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 effect of hypertension on the anatomy, physiology, and course of glomerulonephritis in rats was investigated by inducing deoxycorticosterone acetate-salt hypertension in animals with heterologous immune complex glomerulonephritis and vice versa. The effect of hypertension on glomerulonephritis with different degrees of intensity was also studied. Hypertension increased the proteinuria in the glomerulonephritic rat substantially (p less than 0.01), reduced the creatinine clearance (p less than 0.05), and induced an enormous thickening of the glomerular basement membrane. Furthermore, the life span was shortened (p less than 0.01) when hypertension was induced in nephritic rats, possibly due to insufficient cerebral vascular activity secondary to malnutrition. Glomerulonephritis did not influence the blood pressure in animals with severe protein loss; in rats with minor proteinuria the presence of glomerulonephritis increased the blood pressure. Hypertension lowered the antiserum dose needed to produce pathologic proteinuria (p less than 0.02). Hypertension seemed to increase the amount of glomerular immune deposits in early glomerulonephritis but lowered the amounts of glomerular rat IgG during the course of nephritis. In conclusion, hypertension increases the glomerular damage substantially in rats with heterologous immune complex glomerulonephritis, influences the glomerular deposition of immunoglobulins, and shortens the life span.
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PMID:Effect of hypertension on experimental glomerulonephritis in rats. 669 57

Fabry's disease is a rare familial disorder of glycolipid metabolism which is caused by a deficiency of a lysosomal enzyme alpha-galactosidase. A Finnish family is described in which cornea verticillata was found in the father and 2 daughters. In all cases, there were symptoms suggesting Fabry's disease: febrile episodes the origin of which was not clear, limb pains and, in the case of the father, 20 years of proteinuria with elevated ESR, and hemiplegia and aphasia following a cerebral thrombosis at the age of 43. The diagnosis was confirmed by demonstration of an alpha-galactosidase deficit in the serum and urine of all patients. Deficiency of this enzyme leads to abnormally high urinary tri- and dihexosyl ceramide levels, and this was observed in the father and the elder daughter. At the age of 12, the daughter had loss of vision in her right eye as a result of occlusion of the central retinal artery. Electron microscopic (EM) examination of the father's dermal angioma suggested Fabry's disease. Computerized cranial tomography of the father revealed not only the cerebrovascular condition but also a disease affecting the white matter of the brain.
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PMID:Fabry's disease and cornea verticillata. A report of 3 cases. 679 29

A 4-3/12 old boy with a hypophosphoremic coma (serum phosphorus: 0.4 mg./dl.) is presented. The favoring conditions appear to be related to acute renal failure in polyuric phase with high phosphorus excretion, low phosphorus intake, rapid transit from a catabolic to an anabolic state with previous malnutrition and parenteral feeding, oral aluminum hydroxide gel administration and lung infectious disease. The clinical, biochemical data, evolution and physiologic mechanisms are commented, specially those of erythrocyte, leucocyte and platelet disfunction related to ATP, AMP and 2.3 DPG deficiency. Proteinuria and hematuria during phosphorus depletion are emphasized. The alarm symptoms and treatment are indicated.
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PMID:[Hypophosphatemic coma (author's transl)]. 733 2

Several studies indicate the pathophysiological importance of reactive oxygen species in rats with nephrotic syndrome induced by puromycin aminonucleoside, an experimental model of the human minimal change disease. The role of reactive oxygen species in these rats was further evaluated, examining the effect of dietary deficiency and supplementation of antioxidants (vitamin E and selenium) on biochemical and renal ultrastructural alterations induced by puromycin aminonucleoside. Male Wistar rats, weaned at 3 weeks, were placed on diets normal, deficient or supplemented in vitamin E and selenium for 4 weeks. At the end of this period, rats were divided in two groups: control (sacrificed without any further treatment) and nephrotic (injected with puromycin aminonucleoside and sacrificed 7 and 22 days later). In control rats, the dietary deficiency or supplementation of antioxidants resulted in no significative differences in renal function, proteinuria or kidney ultrastructure. However, kidney lipoperoxidation, kidney glutathione peroxidase activity and circulating levels of vitamin E changed according to the amount of antioxidants in the diet. Seven days after the injection of puromycin aminonucleoside, rats fed normal, deficient or supplemented diets, developed nephrotic syndrome. However, proteinuria, hypoproteinemia, renal dysfunction and ultrastructural alterations were higher in rats fed a deficient diet. In contrast, proteinuria and kidney ultrastructural alterations were lower in rats fed a supplemented diet. Kidney lipoperoxidation and glutathione peroxidase activity increased on day 7 in rats fed a normal or a deficient diet, but not in rats fed a supplemented diet. This study shows that nephrotic syndrome induced by puromycin aminonucleoside in rats is modified by dietary antioxidants (vitamin E and selenium). Dietary supplementation ameliorates it and dietary deficiency exacerbates it.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of dietary antioxidants on puromycin aminonucleoside nephrotic syndrome. 764 24

The effects of low-meat-protein diets on hypercholesterolemia and proteinuria were studied in rats with nephrotoxic serum nephritis. After an injection of nephrotoxic serum, rats were given either a 20% meat-protein diet (20M), an 8.5%-meat-protein diet (8.5M), or a valine-(0.05%)-supplemented 8.5%-meat-protein diet (8.5MV) for 12 days. Urinary protein excreted from the 20M-fed, nephritic control rats increased rapidly and linearly during the initial 3 days, and thereafter the high excretion rate was maintained for up to 12 days. Two low-meat-protein diets (8.5M, 8.5MV) commenced to suppress proteinuria 3 days after feeding and the suppression was preserved during the rest of the experimental periods. Compared with the 20M, both low-meat-protein diets significantly improved hypercholesterolemia induced in this nephritic model. These two diets significantly enhanced the fecal excretion of neutral sterols. They caused neither fatty liver nor severe growth retardation. These effects of 8.5MV were identical to those of 8.5M. The results suggest that low-meat-protein feeding, without amino acid supplementation, improves hypercholesterolemia and proteinuria in nephritis without severe protein malnutrition. The results also suggest that the hypocholesterolemic effect of the low-meat-protein diets may be, at least in part, attributed to increased fecal excretion of steroids.
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PMID:Reduction of hypercholesterolemia and proteinuria in nephritic rats by low-meat-protein diets. 775 76

This article reviews studies that examine the negative effects of urinary and intestinal schistosomiasis on the following nutritional parameters in humans: urinary and faecal blood and iron loss, anaemia and haemoglobin levels, proteinuria, child growth and adult protein-energy status, physical fitness, physical activity, appetite and symptomatology. The conclusions reached are (1) that community-level treatment and control of schistosomiasis in areas where the infection, protein-energy malnutrition, and anaemia are common are to be encouraged and are likely to improve child growth, appetite, physical fitness and activity levels and to decrease anaemia and symptoms of the infection, and (2) that further studies are needed to determine how much and by what means decreases in and treatment of schistosomal infection may improve nutritional status, cognitive and school performance and attendance, and work capacity and productivity in communities with different amounts of parasitism and malnutrition.
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PMID:The impact of schistosomiasis on human nutrition. 811 76

In adults, 12 to 14 g of albumin are synthesized daily. The same quantity is catabolized, essentially by the vascular endothelium and to a lesser degree in renal tubules. During nephrotic syndrome, contrary to what is observed in malnutrition conditions accompanied by hypoalbuminemia, hepatic synthesis is only moderately increased, whereas fractional catabolism is greater than normal. The increase in alimentary protein-intake, which has been proposed to restore the pool of albumin, raises hepatic albumin synthesis, but also its urinary losses, most likely by stimulation of the renin-angiotensin system. A reduction in protein rations lowers proteinuria and improves the hepatic abnormalities of nephrotic syndrome but its longterm nutritional consequences are poorly understood. The association of a converting enzyme inhibitor with a diet moderately restricted in protein content (1 g/kg/day) might constitute a therapeutic satisfactory solution.
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PMID:[Protein metabolism during nephrotic syndrome. Experimental and clinical influence of dietary protein intake]. 823 11

Deficiency of the enzyme glucose-6-phosphatase is the biochemical defect in glycogen storage disease type I (GSD I). Normally this enzyme is present in the liver, intestine and kidneys. The lack of the enzyme in the kidney makes it obvious that glycogen storage will not be restricted to the liver but that also the kidneys will be involved, possibly resulting in renal damage. Glycogen storage in the kidney is most outspoken present in the proximal tubular cells. In case of insufficient metabolic control, a Fanconi-like syndrome can develop, disappearing with improved therapy. Although renal disease has not been considered a problem in GSD I, recent findings indicate that especially in adult patients chronic renal disease is a common complication. In the past gout nephropathy and renal stones were the complications mentioned. Recently it appears that in a considerable number of patients after a period of 'silent' hyperfiltration, renal damage develops with proteinuria, hypertension and renal dysfunction later on. In biopsies of such patients focal glomerulosclerosis is found.
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PMID:Renal complications in glycogen storage disease type I. 831 28

We have previously demonstrated that low-casein diets supplemented with cystine and threonine reduced hyperlipidemia and proteinuria in nephritic rats without noticeable protein malnutrition. In the present study, we examined whether or not a low-casein diet supplemented with methionine, sulfur amino acid other than cystine, and threonine would ameliorate the symptoms without protein malnutrition in rats with nephrotoxic serum nephritis by feeding experimental diets for 10 days. A methionine-threonine-supplemented 8.5% casein diet (8.5 CMT), when compared with a basal 20% casein diet, improved hypoalbuminemia as well as hyperlipidemia and proteinuria without noticeable growth retardation and fatty liver induction in nephritic rats. Fecal bile acid excretion and microsomal cholesterol 7 alpha-hydroxylase activity were enhanced by 8.5CMT feeding. These results suggest that amino acid-balanced low protein diet would have a beneficial effect on the symptoms of nephritis. They also suggest that the hypocholesterolemic action of 8.5CMT may be, at least in part, due to increased fecal bile acid excretion accompanied by elevated microsomal cholesterol 7 alpha-hydroxylase activity.
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PMID:Improvement of hyperlipidemia and proteinuria without noticeable growth retardation by feeding a methionine and threonine supplemented low-casein diet to nephritic rats. 853 82

The adult protein turn-over daily affects 250 grammes, which is equivalent to four times the average daily protein intake. Regulation of synthesis and catabolism appears to occur by independent ways. These systems are altered during the nephrotic syndrome and ultimately lead to a loss of total body nitrogen and a risk for malnutrition. Indeed, during the nephrotic syndrome, muscle protein synthesis is further impaired as the urinary protein losses increase. This may suggest that anabolic compounds are lost in the urine of such patients. A moderate protein restriction (0.8 g/kg BW/day) allows a reduction in proteinuria, as well as pharmacological agents (ACE inhibitors) and should therefore slow the progressive renal insult.
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PMID:[Nephrotic syndrome and protein metabolism]. 892 6


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