Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034186 (pyelonephritis)
 6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aminoglycoside-induced renal damage is enhanced in animals with Escherichia coli pyelonephritis. Bacterial endotoxin is liberated during antibiotic therapy. The toxic effect of endotoxin and tobramycin, alone or in combination, was investigated in primary cultures of rabbit proximal tubular cells grown to confluence in serum-free medium. Sodium-dependent uptakes of Pi and alpha-methylglucopyranoside (MGP) and enzymatic activities (lactate dehydrogenase [LDH] released as a marker of cell necrosis and gamma-glutamyltransferase [GGT] and N-acetyl-beta-D-glucosaminidase [NAG] present in the homogenate as markers of brush border membrane and lysosome integrity) were measured. Cells were exposed to (i) endotoxin (20 mg/liter), tobramycin (1 mM), or endotoxin plus tobramycin for 48 h, or (ii) endotoxin (100 mg/liter), tobramycin (4 mM), or endotoxin plus tobramycin for 72 h. Endotoxin alone did not alter Pi uptake, but tobramycin inhibited Pi uptake through a decrease in Vmax. The effect was not enhanced by the combination of endotoxin and tobramycin. Endotoxin and tobramycin alone exerted no significant effect upon MGP uptake, but strong inhibition of the Vmax was observed after exposure to a combination of endotoxin plus tobramycin, without alteration of the Km. Endotoxin decreased residual GGT activity in the cell homogenate. Tobramycin increased LDH release in the medium and NAG activity in the homogenate. Endotoxin plus tobramycin resulted in an additive effect upon LDH and NAG activities. In conclusion, by disturbing apical membrane integrity, endotoxin increased tobramycin toxicity in vitro in the absence of serum hormonal mediator.
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PMID:Endotoxin-tobramycin additive toxicity on renal proximal tubular cells in culture. 167 35

The uptake of D-glucose, L-aspartate, L-lysine and L-proline was investigated in renal brush border membrane (BBM) vesicles prepared from control, infected or passively-immunized-infected rats. Except L-aspartate, a progressive decrease in the uptake of these nutrients in both infected and immunized-infected groups during the course of infection was observed, but the changes were less apparent in immunized-infected rats than in non-immunized ones. The uptake of L-aspartate was increased in vesicles from early stages of infection but decreased in those from later stages. Also in L-aspartate uptake, the changes were smaller in immunized animals. The uptake of nutrients was detectable earlier than were histopathological alterations of both kidneys. The observations demonstrated that uptake of D-glucose and amino acids in the kidneys is disturbed prior to appearance of histopathological lesions and thus can be used for early detection of the disease. The data also demonstrate that antipili antibodies afford partial protection against ascending pyelonephritis.
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PMID:Transport of nutrients into the renal brush border membrane vesicles as marker in evaluating the role of antipili antibodies in modulation of ascending pyelonephritis in rats. 256 54

Kinetic parameters (Km and Vmax) of renal brush border membrane (BBM) enzymes alkaline phosphatase, maltase, leucine aminopeptidase and gamma-glutamyltranspeptidase were worked out in control, infected and immunized-infected rats. There was no significant change in the Km of all the enzymes studied in three groups. The Vmax of all the enzymes studied decreased significantly (p less than 0.05) 3 or 4 days postinfection and onwards in the left obstructed kidney of infected and immunised-infected animals. However, in the right unobstructed kidney the Vmax of alkaline phosphatase and leucine aminopeptidase increased significantly (p less than 0.05) in the early stages and decreased (p less than 0.05) in later stages in both the experimental groups. The significant difference (p less than 0.05) in the Vmax of infected and immunized-infected groups at various stages of infection revealed the partial protective role of antipili antibody against ascending pyelonephritis.
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PMID:Antipili antibody affords protection against ascending pyelonephritis in rat: evaluated by renal brush border membrane enzymes. 288 98

Kinetic parameters (Km and Vmax) of renal brush border membrane (BBM) enzymes alkaline phosphatase, maltase, leucine-aminopeptidase and gamma-glutamyltranspeptidase were used as markers for the early detection of pyelonephritis. Km of all the enzymes studied remained unaltered. The Vmax of all the enzymes studied were found to be significantly decreased (p less than 0.05) 3 or 4 days postinfection and onwards in the left obstructed kidney. The Vmax of alkaline phosphatase and leucine-aminopeptidase was found to be significantly increased (p less than 0.05) in early stages and decreased (p less than 0.05) in later stages of infection in the right unobstructed kidney. No histopathological lesions confirming pyelonephritis could be seen 7 days postinfection in the left kidney and right kidney remained histopathologically unaltered. This demonstrated that BBM enzymes are much earlier disturbed as compared to histopathological changes.
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PMID:New sensitive markers for the detection of experimental ascending pyelonephritis. 288 3

A sandwich ELISA assay has been formatted from two commercially available murine monoclonal antibodies, URO-4 and URO-4a, directed against a 120,000 dalton glycoprotein, the adenosine deaminase binding protein (ABP), found on the brush border of the renal proximal tubular epithelial cell. Untimed urine samples from 37 normal individuals and urinary ABP less than 0.1 AU; 37 patients with pure glomerular disease had ABP less than 0.4 AU (with 29, or 76% less than 0.2 AU); 10 patients with pre-renal azotaemia had ABP less than 0.6 (with 8, or 80% less than 0.3 AU). In contrast, 79 patients with post-ischaemic acute tubular necrosis had ABP greater than 0.6 AU. Acute renal failure due to myoglobinuria, contrast dye, and aminoglycoside toxicity were all associated with urinary ABP greater than 1.0 AU. In addition, all six patients with acute bacteraemic pyelonephritis had ABP greater than 0.7 AU, as opposed to ABP less than 0.2 AU in the urines of 12 women with acute cystitis. We conclude that this monoclonal antibody based urinary assay is a sensitive measure of renal proximal tubular injury, reliably distinguishes acute tubular from glomerular disease, and may be helpful in differentiating forms of urinary tract infection.
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PMID:Diagnosis of renal proximal tubular injury by urinary immunoassay for a proximal tubular antigen, the adenosine deaminase binding protein. 288 57

Reactive oxygen species have been found to be responsible for the tissue injury caused in experimental pyelonephritis in mice. The extent of lipid peroxidation (as assayed by malondialdehyde formation) was found to be increased significantly (p less than .001) in the infected group as compared to the normal mice. Superoxide dismutase and catalase (oxygen free radical scavengers) showed a significant decrease (p less than .001) in the extent of lipid peroxidation even in the presence of infection. Dimethyl sulfoxide, a hydroxyl ion scavenger, was however found to be effective only at 4 and 7 days postinfection (p less than .001). Allopurinol, an inhibitor of xanthine oxidase, did not significantly (p greater than .05) inhibit the formation of lipid peroxides, even upto 7 days postinfection. There was a significant decrease (p less than .05) in the activities of renal brush border membrane enzymes used as markers of renal tissue damage (i.e. alkaline phosphatase, leucine amino-peptidase and gamma-glutamyl transpeptidase) in the infected group as compared to the normal group. In the presence of superoxide dismutase, dimethylsulfoxide and catalase except allopurinol, the activities of all the enzymes but maltase were found to be increased significantly (p less than .05) as compared to the infected group. There was a significant increase (p less than .01) in the bacterial count in the presence of superoxide dismutase and DMSO in infected mice as compared to the infected control mice. However, no significant difference was observed in the catalase and allopurinol treated groups.
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PMID:Effect of various oxygen free radical scavengers in preventing tissue injury caused by Escherichia coli in pyelonephritic mice. 305 56

Aminoglycosides have a low molecular weight and bind weakly to proteins. They are easily filtered through the glomeruli, bind to phospholipid receptors located on the brush border of proximal tubule cells, and penetrate within the cells by endocytosis. Aminoglycosides decrease lysosomal A and C phospholipase and sphingomyelinase activities. This impairs the degradation of phospholipids, with formation of abnormal intralysosomal structures called myeloid bodies as a result. These myeloid bodies are gradually eliminated from the cells into the lumen of the tubule and excreted in the urine. We studied the urinary excretion of phospholipids following 1, 3, 5 and 10 days of treatment with gentamicin (3 mg/kg/day) or tobramycin (3 mg/kg/day) in patients with acute pyelonephritis. Infection-free, non-treated subjects were used as controls. Patients with a urinary tract infection treated by a quinolone made up a third group. Urinary N-acetyl-beta-D-glucosaminidase (NAG), an indicator of epithelial necrosis, was also evaluated. Results were expressed per ml urine, per mg creatinine and per 24 hours. Only the results expressed per mg creatinine appeared valid. No significant increase in serum creatinine or urinary NAG was found in patients under gentamicin. In the patients with a urinary tract infection not treated with an aminoglycoside, urinary phospholipid excretion on D1 was decreased as compared to controls (p less than 0.01). Urinary phospholipid excretion was never found to be increased in patients under aminoglycosides. No significant difference was found between males and females. Mistaken interpretations occurred if urinary excretion of phospholipids or NAG was not expressed per mg creatinine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Urinary excretion of phospholipids: index of aminoglycoside nephrotoxicity]. 353 46

The uptake of nutrients was investigated in the renal cortical brush border membrane (BBM) vesicles at different stages of ascending pyelonephritis. There was significant difference (p less than 0.05) in the uptake of D-glucose, L-alanine, L-aspartate, L-lysine and L-proline 3 days postinfection and onwards in both right unobstructed and left obstructed experimental kidneys as compared to the sham operated control. The uptake of D-glucose, L-lysine and L-proline was found to be significantly decreased (p less than 0.05) during the course of infection. While uptake of L-alanine and L-aspartate increased (p less than 0.05) in early stages and decreased (p less than 0.05) in later stages of infection. The differential effect was attributed to the compensatory measure and different kinds of transport systems for different types of amino acids.
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PMID:Kinetics of reabsorption of nutrients in renal brush border membrane vesicles from rats with experimental ascending pyelonephritis. 375 10

The uptake of nutrients and activities of membrane enzymes in the kidney were investigated using renal brush border membrane (BBM) vesicles in acute pyelonephritis in rats. A significant decrease (P less than 0.001) in the uptake of D-glucose and L-phenylalanine was observed in both the unobstructed right and obstructed left kidney, while there was a significant increase (P less than 0.001) in the uptake of L-alanine in the left kidney of pyelonephritic rats, demonstrating disturbances in the reabsorption of the glucose and aminoacids in the kidneys. Vmax of alkaline phosphatase, leucine-amino-peptidase and maltase was found to be decreased in the left kidney, suggesting that there was a reduction in the active enzyme molecule number. Km of alkaline phosphatase and leucine-aminopeptidase remained unchanged, while km of maltase decreased in both the right and left kidneys. An increase in the Vmax of alkaline phosphatase and leucine-aminopeptidase and substrate affinity of the maltase in the right kidney demonstrated a compensatory phenomenon for the malfunctioning of the left kidney. This is the first report demonstrating alterations in reabsorption of nutrients and BBM enzymes in experimental pyelonephritis.
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PMID:Pyelonephritis alters the reabsorption of nutrients and brush border membrane enzymes of rat kidney. 390 22

In a survey the present possibilities are outlined to get knowledge about diseases of inner organs with the help of enzyme determinations in the urine. Here it is remarkable that changes of the enzyme excretion appear not only in renal disease with acute renal failure, pyelonephritis, glomerulonephritis, renal infarction and nephroptosis but are also to be observed in primarily extrarenal diseases such as diabetes mellitus, hyperthyroidism, thesaurismoses, myocardial infarction, hypertension, acute pancreatitis, epidemic hepatitis, liver cirrhosis, obstructive jaundice and rheumatoid arthritis. The causes of the changes of enzyme excretions are various. Since enzymes of different origin and localisation behave themselves variably, the simultaneous determination of a brush border marker (e.g. alanine aminopeptidase), a lysosomal enzyme (e.g. beta-glucuronidase or N-acetyl glucosaminidase) and a low molecular enzyme (e.g. lysozyme) is of use for the recognition of renal alterations. By the control of activities of urinary enzymes it is possible to get without risk informations about pathobiochemical processes in the kidney which are not to be gained by means of other methods.
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PMID:[Urinary enzyme excretion in diseases of the internal organs]. 636 87


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