients were divided into three groups according to their urinary protein excretion (UPE): (a) normal proteinuria (less than or equal to 70 mg d-1); (b) microproteinuria (70-500 mg d-1); and (c) macroproteinuria (greater than 500 mg d-1). A significant stepwise increase in mean systolic blood pressure, LDL-cholesterol and fibrinogen levels was observed from the first to the third investigated group of patients. Mean apoprotein B levels were significantly increased in the group with macroproteinuria compared to the other two groups. Significant linear correlations were found between UPE and LDL-cholesterol, total cholesterol, apoprotein B, creatinine, systolic blood pressure and diabetes duration. In summary, it is concluded that the levels of some cardiovascular risk factors increase with the stage of proteinuria in Type 2 diabetes mellitus.
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PMID:Levels of cardiovascular risk factors in type 2 diabetes mellitus are dependent on the stage of proteinuria. 154 31

Experimental animal studies have demonstrated a renal protective effect of ACE inhibition therapy in diabetes mellitus and the remnant kidney model of chronic renal failure. The mechanism of this effect is secondary, at least in part, to the drugs' effects on glomerular hemodynamics. In addition, there is further evidence to suggest that ACE inhibitors may influence other pathogenic mechanisms of progressive renal insufficiency. Preliminary data in clinical studies suggest that ACE inhibition therapy decreases proteinuria and may ameliorate the decline of the glomerular filtration rate in diabetic nephropathy and progressive renal insufficiency of other etiologies. However, before this conclusion can be definite, a large, prospective, randomized clinical trial is required to compare ACE inhibitors to conventional antihypertensive agents. Since calcium channel blockers are metabolically neutral in that they do not increase serum cholesterol or glucose levels and generally do not cause orthostatic hypotension, they may be ideal agents for such a comparison study.
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PMID:Progressive renal insufficiency: the role of angiotensin converting enzyme inhibitors. 155 7

Diabetic nephropathy typically presents more than a decade after diagnosis of diabetes and correlates with the duration of poorly controlled disease. Diabetic nephropathy begins as glomerular hypertension and hyperfiltration, followed by microalbuminuria and the development of hypertension, overt proteinuria, nephrotic syndrome, and a progressive decline in the glomerular filtration rate. Increasing expansion of the glomerular mesangium correlates with loss of function, resulting in uremia. This process eventually leads to the need for dialysis or renal transplantation in 30 percent of patients with insulin-dependent diabetes. By lowering intraglomerular pressure through enhanced glycemic control, inhibition of angiotensin and limitation of protein intake, severe nephropathy may be prevented, delayed or even partially reversed. Treatment must stress control of hypertension.
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PMID:Diabetic nephropathy: early detection, prevention and management. 155 42

In an investigation into the effect of prostaglandin E1 on proteinuria in nephrotic diabetic nephropathy, five patients were treated with 40 micrograms prostaglandin E1 administered intravenously over 2 h twice daily for 4 weeks. The following parameters were compared before and after treatment: protein excretion in urine; total serum protein concentration; serum albumin concentration; creatinine clearance; blood urea nitrogen; and serum creatinine content. A further five patients with nephropathy resulting from non-insulin-dependent diabetes mellitus were selected as controls. Analysis of the results using Student's t-test showed no significant change in any of the parameters before and after treatment.
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PMID:Influence of prostaglandin E1 on slight proteinuria in non-azotaemic diabetics. 156 24


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