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)

Type I glycogen storage disease (GSD-I) is due to the deficiency of glucose-6-phosphatase activity in the liver, kidney and intestine. Although kidney enlargement occurs in GSD-I, renal disease has not been considered a major problem until recently. In older patients (more than 20 years of age) whose GSD-I disease has been ineffectively treated, virtually all have disturbed renal function, manifested by persistent proteinuria; many also have hypertension, renal stones, altered creatinine clearance or a progressive renal insufficiency. Glomerular hyperfiltration is seen in the early stage of the renal dysfunction and can occur before proteinuria. In younger GSD-I patients, the hyperfiltration is usually the only renal abnormality found; and, in some patients, microalbuminuria develops before clinical proteinuria. The predominant underlying renal pathology is focal segmental glomerulosclerosis. Renal stones and/or nephrocalcinosis are also common findings. Amyloidosis and Fanconi-like syndrome can occur, but rarely. The risk factors for developing the glomerulosclerosis in GSD-I include hyperfiltration, hypertension, hyperlipidemia and hyperuricemia. Dietary therapy with cornstarch and/or nasogastric infusion of glucose, aimed at maintaining normoglycemia, corrects metabolic abnormalities and improves the proximal renal tubular function. Long-term trial will be needed to assess whether the dietary therapy may prevent the evolution or the progression of the renal disease.
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PMID:Type I glycogen storage disease: kidney involvement, pathogenesis and its treatment. 202 44

The renal disease in an adult woman with Type 1 glycogen storage disease (GSD) is reported. Since she was 15 years old, several episodes of gouty arthritis had developed. At the age of 18, proteinuria was pointed out. Hepatomegaly, renomegaly out of proportion to the impairment of renal function, hyperuricemia, hyperlipidemia, fasting hypoglycemia and lactic acidemia were observed. The diagnosis of GSD was established on the basis of a glucose tolerance test, glucagon test and liver biopsy. The findings of renal biopsies performed at the ages of 24 and 27 years old suggested that glomerular damage might have preceded the tubulo-interstitial lesion.
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PMID:Renal disease in an adult with type 1 glycogen storage disease. 203 36

The triad of insulin, diet and exercise has been the basis for treatment of diabetes for several decades. However, the choice of sporting activities for young diabetics requires an understanding of: a) the energy metabolism and the adaptation to physical activity in the healthy; b) the metabolic adaptation during physical activity in the diabetic child; and c) the practical recommendations concerning diet and insulin that have to be learned by the children themselves. The healthy child utilises immediately available substrates, such as ATP and creatine phosphate in much the same fashion as the adult. However, the capacity for anaerobic degradation of glycogen and glucose seems limited in the muscles of children relative to that of adults. Consequently, the adaptation to resistance exercise should be undertaken with prudence in children and adolescents. The release of insulin tends to decrease during effort. Diverse hypotheses have been proposed to explain this phenomenon. However a low concentration of insulin is required: insulin is said to play a "permissive" role. In diabetic children, an adequate insulin therapy is required to allow the full benefit of muscular activity on glucose assimilation and to reach the same level of physical performance as the non-diabetic. In the case of insufficient metabolic control, exercise can provoke severe hypoglycaemic episodes, even after muscle activity has ceased, or increase glucose levels and lead to ketoacidosis. Regular physical training induces a reduction in postexercise proteinuria measured in diabetic adolescents but its role in metabolic control remains controversial.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Sports and diabetes in children and adolescents]. 206 55

Genetically diabetic mice (db/db) were given 50 mg/kg body weight/day substance L, a nontoxic basic amino acid and compared to control diabetic mice without treatment. The oral administration of the compound was started at the age of 3 months and the animals were sacrificed at the age of 7 months. No adverse effects were observed in animals given the substance L. Total food consumption, drinking water intake and body weight were comparable between the groups. Nonenzymatic glycosylation of serum proteins and hemoglobin was not significantly different in the groups. Renal pathological lesions in the control diabetic mice showed glomerular mesangial expansion and on electron microscopy thickened glomerular basement membranes with a mean thickness of 3,204 +/- 186 A. Treated animals showed significantly less mesangial crescents and thinner glomerular basement membrane thickness of 2,520 +/- 252 A (p less than 0.01). The experimental animals showed in addition a lower mean kidney weight. Glomerular but not tubular proteinuria was reduced in the treated group. Basement membrane collagen type IV isolated from kidneys of experimental animals was more soluble in acidity and showed a lower degree of cross-linking as evaluated by SDS-polyacrylamide gel electrophoresis. We conclude that substance L is beneficial to diabetic renal changes. We suggest that this positive effect could be due to the inhibition of glucose-mediated abnormal cross-linking of collagenous structures by the interaction of substance L with reactive carbonyl residues of glycosylation adducts of collagen. Other possible mechanisms are discussed.
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PMID:The effect of substance L on glucose-mediated cross-links of collagen in the diabetic db/db mouse. 207 11

A corticosteroid- and furosemide-induced excessive increase in proteinuria developed in a 34-year-old nephrotic patient with focal glomerulosclerosis. The concentration of urinary protein increased almost in parallel with that of urinary glucose. This finding indicates that corticosteroids and/or furosemide can promote the disturbance of the tubular reabsorption mechanism together with increases in glomerular permeability and glomerular filtration rate.
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PMID:Corticosteroid- and furosemide-induced increase in proteinuria in nephrosis. 208 3

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

To evaluate the screening tests for cadmium-induced renal tubular dysfunction, qualitative and quantitative tests for urinary protein and glucose have been done in 146 urine samples obtained from subjects who had lived in the cadmium-polluted Jinzu River basin in Toyama Prefecture, Japan. The subjects consisted of 66 men and 80 women aged 55 to 71 years with beta 2-microglobulinuria exceeding 1,000 micrograms/g creatinine. The results obtained from this study were as follows; 1) The positive reaction (above 1+) for protein by the dipstick method was seen in 19.7% of men and 20.0% of women, and for glucose using Tes-tape in 48.5% of men and 33.8% of women. 2) The geometric means of protein and glucose concentrations in urine were 16.4 mg/dl and 12.7 mg/dl in men, and 14.2 mg/dl and 6.8 mg/dl in women, respectively. 3) The criteria of the primary screening in the health survey system for the residents in cadmium-contaminated areas conducted by the Japan Environment Agency were a proteinuria level exceeding 10 mg/dl and a glucosuria above (+/-) with Tes-tape. Nearly all subjects with urinary beta 2-microglobulin exceeding 30 mg/g creatinine were screened by these criteria in both sexes, whereas only 52.9% of men and 30.0% of women who had urinary beta 2-microglobulin between 10 to 30 mg/g creatinine could be screened in this manner. These results indicate that semiquantitative tests are insufficient as initial tests for screening cadmium-induced renal tubular dysfunction.
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PMID:[Evaluation of qualitative and quantitative tests for proteinuria and glucosuria as screening tests for cadmium-induced renal tubular dysfunction]. 209 27

The prevailing blood-glucose level has been found to influence renal haemodynamics in type 1 (insulin-dependent) diabetes mellitus. In a group of 48 type 1 diabetic patients with normal serum creatinine (less than 120 mumol l-1) and without persistent proteinuria, no relationship was present between blood glucose, corrected to near normoglycaemia (6.8 [6.2 to 7.3] mmol l-1 (median [95% confidence interval]), and glomerular filtration rate (GFR), effective renal plasma flow (ERPF) determined with 125I-iothalamate and 131I-hippuran respectively. GFR tended to increase (2 [-1 to +4] ml min-1 1.73 m-2, 0.05 less than P less than 0.10) and ERPF did not change after a blood glucose rise of 7.9 (7.0 to 8.9) mmol l-1, achieved by an intravenous glucose load in 31 patients. The individual changes in GFR and ERPF were correlated (r = 0.60, P less than 0.005). The changes in GFR were inversely related to baseline blood glucose (r = -0.45, P less than 0.02), but not to baseline GFR. GFR increased (3.5 [0 to +12] ml min-1 1.73 m-2, P less than 0.01) if baseline blood glucose was less than or equal to 6.8 mmol l-1 (n = 16) but ERPF did not. Achievement of near normoglycaemia before measurement of kidney function in type 1 diabetes appears to reduce the influence of variation in glycaemia on renal haemodynamics and thus would improve comparison between and within individuals. Moderate hyperglycaemia can cause a small rise in the glomerular filtration rate.
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PMID:Renal haemodynamic changes in response to moderate hyperglycaemia in type 1 (insulin-dependent) diabetes mellitus. 211 86

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

Thrombomodulin is an endothelial cell membrane protein acting as a cofactor for the activation of plasma protein C. Recently, it was found that soluble forms of thrombomodulin exist in plasma. Although the physiological significance of circulating thrombomodulin is presently obscure, it may reflect injury of the endothelial cell. In the present study, we examined plasma thrombomodulin concentrations in 106 Type 2 (non-insulin-dependent) diabetic patients. Plasma thrombomodulin was determined by a sandwich ELISA employing monoclonal anti-thrombomodulin antibodies. The patients with proteinuria had higher plasma thrombomodulin concentrations (61.0 +/- 36.0 ng/ml) compared to the patients without proteinuria (33.6 +/- 9.5 ng/ml, P less than 0.001) and control subjects (32.8 +/- 6.5 ng/ml, P less than 0.001). Plasma thrombomodulin concentrations were positively correlated with the level of serum creatine, blood urea nitrogen, urinary albumin and urinary beta 2-microglobulin (P less than 0.001 for each), but not with fasting plasma glucose, hemoglobin A1c or fructosamine. Elevated plasma thrombomodulin was also observed in the patients with pre-proliferative (63.4 +/- 28.9 ng/ml) or proliferative retinopathy (57.4 +/- 34.7 ng/ml), but not in the patients with non-proliferative retinopathy (33.5 +/- 12.9 ng/ml) or those without retinopathy (32.4 +/- 8.9 ng/ml). Even in the 81 diabetic subjects without proteinuria as determined by a dip and read method, and whose serum creatinine was lower than 1.0 mg/dl, the plasma thrombomodulin concentration was significantly higher in the patients with pre-proliferative (41.5 +/- 4.4 ng/ml) and proliferative retinopathy (41.0 +/- 12.8 ng/ml) compared to the patients without retinopathy (32.2 +/- 8.8 ng/ml) and those with non-proliferative retinopathy (31.9 +/- 7.8 ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma thrombomodulin concentration in diabetes mellitus. 217 97


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