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Query: UMLS:C0034186 (pyelonephritis)
 6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Over a 7-year period, 15 pregnant women admitted to Parkland Memorial Hospital for acute pyelonephritis developed respiratory insufficiency characterized by dyspnea, tachypnea, hypoxemia, and radiographic evidence of pulmonary infiltrates. Clinical manifestations usually appeared 24 to 48 hours after the patient was admitted and varied from mild respiratory distress to pulmonary failure in three; these three required tracheal intubation and mechanical ventilation. We found no evidence that pulmonary edema was caused by intravenous fluid overload. Oxygen therapy and ventilation were given to maintain the arterial PO2 at 80 mm Hg or greater, and erythrocyte transfusions were given to six women to correct anemia. Women with pulmonary injury were more likely to have multisystem derangement than a control group without respiratory involvement, but there were no clinical risk factors that were predictive at admission. This syndrome was probably caused by permeability pulmonary edema, likely mediated by endotoxin-induced alveolar-capillary membrane injury since other evidence of endotoxemia was common. Thrombocytopenia, hemolysis, intravascular coagulation, renal dysfunction, and transient cardiomegaly concomitant with hyperdynamic ventricular function are all explicable from endotoxin effects.
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PMID:Pulmonary injury complicating antepartum pyelonephritis. 357 94

The favourable effect of gentamicin and its combination with furosemid was shown in treatment of rats with experimental pyelonephritis. However, alongside the favourable effect, a danger of the gentamicin nephrotoxic effect, especially in combination with furosemid was noted. The nephrotoxic effect was evident from foci of distrophic and necrobiotic changes in the epithelium of the convoluted tubules, impairment of the cortical hemodynamics and development of the cortical hypoxia of the kidneys resulting in severe renal insufficiency. Gentamicin had no direct inhibitory effect on the tissue respiration, did not block the oxygen uptake and oxidative phosphorilation in isolated mitochondria. To prevent the development of the nephrotoxic effect of gentamicin and its combination with furosemid strict and effective control of the antibiotic plasma levels is necessary. Informative tests for the control of the renal function are the concentration parameters of creatinine and urea, especially at the beginning of the pathological state when the level of hyperazotemia is still of a low informative value. The diurnal urine excretion is not an important informative index of renal function.
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PMID:[Use of gentamycin and furosemide in acute pyelonephritis (an experimental morphological study)]. 736 27

We investigated the influence of granulocyte colony-stimulating factor (G-CSF) on bactericidal activities of macrophages and polymorphonuclear leukocytes (PMNs) from experimental pyelonephritis in leukocytopenic rats, in order to clarify the usefulness of G-CSF for opportunistic pyelonephritis. We prepared three groups of experimental pyelonephritis, i.e., G-CSF administration group (group-1), cyclophosphamide (CPA) administration group (group-2), and CPA and G-CSF administration group (group-3). And we measured the active oxygen generation of peritoneal macrophages and PMNs in each group. On the other hand, we produced pseudomonal pyelonephritis in each group, and compared the survival rate of each group for 7 days. G-CSF enhanced active oxygen generation of peritoneal macrophages and PMNs, significantly. Furthermore, G-CSF improved the survival rate of pseudomonal pyelonephritis in leukocytopenic rats. These results indicate that G-CSF enhanced bactericidal activities of macrophages and PMNs in vivo, and prevents dissemination of infections.
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PMID:[Influence of granulocyte colony-stimulating factor on bactericidal activities of macrophages and polymorphonuclear leukocytes]. 750 94

Although emphysematous pyelonephritis has been recognized for more than a hundred years, the actual etiology is still unknown. Glucose fermentation has been implicated as a mechanism of gas formation. We report a case of emphysematous pyelonephritis in which real-time ultrasonography demonstrated intravascular gas bubbles originating in the involved kidney, and passing into the inferior vena cava and hepatic veins. Gas from the affected kidney was analyzed by chromatography; the result showed hydrogen 10.5%, carbon dioxide 39%, nitrogen 49.6% and oxygen 0.8%. The clinical presentation and the results of gas analysis implicate a critical condition that bacteria proliferated rapidly by mixed acid fermentation of glucose. Additionally, the finding of gas production and transportation could explain the previous hypothesis of gas transport. In this critical situation immediate drainage with medical intervention is indicated to treat this life threatening condition.
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PMID:Gas in hepatic veins: a rare and critical presentation of emphysematous pyelonephritis. 825 88

The close similarities between the urinary tract of primates make it possible to use the monkey as a model for understanding the pathophysiology of pyelonephritis in the human. Basically, experimental protocols consist in introducing uropathogenic strains of E. coli into the bladder and/or the ureter in the monkey and to determine early and late consequences of the subsequent renal tissue infection. Lesions appear within the first minutes of bacterial invasion. They result from the virulence of the parasite, which pertains to multiple factors, with a prominent role of fimbrial adhesion. However, the defense mechanisms of the host better explain the renal tissue insult. They comprise early ischoemia due to granulocyte aggregation within the renal capillaries, followed by damage due to oxygen free radicals which are generated during reperfusion. The primate model of pyelonephritis is extremely useful to understand most clinical, functional and radiological events observed in the course of human pyelonephritis. This model also serves to test pharmacological manoeuvres aimed at preventing the renal tissue injury of pyelonephritis.
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PMID:[Contribution of experimental pathology to the understanding of human pyelonephritis]. 837 12

In the pathogenesis of glomerulonephritis, acute renal failure, pyelonephritis and other diseases of the kidneys oxygen radicals are involved. Some types of glomerulonephritis are characterized by infiltration of the glomeruli by neutrophils and monocytes which can form oxygen radicals (superoxide, hydrogen peroxide). The increased amount of cAMP in glomeruli can be due to oxygen radicals. Cyclic nucleotides modulate the inflammatory or immune response in glomerular disease and play a part in the action of local mediators of the inflammation. Oxygen radicals act as second messenger for the activation of cytokines via NF-kappaB transcription factor, they stimulate the formation of TNF-alpha, IL-1, IL-6 and influence the expression of monocyte-specific cytokines (CSF-1 and MCP-1). Radicals formed by the system myeloperoxidase--hydrogen peroxide--halogen derivatives activate proteolytic enzymes (proteinases) which break down collagen and other components of the extracellular matrix present in the basal membrane of glomeruli and in the mesangium. Oxygen radicals and proteinases can cause and amplify glomerular damage. Glucocorticoid administration leads to an increased activity of endogenous antioxidant enzymes in the glomerulus and reduced the of lipid peroxidation.
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PMID:[The role of oxygen radicals in the pathogenesis of glomerulonephritis]. 859 8

Pyelonephritis is the most common urinary tract infection in females, but the pathogenetic mechanisms are not well understood. Reactive oxygen species (ROS) have been implicated as cause of injury in several renal diseases. In this study, we have demonstrated the role of ROS in pathogenesis of pyelonephritis in Balb/c mice. A clear correlation between extent of ROS generation and subsequent lipid peroxidation and DNA damage in kidneys was observed during the course of infection, from 2 to 14 days. Activities of brush border membrane marker enzymes were also significantly altered. Administration of antioxidants, superoxide dismutase, catalase and dimethylsulfoxide significantly reversed the histopathological changes, reduced the extent of lipid peroxidation in renal brush border membrane, and also reversed the altered enzyme activities to near normal situation. These results clearly suggest that interaction of ROS with various cellular organelles in kidneys has a significant deleterious effect, and this could be the underlying mechanism for renal dysfunction in pyelonephritis.
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PMID:Reactive oxygen species-mediated tissue injury in experimental ascending pyelonephritis. 877 Sep 45

Pyelonephritis is the most common urinary tract infection affecting females of all age groups. Despite concerted efforts the mechanism of renal injury in pyelonephritis is not clearly understood. In the present study we have made an attempt to characterise the mediators of inflammatory insult in an experimental model of ascending pyelonephritis. Mice infected with Escherichia coli O6:K13:H1 were sacrificed at 2, 7 and 14 days post-infection. Luminol-dependent chemiluminescence response, NADPH oxidase, acid phosphatase, beta-glucuronidase and N-acetyl-beta-D-glucosaminidase activities were monitored in circulating as well as renal phagocytic cells in order to determine the role of reactive oxygen species and lysosomal enzymes in genesis of renal injury. We have demonstrated that reactive oxygen species are generated at the initiation of infection and the levels increase progressively during the course of infection. While intracellular release of lysosomal enzymes was seen in all groups, extracellular release was primarily observed at 7 and 14 days post-infection only. The results indicate that while reactive oxygen species play a significant role in tissue injury during all stages of infection, lysosomal enzyme release in extracellular milieu augments tissue destruction at later stages only.
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PMID:Oxygen-dependent and -independent mechanisms of renal injury in experimental ascending pyelonephritis. 882 96

Immunological examination (T- and B-cell immunity, metabolic activity of phagocytes) was conducted in 10 patients with primary and 21 patients with secondary chronic pyelonephritis in the phase of latent inflammation resistant to conventional antibacterial therapy versus 12 patients free of this disease. It was found that immunoreactivity in the above patients was compromised as shown by quantitative and qualitative deficiency of T-cell immunity (a fall in the absolute number of CD3+, absolute and relative content of CD2+DR+, changed proportion of T-lymphocyte subpopulations, low activity of oxygen-dependent anti-infection systems of phagocytes). B-system immunity did not much change for the worse. In primary chronic pyelonephritis immunoreactivity was affected more seriously.
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PMID:[The immune status of patients with primary and secondary chronic pyelonephritis]. 892 23


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