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)

Studies to determine the effect of kidney parenchymal infection upon urinary lactic dehydrogenase (ULDH) isoenzyme composition were performed in 12 female Sprague-Dawley rats on Day 0 and on Days 2, 5, and 10, after experimental inducement of Escherichia coli pyelonephritis. An additional group of 12 animals was subjected to similar experimental manipulations and served as sham controls. Repeated 12-h urine collections revealed lower urine osmolalities and significantly higher levels of ULDH 5 excretion in the experimental than in the sham operated animals (P less than 0-05). These differences persisted for the length of the experiment (10 days). Leucocyte excretion rates were also higher in the experimental than in the sham group, and a high correlation with ULDH 5 activity was demonstrated (r = 0-815). No other evidence that the two variables may be causally related was found.
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PMID:Urinary LDH isoenzyme 5 excretion in experimental pyelonephritis. 32 11

The triad of elevated SGOT and lactic dehydrogenase levels, positive blood and urine cultures, and acute renal failure was noted in a patient with severe pyelonephritis. Bilateral medullary necrosis was found on biopsy and at postmortem examination. These findings may help establish a prompt antemortem diagnosis.
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PMID:Nonobstructive pyelonephritis initially seen as acute renal failure. 34 38

In 39 children with urinary infection renal capacity of concentration, serum C-reactive protein and presence of urinary lactic dehydrogenase are studied pointing to the establishment of the topography of the damage. C-reactive protein levels higher than 20 micrograms/ml are 100 per 100 reliable in the diagnosis of pyelonephritis. Moreover, value of this test is confirmed as a guide of therapeutic efficacity. Difficulty of concentrating urine above 800 mOsm/l is 70 per 100 reliable and is a useful method for demonstrating parenchymal damage. The urinary lactic dehydrogenase was superior to 20 units/l in 64 per 100 of the cases, but other studies are necessary for interpretation of these data. These findings are similar to those obtained in the study of the isoenzymes.
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PMID:[Value of the C reactive protein, urinary lactic dehydrogenase and renal capacity of concentration in the topographic diagnosis of the urinary infection in infancy (author's transl)]. 69 17

In patients with chronic pyelonephritis (n = 17), nephrotic syndrome (n = 7) and hyperthyroidism in comparison to a reference group of healthy persons (n = 17) total activity and isoenzymes of the lactate dehydrogenase in the urine were determined. Only in patients with pyelonephritis is not regularly increased activity of the total lactate dehydrogenase a clear increased excretion of the isoenzymes IV and V is established. The isoenzyme pattern shows a dependence on the content of leucocytes in the urine and normalizes in renal infections only in a therapeutic effect.
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PMID:[Diagnostic value of LDH-isoenzyme determination in the urine]. 91 May 32

Urinary lactic dehydrogenase (U-LDH) isoenzyme assays were performed on ch2) as well as normal controls (N = 24). Docuemntation of bladder and kidney infection was accomplished by means of the bladder washout test, culture of ureteric urine (in patients with urinary diversion), kidney function studies including the maximal urine concentration test, clinical symptomatology and radiologic appearance of the urinary tract. Total U-LDH in normal children (10.8 +/- 1 mU/ml) was lower than in patients with bladder (27.0 +/- 3.9 mU/ml) or kidney (226 +/- 67.3 mU/ml) infections (P less than 0.005). In normal children isoenzymes 1 and 2 predominated (LDH-1 migrates fastest to anode -- fast zone pattern). In patients with bladder infections, the isoenzyme patterns varied but the concentration of isoenzyme 5 (3.1 +/- 0.8 mU/ml) was lower (P less than 0.005) than in patients with kidney infections (120 +/- 39 mU/ml). In the latter, isoenzymes 4 and 5 predominated (slow zone pattern). Since overlap between kidney and bladder infections regarding isoenzyme 5 concentrations (at 3 SD) occurred in only one individual (patient 37), a correct differential diagnosis using U-LDH-5 alone would have been possible in 94% of the children with pyelonephritis or 97% of the total patient population (kidney + bladder).
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PMID:Urinary lactic dehydrogenase isoenzyme 5 in the differential diagnosis of kidney and bladder infections. 117 77

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

Proteus mirabilis, a common agent of nosocomially acquired and catheter-associated bacteriuria, can cause acute pyelonephritis. In ascending infections, bacteria colonize the bladder and ascend the ureters to the proximal tubules of the kidney. We postulate that Proteus species uses the HpmA hemolysin and urease to elicit tissue damage that allows entry of these bacteria into the kidney. To study this interaction, strains of Proteus mirabilis and P. vulgaris and their isogenic hemolysin-negative (hpmA) or isogenic urease-negative (ureC) constructs were overlaid onto cultures of human renal proximal tubular epithelial cells (HRPTEC) isolated from kidneys obtained by immediate autopsy. Cytotoxicity was measured by release of soluble lactate dehydrogenase (LDH). Two strains of P. mirabilis inoculated at 10(6) CFU caused a release of 80% of total LDH after 6 h, whereas pyelonephritogenic hemolytic Escherichia coli CFT073 released only 25% at 6 h (P less than 0.012). Ten P. mirabilis isolates and five P. vulgaris isolates were all hemolytic and cytotoxic and produced urease which was induced by urea. The HpmA hemolysin is apparently responsible for the majority of cytotoxicity in vitro since the hemolysin-negative (hpmA) mutants of P. mirabilis and P. vulgaris were significantly less cytotoxic than wild-type strains. P. mirabilis WPM111 (hemolysin negative) was used to test the effect of urease-catalyzed urea hydrolysis on HRPTEC viability. In the presence of 50 mM urea, WPM111 caused the release of 42% of LDH versus 1% at 6 h in the absence of substrate (P = 0.003). We conclude that the HpmA hemolysin of Proteus species acts as a potent cytotoxin against HRPTEC. In addition, urease apparently contributes to this process when substrate urea is available.
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PMID:Cytotoxicity of the HpmA hemolysin and urease of Proteus mirabilis and Proteus vulgaris against cultured human renal proximal tubular epithelial cells. 203 63

Acute pyelonephritis, a complication of Escherichia coli bacteriuria, must represent a bacterial invasion through the kidney epithelium. To study this process, we overlaid bacterial suspensions onto monolayers of cultured human kidney proximal tubular epithelial cells and measured cytotoxicity by release of lactate dehydrogenase (LDH). Thirty-four isolates cultured from patients with acute pyelonephritis were screened for the ability to cause pyelonephritis in CBA mice by transurethral challenge. The eight most virulent strains (greater than or equal to 70% of mice challenged developed greater than or equal to 10(3) CFU/g of kidney after 48 h) were selected for study. Each strain displayed mannose-resistant hemagglutination of human O erythrocytes; three strains were phenotypically and genotypically hemolytic. Pyelonephritogenic strains were significantly more cytotoxic (30.1 +/- 9.5% LDH release after 18 h) than eight fecal control strains (13.5 +/- 11.5% LDH release; P = 0.0068). We selected the most cytotoxic strain, CFT073, for further study. Sterile filtrate from this hemolytic strain was significantly more cytotoxic than was the filtrate of the fecal control strain, FN414. Transposon mutagenesis of CFT073 with TnphoA abolished hemolytic activity and cytotoxicity by both whole cells and sterile filtrate. Southern blot analysis revealed that the Tnphoa insertion mapped to the E. coli chromosomal hly determinant within a 12-kilobase SalI restriction fragment. Transformation of a nonhemolytic strain, CPZ005 with plasmid pSF4000, which carries a cloned hemolysin determinant, resulted in highly elevated cytotoxicity. Light micrographs of proximal tubular epithelial cell cultures demonstrated cell damage by pyelonephritogenic strains that was not induced by a fecal strain or the hemolysin-deficient mutant. Results indicate that pyelonephritogenic E. coli strains are more frequently cytotoxic for a putative target, that is, human renal tubular epithelium, than are fecal isolates. Hemolysin, in some strains, is apparently responsible for this cytotoxicity.
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PMID:Pyelonephritogenic Escherichia coli and killing of cultured human renal proximal tubular epithelial cells: role of hemolysin in some strains. 218 40

Enzyme levels of lactate dehydrogenase (LDH), alpha-hydroxybutyrate dehydrogenase (HBDH), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured in the cytosol of renal cortex samples from either normal and pathologic kidney tissue. The mean enzyme activity values, expressed in Units per gram of cytosolic protein decreased in the following order: normal cortex (LDH = 4,299 +/- 654; AST = 522 +/- 101; ALT = 197 +/- 44). chronic pyelonephritis (LDH = 2,360 +/- 876; AST = 297 +/- 117; ALT = 90 +/- 48), hydronephrosis (LDH = 2,208 +/- 1,264; AST = 279 +/- 165; ALT = 82 +/- 61), pyonephrosis (LDH = 1,410 +/- 596; AST = 158 +/- 69; ALT = 23.4 +/- 16.4) and renal tuberculosis (LDH = 1,149 +/- 481; AST = 93 +/- 34; ALT = 5.6 +/- 2.8). The decrease in the enzyme activities paralleled tissue damage and it was shown to affect cellular functionality in relation with energy and amino acid metabolism.
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PMID:Cytoplasmic enzyme activities involved in energy and amino acid metabolism in pathological human renal cortex. 324 90

This investigation was a systemic study on an adult population of urinary lactate dehydrogenase (LDH) isoenzyme analysis for the distinction between upper and lower urinary tract infections. The study included 160 urine samples from patients and healthy individuals. On the basis of clinical symptoms, urinary bacterial colony counts, renal function tests and radiologic findings, the adults were divided into pyelonephritis group, cystitis group, pelvic lesion group, and control group. This technique correctly identified 23 of 26 patients with pyelonephritis by the presence of elevated LDH-V (over 10 percent) and all of 12 patients with cystitis by the presence of elevated LDH-I (over 60 relative units) but low LDH-V (below 10 percent or lower than LDH-I). In the pelvic group, the results of eight patients were consistent with cystitis and four with pyelonephritis. Our study confirms the sensitivity and specificity of the LDH isoenzyme technique for the differential diagnosis of urinary tract infection on adult patients and is consistent with previous studies on pediatric patients. However, one should be cautious to interpret the results of LDH isoenzymogram before extra-urinary tract lesions are excluded.
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PMID:Urinary lactate dehydrogenase isoenzyme analysis in adult population. 397 May 16


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