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)

Long-term protein intake may have pathogenic influence on development of late diabetic complications. A review of the latest results in insulin-dependent diabetic patients shows that short-term lowering of protein intake reduces the characteristic early glomerular hyperfiltration as well as microalbuminuria and proteinuria in diabetic nephropathy. A sustained beneficial effect on the progression rate of nephropathy may be achieved. Based on this evidence it is advisable to avoid the traditionally high protein intake in diabetes. We suggest a protein-controlled diet--with protein comprising 14 energy %--as a goal in uncomplicated diabetes. In patients with progressive albuminuria or proteinuria prescription of a low-protein diet with 10% protein should be considered as supplementation to antihypertensive treatment. At present we do not find sufficient evidence for suggesting an intake of 10% protein (corresponding approximately to recent recommendations on 0.8 g prot/kg body weight) also in uncomplicated diabetes. Both a 10 and 14% protein diet will differ somewhat from the diet of the background population and the present diet of many diabetic patients. Therefore the introduction of such diets requires a careful individualized diet therapy in which repetitive evaluation and estimation of compliance are performed. A reduction of protein intake to 10 energy % represents a profound diet intervention.
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PMID:Reducing protein in the diabetic diet. 207 71

The precise pathogenesis of human diabetic kidney disease and the factors responsible for the susceptibility to it remain to be established. However, there is now evidence that renal disease clusters in families and that genetic factors are of central importance in determining liability. A predisposition to arterial hypertension has been suggested as playing a contributory role in the development of kidney disease. Genetically controlled hypertrophic processes may be implicated in the susceptibility to arterial wall damage and glomerular injury in diabetes. This suggestion derives from the observation that the fibroblasts of patients with diabetic nephropathy show a higher Na+/H+ antiport activity and a greater 3H-thymidine incorporation into DNA than fibroblasts of diabetic patients without nephropathy. The first sign of renal damage is the appearance of microalbuminuria and of a small elevation in arterial pressure, changes associated with significant mesangial expansion. Microalbuminuria is associated with abnormalities of lipoprotein profiles possibly as a consequence of insulin-resistance-induced hyperinsulinemia. It could be postulated that the environmental changes brought about by diabetes lead in susceptible individuals to increased systemic and intraglomerular pressure on the one hand and mesangial expansion on the other. These two processes would cause proteinuria and glomerulosclerosis. Lipid abnormalities would further aggravate the renal histological damage and, in combination with hypertension, contribute to the accelerated atherosclerosis typical of patients with diabetic kidney disease. A vicious circle would thus be triggered of reduction in renal function, more hypertension, more proteinuria, more glomerular obsolence, more hyperlipidemia and eventually end-stage renal failure or premature cardiovascular death.
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PMID:Mechanisms of diabetic renal and cardiovascular disease. 207 90

Diabetic nephropathy continues to be a common complication and has an unfavorable prognosis. Metabolic and hemodynamic factors determine the natural history of the condition. Of importance for the prognosis is the detection of nephropathy at an early stage. Such early diagnosis is not possible through the detection of microalbuminuria (incipient nephropathy stage). At this stage, further progress can be reversed by optimizing the metabolic situation and initiating early treatment of increasing blood pressure. For this reason, all diabetics should be submitted to early screening for microalbuminuria. When proteinuria persists (clinically manifest nephropathy stage), renal function usually declines progressively. Vigorous treatment of hypertension, optimal metabolic management, and normalization of protein intake can slow down the rate of continued loss of renal function.
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PMID:[Diagnosis and therapy of diabetic nephropathy]. 208 27

Recently the beneficial effects of captopril (angiotensin-converting-enzyme inhibitor) on diabetic nephropathy, especially proteinuria, have been reported by some investigators. The mechanism whereby proteinuria is reduced, however, have not been clarified yet. The present study was undertaken to evaluate the effects of captopril on urinary albumin excretion in relation to urinary prostaglandins (PGs) excretion in patients with non-insulin-dependent diabetes mellitus (NIDDM). Captopril (37.5 mg/day) was orally administered to 13 diabetic patients for an eight-week period. A single administration of captopril (12.5 mg) was performed in the same patients. The spot urine samples were collected in the early morning and 2 hr after the single administration of captopril. The albumin index (mg/gram-creatinine) was markedly decreased in eight patients (Group A) within four weeks, but no decrease was found in five patients (Group B). Furthermore, in Group A, by the single administration of captopril urinary excretions of 6-keto-PCF1 alpha (a stable metabolite of PGI2) and PGE2 were significantly (p less than 0.05) increased while urinary TXB2 (a stable metabolite of TXA2) excretion did not change significantly. The urinary 6-keto-PGF1 alpha/TXB2 ratio, which is significantly (p less than 0.05) low in diabetic patients was significantly (p less than 0.01) increased up to the normal value in Group A. In Group B, however, there were no significant changes in urinary PGs excretion. These results suggest that captopril enhances the production of intrarenal vasodilatory PGs such as PGI2 and PGE2, which may be deeply involved in the reduction of intraglomerular capillary pressure and urinary protein excretion in diabetic patients.
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PMID:Effects of captopril on urinary excretion of albumin and prostaglandins in patients with diabetic nephropathy. 209 82

We have studied the long term effects of captopril therapy on proteinuria in ten patients with non-insulin-dependent diabetes mellitus with hypertension and nephropathy. There were 7 males and 3 females, with a mean age of 53.3 +/- 10.6 years. After a run-in period of two weeks, therapy with captopril was started. The following parameters were studied: serum glucose, sodium, potassium, cholesterol and triglycerides, glycosylated haemoglobin, renal function and 24 hour urine protein excretion before and at six month intervals for up to 24 months. Average BP fell significantly from 182.5 +/- 28/95 +/- 7.1 to 146 +/- 16.7/76 +/- 18.1 mmHg although no significant changes were seen in the biochemical parameters studied, except a reduction in 24 hour urine protein excretion from 3.86 +/- 2.85 to 0.88 +/- 1.08 g/24 h after 24 months of treatment (P less than 0.01). No correlation was observed between the reduction in proteinuria and any other parameters studied. Our results confirm the reduction of proteinuria in patients with type II diabetes mellitus and stable diabetic nephropathy treated with captopril. This effect was maintained for a period of 24 months.
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PMID:Long term follow-up of the effect of captopril on severe proteinuria in hypertensive diabetic patients. 209 9

Fifty-nine streptozotocin-induced diabetic rats, not treated with insulin clearly demonstrated one of two protein excretion patterns based on urinary albumin and IgG excretion rates. 63% (35/59) of the diabetic rats developed significantly elevated albumin excretion rates (incipient proteinuria) when compared to age-matched control animals. This condition progressed to a highly elevated albuminuria and increased IgG excretion (overt proteinuria). Analysis of IgG subclass content in these diabetic proteinuric rat urines showed that there was a selective excretion of IgG2b into the urine at a time that correlated with the onset of overt proteinuria. This IgG subclass comprised approximately 75% of the total IgG excreted during progressive nephropathy (in some animals, 100%) and was unique as it was not the predominant subclass in the serum of this group of animals. The other 37% of the diabetic rats (22/59) did not develop either incipient or overt diabetic nephropathy. In fact, some animals in this group had statistically less albumin and/or IgG in their urine than control rats. The subclass IgG2c was detected sporadically in the urine of these diabetic non-proteinuric rats throughout the chronological study even though it was the IgG subclass that comprised the lowest serum concentration of all four IgG subclasses. In control rats (total of 19), urinary albumin and low levels of the subclass IgG2a were detected throughout the chronological study; both of which increased with the age of the rat. However, in contrast to diabetic rats, the subclasses IgG1 and IgG2b were not detected in the urine of control rats until late in the chronological study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunoglobulin subclasses in the urine of control and streptozotocin-induced diabetic rats and their role in the development of diabetic nephropathy. 213 8

The prevalence of microalbuminuria and persistent proteinuria was studied in a population of 801 diabetic patients (535 with type II and 266 with type I diabetes). Urinary albumin excretion rate (AER) was measured on morning samples by laser nephelometry. Normoalbuminuria, as defined, in the absence of contaminated urine, by an albumin: creatinine (A/C) ratio below 2, was found in 551 patients, microalbuminuria (NC greater than or equal to 2 with AER below 200 mg/l) in 190 patients and persistent proteinuria (AER greater than or equal to 200 mg/l) in 60 patients. Microalbuminuria was present in 48 (18 p. 100) IDDM patients and 142 NIDDM patients. In IDDM patients, AER increased with the duration of the disease with no apparent influence of age at the onset. The prevalence of hypertension was 25 p. 100 and 61 p. 100 in IDDM patients with microalbuminuria and macroproteinuria respectively versus 10 p. 100 in patients with normoalbuminuria. This prevalence increased in NIDDM patients from 39.3 p. 100 with normoalbuminuria to 40.8 p. 100 and 76.2 p. 100 with microalbuminuria or macroproteinuria respectively. Proliferative retinopathy in type I and type II patients with normal AER was 7.4 p. 100 and 1.2 p. 100 respectively increasing to 15.2 p. 100 and 8.9 p. 100 with microalbuminuria and 27.8 p. 100 and 23.1 p. 100 with macroproteinuria. The prevalence of coronary disease increased from 4 to 10.4 p. 100 in patients with type I diabetes and microalbuminuria. The prevalence of cardiac failure increased from 1.5 to 2.1 p. 100 in type I diabetics and from 3.2 to 7.8 p. 100 in type II diabetics in the presence of microalbuminuria. Patients with microalbuminuria had increased levels of glycosylated hemoglobin A 1C but statistical difference was only obtained for patients with type II diabetes. Routine analysis of AER in diabetics allows early detection of diabetic nephropathy and emphasizes the need for tight metabolic and blood pressure control. Hypertension can be detrimental to nephropathy but might also initiate renal lesions in NIDDM patients.
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PMID:[Microalbuminuria and diabetic nephropathy. Detection and correlation with other degenerative complications]. 214 8

The role of specific risk factors in the development of diabetic nephropathy was examined among noninsulin-dependent diabetic subjects attending the Diabetes Clinic of Christian Medical College Hospital, Vellore during 1986-87. Seventy-three subjects with normal protein excretion (less than 150 mg/24 hr) were compared with 66 microproteinuric (150-500 mg/24 hr) and 61 macroproteinuric subjects (greater than 500 mg/24 hr). The risk factors included family history of diabetes, tobacco use, dietary habits and metabolic control; the latter was assessed from an average of 5 clinic blood sugar determinations done annually per patient. Patients who had developed proteinuria were characterized as mostly men, with increased tobacco consumption and early onset of proteinuria in relation to duration of diabetes. The mean blood sugar value was significantly high in both the proteinuric groups compared to the group with no proteinuria (p less than 0.01). There was a striking increase in the prevalence of ischemic heart disease, hypertension and retinopathy in the macroproteinuric group compared to the other two groups (p less than 0.01). It is concluded that the risk of developing nephropathy was significantly higher in men, in smokers and in those with poor metabolic control (mean postprandial blood sugar more than 200 mg/dL). Furthermore, it was clearly evident from our study that the diabetic subjects with nephropathy had a higher incidence of hypertension, retinopathy, hyperlipidemia and ischemic heart diseases.
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PMID:Nephropathy in noninsulin-dependent diabetes mellitus: comparative study with normoproteinuric and microproteinuric subjects. 214 34

Twenty-three nonobese KK mice with abnormal tolerance to glucose, hyperinsulinemia with insulin resistance and human diabetic-like nephropathy were treated with either saline (12 mice) or glipizide, an oral hypoglycemic compound, 1 mg/kg, (11 mice) from 120 to 360 days of age. These mice develop significant increases in mesangial volume and matrix by 40 days of age. Oral glucose tolerance (OGTT), glucosyltransferase and N-acetyl-beta-glucosaminidase (enzymes involved in synthesis and degradation of kidney glycoproteins, respectively) in the kidney and serum, 24-hr proteinuria, and light microscopy studies of the kidney were performed. Glipizide-treated mice improved their OGTT. There was no difference in body weight; however, a 16% decrease (P less than 0.05) in kidney weight was observed in glipizide-treated mice. Both enzymes were significantly increased in the kidneys of mice treated with glipizide. No difference in serum enzymes was found between the two groups of mice. About 58% of the saline-treated mice had moderate glomerulosclerosis. By contrast, only 27% of glipizide-treated mice had moderate glomerulosclerosis. Also, a significant decrease in proteinuria was found in glipizide-treated mice. These data suggest that glipizide improves glucose metabolism, decreases kidney size, prevents kidney glycoprotein and mesangial matrix accumulation, and reduces proteinuria in type II diabetic KK mice. This indicates that good glycemic control prevents further progression of established diabetic nephropathy in animals.
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PMID:Diabetic microangiopathy in KK mice. VI. Effect of glycemic control on renal glycoprotein metabolism and established glomerulosclerosis. 214 55

Blood rheology was investigated in patients with diabetic nephropathy and progressive renal insufficiency, and compared with similar non-diabetic patients and healthy control subjects. Plasma viscosity and whole blood viscosity at standardized haematocrit were elevated to a comparable degree in the two patient groups, but erythrocyte deformability was normal. In diabetic patients, the rate of progression of renal failure showed weak, but significant, correlations with plasma viscosity (rs = 0.50, p = 0.005), standardized whole blood viscosity (rs = 0.41, p = 0.021), plasma fibrinogen (rs = 0.46, p = 0.010), C reactive protein (rs = 0.40, p = 0.023), and proteinuria (rs = 0.52, p = 0.003). Both plasma viscosity and plasma fibrinogen correlated significantly with proteinuria (rs = 0.45, p = 0.012 and 0.40, p = 0.027, respectively). Rheological abnormality is probably a manifestation of increased acute phase proteins, but it remains to be determined whether these are the cause or the effect of the renal injury. Abnormal blood rheology may be a risk factor for the progression of renal failure in diabetic nephropathy.
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PMID:Blood hyperviscosity and its relationship to progressive renal failure in patients with diabetic nephropathy. 214 85

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