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)

Infection-induced suppressor cells may be associated with a depression of cell-mediated immune (CMI) mechanisms in pyelonephritis. In the present study, cell viability and cell to cell contact were established as prerequisites for immunosuppression and the role of mononuclear phagocytic cells and polymorphonuclear leukocytes, as immunoregulatory cells affecting CMI, was also examined. Fractionation of spleen cell suspensions was carried out using carbonyl iron, nylon wool, glass beads, and sephadex. These procedures restored mitogenic responsiveness to splenic lymphocytes from pyelonephritic animals, and it was possible to isolate cells with accessory and suppressor activity from nylon wool columns. Elutable cells (that is, cells which adhere to the column but could be recovered by the addition of EDTA) were characteristically accessory cells and increased the mitogenic responsiveness of normal lymphocytes. Adherent splenocytes which suppress mitogenic responses were isolated from pyelonephritic animals. Additionally, neutrophils, at concentrations readily demonstrable in lesions, depressed CMI responses in vitro. With this information available it should now be possible to carry out a detailed analysis of the cellular mechanism by which CMI in renal infection is depressed.
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PMID:Infection-induced immunosuppression in pyelonephritis: characteristics of the suppressor cell(s). 622 63

Our investigation of cefotiam in pediatric infection produced the following results: 1. Cefotiam was administered intravenously by one shot or drip infusion in 20 patients with infectious diseases. These diseases consisted of 13 pneumonia, 3 upper respiratory tract infections, 3 pyelonephritis, 2 other urinary tract infections and one purulent meningitis. Cefotiam was effective in all cases. 2. Transient elevation in serum GOT, GPT, Al-P and LDH was observed in 3 cases. But other side effect was not noted in any cases.
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PMID:[Clinical studies on cefotiam in pediatric infections (author's transl)]. 627 Apr 18

The therapeutic efficacy and pharmacokinetics of the cephalosporins ceftazidime, ceftizoxime, cefotaxime and HR 221 were studied in animal experiments. The animal model used was experimental estrogen-induced or non-induced chronic Escherichia coli pyelonephritis in rats. The animals were treated with 5 mg cephalosporin/kg twice daily for one week. Each of the cephalosporins tested led to a significant decrease in renal bacterial counts, in spite of the low doses given. Ceftazidime was significantly more active than HR 221 in both experimental models, although the serum levels of HR 221 were higher and were maintained for a longer period of time than those of ceftazidime. Differences in pharmacokinetic properties (influenced by metabolic stability and protein binding) could be the reason for the differences in therapeutic activity, since the in vitro antimicrobial activity of each of the cephalosporins tested was very similar against the test strain.
Infection 1983
PMID:Ceftazidime, ceftizoxime, cefotaxime and HR 221 in experimental chronic Escherichia coli pyelonephritis in rats. 629 68

Twenty-one hospitalized patients with infectious diseases were randomly assigned to receive either thienamycin formamidine/renal dipeptidase inhibitor or cefazolin. Infections treated included septicaemia, pneumonia, osteomyelitis, pyelonephritis, cellulitis and cutaneous abscesses. All eleven patients treated with thienamycin formamidine/renal dipeptidase inhibitor responded well to therapy. One of the ten patients treated with cefazolin developed a superinfection with Pseudomonas aeruginosa. Side effects detected were minor in both groups.
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PMID:A randomized study comparing clinical efficacy and safety of thienamycin formamidine (MK0787)/renal dipeptidase inhibitor (MK0791) and cefazolin. 635 77

In patients with recurrent pyelonephritis, the pathogenetic events proceed through intestinal colonization, spread to the urinary tract and persistence, seemingly uninterrupted by host defense mechanisms. The factors responsible for the deficient bacterial clearence from the kidneys of these patients, and the genetic control, have not been identified. The susceptibility to colonization has been linked to an increased receptivity for attaching bacteria of the uroepithelia, and to an overrepresentation of the P1 blood group phenotype. To evaluate the role of defects in host defense for the susceptibility to pyelonephritis, experimental UTI in mouse strains with known deficiencies was used. A highly significant increase in susceptibility was noted for C3H/HeJ compared to C3H/HeN mice. The bacterial recovery was inversely correlated to the mitogenic response to LPS. Back-cross analysis revealed a linkage of susceptibility to the Lpsd/Lpsd genotype. In contrast, T and B lymphocyte and complement (C5) defects had little effect on the clearance of Escherichia coli from the kidneys. It is concluded that the inflammatory mechanisms induced by LPS are essential for resistance to experimental pyelonephritis.
Infection
PMID:Genetic factors in host resistance to urinary tract infection. 637 64

More attention should be directed to upper urinary tract infections as they cause renal parenchymal damage. Recently, many reports on antibody-coated bacteria (ACB) in urological diseases have been made. We performed ACB tests in 68 cases of urological infectious diseases. The tests were made according to Thomas' method. Anti-human immunoglobulin IgG, IgA, and IgM rabbit sera were used. The results were compared using the chi-square analysis. ACB-positive were 0 approximately 15% of the cases of acute cystitis, 33 approximately 67% of the cases of chronic cystitis, 30 approximately 60% of the cases of prostatitis and urethritis, and 60 approximately 90% of the cases of pyelonephritis. The percentage was higher in the patients who had indwelling catheters than in those who did not. The ACB test was suggested to be helpful in diagnosing upper urinary tract infection in the female patients who did not have indwelling catheters. But there was the danger of making an incorrect diagnosis with this test on male patients who had indwelling catheters, and those with prostatitis or urethritis, and on female patients with indwelling catheters.
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PMID:[Urinary tract infection : clinical significance of antibody-coated bacteria]. 638 63

The structural basis for the cross-reactivity between the Escherichia coli K13, K20 and K23 capsular polysaccharides is the ----)-beta-ribofuranosyl-(1----7)-beta-2-keto-3-deoxyoctonate polymer. Monoclonal antibodies against E. coli K13 which require O-acetyl-2-keto-3-deoxyoctonate for binding were further investigated. Such antibodies, of both the IgG and the IgM isotype, opsonized E. coli K13 in vitro and protected against intraperitoneal infection in mice as well as ascending pyelonephritis in rats. A monoclonal IgG1 anti-idiotype, specific for the K13 polysaccharide combining site of a protective IgM idiotype, primed for protection against intraperitoneal infection with live E. coli K13 following K13 injections at four as well as 12 weeks of age. the K13 polysaccharide alone did not immunize and protect. The monoclonal anti-K13 idiotype only primed for protection at four weeks of age. These findings suggest a strong effect of a single idiotype on the outcome of a bacterial infection.
Infection
PMID:Studies on immunity against Escherichia coli K13 with monoclonal anti-K13 and anti-anti-K13. 638 95

We studied the effect of D-glucaro-1,5-lactam on aminoglycoside-induced nephrotoxicity in rats. Parameters of nephrotoxicity were urinary excretion of tubule cells and malate dehydrogenase. When given in appropriate doses, either i. m. or via an oral tube, D-glucaro-1,5-lactam significantly reduced the excretion of cells and enzymes during the administration of gentamicin, tobramycin, dibekacin, netilmicin and ribostamycin. It did not impair the therapeutic efficacy of ribostamycin in the experimental treatment of acute pyelonephritis in rats. The protective effect of D-glucaro-1,5-lactam could be ascribed to its inhibition of beta-glucuronidase, an enzyme which is located in renal lysosomes and which is activated by aminoglycosides.
Infection
PMID:Animal studies on the reduction of aminoglycoside-induced nephrotoxicity by D-glucaro-1,5-lactam. 688 75

There have been no reports suggesting that a genetic component may affect host resistance to renal infection. In rats with experimentally induced unilateral pyelonephritis, consistent level of infection was achieved in the directly challenged (left) kidneys. Retrograde infection in the unmanipulated (right) kidneys was found to be strain dependent in these animals. Infection was readily established in the right kidneys of the AS2 and HO strains but not in the DA strain; however, infection was established in all unmanipulated kidneys of the DA X AS2 F1 hybrid, whereas eight of 10 kidneys from the DA X HO hybrid remained uninfected. These results suggest that host resistance to retrograde renal infection in the rat strains studied was genetically determined, although the relevant host factor(s) has not yet been identified.
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PMID:Genetic factors and host resistance in experimental pyelonephritis. 688 95

Using 44 anti-O sera 789 Escherichia coli strains isolated from the urine of patients with urinary tract infections were typed. Of the 119 E. coli strains from the urine of children, 49.6% were O-typable; only 3.4% were rough strains. Of 357 strains from pregnant women, 47% were O-typable; 12.1% were rough strains. The largest proportion of O-typable E. coli strains was found among 314 strains isolated from adults with recurrent urinary tract infections (55.4% of the 314 strains); 8% were rough strains. The higher proportion of E. coli rough strains in adults, including pregnant women, indicate that once a pyelonephritis process has been established by virulent smooth strains in childhood, it can be sustained by rough strains at a later stage. Certain O serotypes were found to occur with a variable frequency in the individual patient groups. Enteropathogenic E. coli strains were seldom found in any of the three groups.
Infection 1980
PMID:[Escherichia coli o serotyping in different patient groups with urinary tract infections (author's transl)]. 698 60


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