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 induction of nephrotoxic nephritis in rats with rabbit antibodies preparation results in proteinuria, hypoproteinemia and hyperlipidemia with little glomerular lesions. A study of some hydrolases in cortex and medulla on one hand and glomerular and tubules on the other, showed changes in the activities of following enzymes. 1) A 20-30 % decrease in Na+, K+ dependent ATP-ase in whole kidney. 2) A 20 % decrease in beta-galactosidase activity in glomerular and medulla. 3) A 20 % increase of arylsulphatase A activity in tubules. These results are discussed in the light of the present knowledge of sulphatide metabolism in kidney.
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PMID:[Experimental nephrotic syndrome in the rat. Biologic parameters and study of several hydrolases in different purified kidney fractions]. 20 50

To elucidate the relationship between the high concentration of taurine in platelets and platelet aggregation in patients with EPH gestosis (gestosis with edema, proteinuria and hypertension), platelet aggregation and the platelet release response (release of ATP and beta-thromboglobulin) were studied in the washed platelet suspension (PS) obtained from normal pregnant or non-pregnant women and EPH gestosis patients. Platelet aggregation and platelet release response were significantly lower in EPH gestosis patients than in normal pregnant and non-pregnant women. Platelet aggregation, platelet release response induced by ADP and collagen and the aggregation induced by A23187 were inhibited in taurine-loaded PS from non-pregnant women. These results suggest that the decrease of platelet aggregation in EPH gestosis patients was caused by high concentrations of taurine in platelets, which may inhibit the intracellular Ca2+ movement and platelet release response. Therefore, taurine appears to have a protective effect against the hyper-coagulative state in EPH gestosis.
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PMID:Effect of taurine concentration on platelet aggregation in gestosis patients with edema, proteinuria and hypertension. 144 48

Extracellular adenine nucleotides are considered mediators of inflammation because they modulate functions of neutrophils and platelets. Until now, this role for adenine nucleotides has not been studied in vivo. In particular in the rat kidney, where ATP- and ADPase activity is present in the glomerular basement membrane, studies about the role of nucleotides may increase our understanding of the dynamics of glomerulonephritis (GN). Therefore, we examined effects of adenine derivatives ATP gamma S, ADP beta S and 2chloro-adenosine (2chloro-ADO) in vitro and during anti-Thy1 GN. The in vitro results show that ADP beta S and ATP gamma S are not degraded by glomerular nucleotidases but, on the other hand do stimulate O2- production of peritoneal exudate cells (PEC). In contrast, 2chloro-ADO significantly inhibits O2- production of peritoneal exudate cells. For in vivo studies rats were rendered nephritic by intravenous injection of monoclonal anti-Thy1 IgG (5 mg/kg body weight). Subsequently, rats were treated with saline (group 1, N = 10), 2chloro-ADO (group 2, N = 10), ADP beta S (group 3, N = 10) or ATP gamma S (group 4, N = 10). All analogs (10 mg/kg body weight) were administered both at t = 0 and t = 12 hour. After 24 hours, rats were sacrificed and kidneys were examined histochemically. In an additional group of nephritic rats (N = 5) proteinuria was studied after 2-chloro-ADO treatment. Results show increased intraglomerular platelet aggregation in nephritic rats treated with ADP beta S, whereas 2chloro-ADO inhibits aggregation significantly as compared with nephritic rats receiving saline. The percentage of granulocytes producing O2- is significantly increased in glomeruli after treatment of nephritic rats with ATP gamma S, whereas cell influx itself is not changed. In contrast, 2chloro-ADO inhibits intraglomerular O2- production, which is associated with the complete inhibition of proteinuria in the early phase of anti-Thy1 GN. These data demonstrate significant pro-inflammatory activities of extracellular adenine nucleotides during anti-Thy1 GN suggesting an anti-inflammatory role for glomerular ATP/ADPase, which in concert with 5' nucleotidase converts ATP and ADP to antiinflammatory ADO.
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PMID:Modulation of anti-Thy1 nephritis in the rat by adenine nucleotides. Evidence for an anti-inflammatory role for nucleotidases. 153 30

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

To clarify the ultrastructural changes of renal proximal tubulus in initial nephropathy having microalbuminuria, we observed 80 biopsies of non-insulin-dependent diabetics by light and electron microscopically morphometric analysis. The patients were divided into four groups; group I; no proteinuria (p.u.) & normal serum creatinine (Cr.); less than 1.5 mg/dl, group II; p.u. less than or equal to 0.5 g/day & normal Cr., group III; p.u. greater than 0.5 g/day & normal Cr., group IV; Cr. greater than 1.5 mg/dl. Age-matched 20 normal patients and 40 patients with IgA-nephropathy (20 cases with Cr. less than or equal to 1.5 mg/dl, 20 cases with Cr. greater than 1.5 mg/dl) were used as controls. In diabetics in Group I and II, significant changes were as follow. 1) general mitochondrial enlargement in size in proximal tubular cells, and significantly related to the level of fasting blood glucose, 2) enlargement of proximal tubular cells and their nuclei in size, 3) thickening of the proximal tubular basement membrane, and in group I, it indicated to get worse in future, 4) no relationship between the mitochondrial enlargement and other parenchymal parameters such as glomerular sclerotic change, interstitial fibrosis, luminar narrowing of arterioles and prognosis. Glomerular nodular-lesion, glomerular sclerotic change, and cortical tubulointerstitial fibrosis only appeared in the advanced stages; Group III and IV. We concluded that mitochondrial enlargement could be caused by the initially urinary excretion of low molecular proteins and microalbumin in diabetics, probably due to disturbances of ATP synthesis, reduction of active transport, and finally decreased of reabsorption in the proximal tubulus.
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PMID:[Mitochondrial enlargement of renal proximal tubulus as a cause of microalbuminuria in non-insulin dependent diabetics]. 228

The isolated kidney perfused with modified Krebs-Henseleit buffer with amino acids yields heavy proteinuria associated with reduced ATP levels characteristic of partial ischemia. These conditions are associated with a similar perfusion time dependent release of degraded vascular [35S]heparan sulfate proteoglycan into the perfusate solution which included a 60% loss of [35S]macromolecular material from the glomerulus after 2h of perfusion. Small amounts of [35S]macromolecular material were found in the urine and lymph. These results demonstrate that partial ischemia promotes a specific response in the overall renal vasculature, probably involving oxygen reactive metabolites, that results in the preferential release of heparan sulphate from the basement membrane and endothelial cells on the luminal side of the capillary wall.
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PMID:Partial ischemia and proteinuria during isolated kidney perfusion is accompanied by the release of vascular [35S]heparan sulfate. 253 69

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. 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. If a diabetic child or adolescent follows individual recommendations concerning diet and insulin, he or she can perform physical activity much the same as a young non-diabetic. These recommendations include: (a) self-measurement of blood glucose concentration before and after exercise; (b) ingestion of carbohydrates before, during, and after exercise; (c) reduction of the insulin dose during and immediately after exercise; and (d) not choosing an injection site involved with muscular work. The only prohibited sports are those which constitute a danger to the diabetic child by provoking an eventual hypoglycaemia. The best sports are those that require progressive physical effort and that are spread out over several hours.
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PMID:Sport and the diabetic child. 265 64

Prolonged cadmium exposure has been associated with proteinuria, calcuria and loss of calcium from bones in humans. Previous studies have shown that kidney uptake of cadmium in vivo results from proximal tubule absorption of the circulating cadmium metallothionein complex (CdMT), and intracellular release of the Cd2+ ion prior to induction of renal metallothionein. Parenteral administration of CdMT has been found to selectively damage the proximal tubule cell lysosome system with development of a tubular proteinuria pattern similar to that observed under chronic exposure conditions. The present studies also demonstrate a concomitant calcuria but no changes in the excretion of other electrolytes or glucose using this model. These marked changes in renal calcium metabolism occurred in the absence of mitochondrial damage, changes in total, Na/K or Mg-stimulated ATPase activities, renal ATP levels, membrane 45Ca2+ transport or overt tubule cell necrosis during an 8 hour period following CdMT injection. Proteinuria and calcuria were prevented by prior zinc induction of the renal MT pool. Data from these studies indicate that renal proximal tubule cell uptake and degradation of the circulating CdMT complex produces both a marked proteinuria and calcuria. The calcuria does not appear to stem from changes in renal energy metabolism or membrane transport of this element but is probably a secondary result of calcium binding to excreted proteins which are increased in urine to a similar extent. The studies also suggest that zinc status and maintenance of the renal ZnMT pool may play an important role in regulating cadmium-induced renal proteinuria and calcuria by preventing Cd2+ perturbation of the proximal tubule cell lysosome system.
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PMID:Mechanism of cadmium-metallothionein-induced nephrotoxicity: relationship to altered renal calcium metabolism. 282 68

In previous studies from this laboratory it has been shown that ATP-ase activity in situ in the glomerular basement membrane (GBM) is clearly reduced in rats rendered nephrotic after treatment with adriamycin (ADR). The question was raised whether this reduction of ATP-ase activity in the GBM is due to toxic activity of ADR or rather a result of the nephrotic condition per se. Therefore, we studied ATP-ase activity using the cerium-based method in kidneys from ADR-treated rats without proteinuria (48 hr after ADR injection), or with proteinuria (approximately 150 mg/24 hr) several weeks after ADR injection. Also kidneys from rats rendered nephrotic by surgical ablation and from non-nephrotic rats treated with local X-irradiation (2000 rads) as well as from normal control rats were studied. The results show that in the GBM of ADR-treated or irradiated rats, clear reduction of ATP-ase activity is observed irrespective of their proteinuria, whereas in the GBM of rats rendered nephrotic by renal ablation (approximately 156 mg/24 hr mean protein excretion) no reduction of enzyme activity is found. It is concluded that decreased ATP-ase activity of the glomerular filtration barrier in ADR-treated rats is due to an early toxic activity of this drug and not a result of the nephrotic state per se. In view of the identical results in X-irradiated rats, it is likely that ADR may act through production of toxic radicals leading to damage of this membrane-associated enzyme system.
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PMID:Decreased ATPase activity in adriamycin nephrosis is independent of proteinuria. 295 30

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


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