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)

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.
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PMID:Risk factors for coronary heart disease in diabetes mellitus. 152 26

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

Renal protection is defined as an attenuation or significant slowing of the irrevocable decrease in renal function over time, which occurs subsequent to renal dysfunction. Control of systemic hypertension by whatever means exerts a renal protective effect. Evidence suggesting a specific action of individual antihypertensive agents is less certain. Calcium antagonists may exert a specific renal protective effect. Experiments in rats with reduced renal mass, desoxycorticosterone-induced hypertension, chronic angiotensin II infusion, and in spontaneously hypertensive rats support such a view. In three crossover trials, calcium antagonists reduced proteinuria in patients with type 2 diabetes mellitus. Preliminary data from a single prospective trial in patients with renal insufficiency offer additional support; however, definitive conclusions cannot be reached without further trials. In particular, comparative trials of different classes of antihypertensive agents with equal blood pressure control are needed. Thus far, only reducing systemic blood pressure per se has been shown to be of value in attenuating hypertension-induced renal dysfunction in humans.
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PMID:Are calcium antagonists of value in ameliorating the course of chronic renal disease? 161 61

Diabetic nephropathy is the most important complication of diabetes, because it is a major cause of morbidity and mortality for diabetic subjects. Since not all subjects with diabetes are at risk of developing this complication, we conducted a study to determine if heredity might be a possible risk factor for diabetic nephropathy in non-insulin dependent diabetes. Twenty-one factors including inheritance of nephropathy and hypertension were investigated in 109 individuals with NIDDM: 50 patients without proteinuria (Group I), 20 patients with intermittent proteinuria (Group II), and 39 patients with continuous proteinuria (Group III) matched for age and duration of diabetes. Of those patients, 55 patients with inheritance of diabetes were also divided into three groups: 29 patients without proteinuria (Group I), 9 patients with intermittent proteinuria (Group II), and 17 patients with continuous proteinuria (Group III). Individuals in Groups II and III has significantly higher frequency of inheritance of diabetic nephropathy than those in Group I, and also individuals with inheritance of diabetic nephropathy had significantly higher frequency of diabetic nephropathy than those without it. Frequency of hypertension, retinopathy and body mass index in the past were significantly higher in subjects in Groups II or Group III than in those in Group I. There were no significant differences between subjects in Groups II and III. These findings suggest that susceptibility to diabetic nephropathy in NIDDM may be hereditary, although hypertension and obesity may also be important risk factors for diabetic nephropathy.
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PMID:[The possibility of hereditary factors in the susceptibility to diabetic nephropathy in NIDDM]. 163 29

Many lipoprotein abnormalities are seen in the untreated, hyperglycemic diabetic patient. The non-insulin-dependent diabetic (NIDDM) patient with mild fasting hyperglycemia commonly has mild hypertriglyceridemia due to overproduction of TG-rich lipoproteins in the liver, associated with decreased high-density lipoprotein (HDL) cholesterol levels. The more hyperglycemic untreated NIDDM and insulin-dependent diabetic (IDDM) patient have mild to moderate hypertriglyceridemia due to decreased adipose tissue and muscle lipoprotein lipase, (LPL) activity. These patients also have decreased HDL cholesterol levels associated with defective LPL catabolism of TG-rich lipoproteins. Treatment of diabetes with oral sulfonylureas or insulin corrects most of the hypertriglyceridemia and some of the decrease in HDL cholesterol. The abnormality in adipose tissue LPL activity corrects slowly over several months of therapy. The treated IDDM patient often has normal lipoprotein levels. The treated NIDDM patient may continue to have mild hypertriglyceridemia, increased intermediate-density lipoprotein levels, small dense low-density lipoproteins (LDL) with increased apoprotein B, and decreased HDL cholesterol levels. The central, abdominal distribution of adipose tissue in IDDM is associated with insulin resistance, hypertension, and the above lipoprotein abnormalities. Improvement in glucose control, in the absence of weight gain, leads to lower triglyceride and higher HDL cholesterol levels. In addition, the diabetic patient is prone to develop other defects that, in themselves, lead to hyperlipidemia, such as proteinuria, hypothyroidism, and hypertension, treated with thiazide diuretics and beta-adrenergic-blocking agents. When a diabetic patient independently inherits a common familial form of hypertriglyceridemia, he might develop the severe hypertriglyceridemia of the chylomicronemia syndrome.
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PMID:Pathophysiology of hyperlipidemia in diabetes mellitus. 171 Jul 39

In order to provide further insights into the conflicting reports of associations between diabetes and uric acid metabolism, we studied 175 adult diabetic patients (56 IDDM, 119 NIDDM) and 114 matched control subjects. Plasma uric acid (PUA) concentrations were not significantly different between diabetic and control subjects, despite increased urinary urate in diabetic patients. There were no significant associations, in diabetic patients, between PUA and (i) type of diabetes, (ii) glycaemic control, (iii) retinopathy and (iv) proteinuria. Plasma urate did not correlate with the KG constant for glucose disposal rate during IVGTT, thus indicating that PUA may not be related to insulin action. In a separate study, PUA rose sharply, peaking at 30 min, and fell subsequently in both newly diagnosed NIDDM patients (n = 20) and subjects with impaired glucose tolerance (n = 15) in response to standard OGTT, in contrast to normal controls (n = 35) in whom PUA rose gradually to a peak at 120 min. Mean rise in PUA from baseline to peak was significant (P less than 0.05) in the diabetic group only. These differences in PUA response during an OGTT between subjects with abnormal glucose metabolism and normal controls may be a feature in the metabolic evolution of diabetes and need further investigation.
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PMID:Plasma urate in diabetes: relationship to glycaemia, glucose disposal, microvascular complications and the variations following oral glucose. 175 87

Type 2, non-insulin-dependent diabetes mellitus accounts for 60% of the end-stage renal disease attributed to diabetes in the United States, yet little is known about glomerular function or the development of renal disease in this type of diabetes. The Diabetic Renal Disease Study (DRDS) is a longitudinal study designed to elucidate the natural history of renal disease and to characterize glomerular function throughout the course of renal disease in type 2, non-insulin-dependent diabetes mellitus. The study is being conducted among the Pima Indians from the Gila River Indian Community in Arizona because they experience a very high rate of type 2 diabetes mellitus, which often develops at a young age and which is frequently associated with the development of renal disease. Glomerular filtration rate, renal plasma flow, albumin and IgG excretion, level of vasoactive hormones, retinal damage, and glomerular capillary permeability to dextrans of different sizes will be assessed at regular intervals over 48 months in six groups of subjects representing a range of glucose tolerance from normal to diabetes, and among the diabetic subjects, a range of proteinuria from normal to overt diabetic nephropathy. The DRDS is designed to provide new information on the functional determinants of renal disease in type 2, non-insulin-dependent diabetes mellitus and will serve as the basis for designing intervention strategies.
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PMID:Renal function in non-insulin-dependent diabetes mellitus: purposes and design of the Diabetic Renal Disease Study. 177 50

Type 1 and type 2 diabetes mellitus are both characterized by increased cardiovascular mortality and morbidity. Since several reports have indicated that apolipoprotein (a) [apo(a)] levels are positively associated with an increased risk of macrovascular disease, we investigated whether apo(a) levels are elevated in both types of diabetes mellitus and may thus represent an independent risk factor for atherosclerotic disease. Apo(a) concentrations in type 1 diabetic patients were not significantly different from matched controls (276 +/- 78 vs 149 +/- 46 units/l). Type 2 diabetic patients had considerably higher levels of apo(a) than matched controls (471 +/- 89 vs 221 +/- 61 units/l, P = 0.06), though the difference was not statistically significant. However, concentrations of apo(a) were above 300 units/l in 36% of type 1 and 67% of type 2 diabetic patients, but in only 14% and 25% respectively of matched control subjects. Plasma triglycerides were positively and independently correlated with apo(a) levels in both diabetic and non-diabetic subjects. On the other hand, no significant correlation was found between apo(a) levels and glycosylated haemoglobin, total cholesterol or high density lipoprotein cholesterol in any of the groups studied. In conclusion, apo(a) levels are not significantly elevated either in type 1 or type 2 diabetic patients without proteinuria and in moderate metabolic control; however, levels above 300 units/l were 2.6 times more frequent in both types of diabetes mellitus than in carefully age-, sex-, and weight-matched control subjects.
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PMID:Apolipoprotein (a) levels in type 1 and type 2 diabetes mellitus. 177 52

The beneficial effects of conventional long treatment on declining renal function in diabetic nephropathy (non-insulin-dependent diabetes mellitus, NIDDM) were evaluated retrospectively. One hundred NIDDM patients with overt proteinuria were followed for more than three years. Clinical data before and after various regimens of treatment were compared statistically. Treatment included a calcium antagonist (CaA), alpha-methyl dopa (AMD), an alpha-blocker (ABL), angiotensin converting enzyme inhibitor (ACEI), anti-platelet agents (APL), essential amino acids (EAA), and an oral absorbent (AST-120). Changes in renal function were analyzed by comparing the degree of slopes of regression rate of the reciprocals of serum creatinine levels (R1/Cr). Administration of ACEI and EAA resulted in R1/Cr improvement after the initiation of treatment (p less than 0.05). It appears that the administration of EAA and ACEI are beneficial with regard to protection against renal failure in NIDDM patients with diabetic nephropathy.
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PMID:Ameliorating effects of conventional therapy on declining renal function in patients with diabetic nephropathy. 181 52

To determine the effectiveness of dietary protein restriction on proteinuria in patients with non-insulin dependent diabetes (NIDDM), 14 diabetic patients with overt nephropathy were placed on either a low protein diet (N = 7) or conventional protein diet (N = 7) for one month. After the study period, daily urinary protein excretion rates decreased significantly, from 3.2 +/- 0.4 to 1.9 +/- 0.4 g/day, and serum albumin levels increased from 3.3 +/- 0.2 to 3.7 +/- 0.5 g/dl only in the low protein diet group, without any significant changes in either serum creatinine levels or creatinine clearance. These findings suggest that dietary protein restriction has a beneficial role in the treatment of NIDDM patients with overt nephropathy.
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PMID:Effect of dietary protein restriction on proteinuria in non-insulin-dependent diabetic patients with nephropathy. 182 Apr 50


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