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

Complications are the major causes of illness and death after burning and most of them stem from the burn wound. Their origin and importance are reviewed with emphasis on problems and growing points in knowledge. Fluid leakage from the circulation into the burn is the cause of hypovolemic shock, but the underlying permeability changes in the burn are only partly understood. Other nonbacterial complications include acute cardiac failure, acute anemia, hemolytic jaundice, renal failure, encephalopathy, complex hypermetabolic effects including pseudodiabetes, gastric and duodenal ulceration, deep vein thrombosis and pulmonary embolism, pulmonary and glomerular microthrombosis, hepatic jaundice, and arterial thrombosis. Involvement of the airway in conflagrations carries special hazards like glottic edema and inhalation of irritant fumes. Nowadays, bacterial causes are dominant and these remain the main challenge. Bacterial infection and invasion of the burn are usually responsible for septicemia, bronchopneumonia, and pyelonephritis although other sources also contribute. Indirect manifestations of septicemia include paralytic ileus, acute gastric dilatation, toxic myocarditis, and some cases of renal failure. Therapeutic complications like agranulocytosis, thrombocytopenia, and colitis occur at times. High concentrations of oxygen given therapeutically can produce fatal aseptic hypoxic pneumonitis.
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PMID:A review of the complications of burns, their origin and importance for illness and death. 44 73

P-fimbriated Escherichia coli, which cause nonobstructive pyelonephritis, adhere to a specific urothelial glycolipid receptor. In either the presence or absence of reflux (in the area of turbulent urine flow) these bacteria ascend the ureter and cause a decrease in ureteral motility. Endotoxin causes peristalsis to cease, leading to ureteral dilatation and change in papillary shape, thus allowing intrarenal reflux and adherence of the bacteria to renal tubules. Bacterial infection of a refluxing ureter may cause reflux to persist. Once the bacteria reach the kidney rapid effects occur at the cellular level with activation of complement followed by granulocytic aggregation and capillary obstruction, causing renal ischemia and damage during reperfusion. In addition, during phagocytosis the respiratory burst occurs, releasing toxic oxygen molecules, which leads to renal tubular death, invasion of the interstitium, microabscess and renal scar formation, that is chronic pyelonephritis, which equates with reflux nephropathy.
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PMID:Vesicoureteral reflux and pyelonephritis in the monkey: a review. 143 97

The mechanism of tissue injury at the cellular level by following the chemiluminescence response of various phagocytes in E. coli induced experimental pyelonephritis in mice was investigated. There was a marked increase in the capacity of various phagocytic cells viz; renal neutrophils and macrophages peritoneal macrophages, blood monocytes and neutrophils to produce reactive oxygens species through the respiratory burst activity as monitored by the chemiluminescence response. The chemiluminescence response was observed to be increased significantly (p less than 0.001) with increasing days post infection in all phagocytic cells. However, the quantity of total reactive oxygen species produced per million cells was much more in the renal and peritoneal macrophages as compared to blood monocytes and neutrophils. The peak chemiluminescence response time was observed to be decreased from 4 to 2 minutes with the progression of the diseases. The implications of these findings have been discussed.
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PMID:Chemiluminescence response of phagocytes in E. coli induced experimental ascending pyelonephritis. 161 96

Levels of R proteins, immunoglobulins A, M, and G, natural anti-sheep erythrocyte antibodies, active oxygen (superoxide) were measured in the neutrophilic leukocytes in pregnant females at a risk for late gestosis. The examinees were found to have high levels of R proteins, IgA, IgM, natural anti-sheep erythrocyte antibodies, neutrophils capable to restore NST, and low levels of IgG. Teen-agers, old-year primiparas, pregnant females with a history of pyelonephritis, obesity, neuropathy in the prior labour, and hypertensive vegetovascular dystonia constituted a gestosis-risk group. The R-protein test should be considered to be the most informative indicator of a gestosis risk.
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PMID:[Immunity indices in the diagnosis of pretoxicosis in women with an increased risk for the development of late toxicosis]. 165 May 37

Oxidant injury has been implicated in the pathogenesis of inflammatory, metabolic and toxic insults, in ischemic-reperfusion injury, and in carcinogenesis, aging and atherosclerosis. Oxidant injury is initiated by free radicals and reactive oxygen molecules which are generated by activated neutrophils, monocytes, and mesangial cells, during normal and abnormal metabolic processes, and from the metabolism of exogenous drugs and toxins. When cells and organs are exposed to oxidant stress, several different antioxidant defense mechanisms operate to prevent or limit oxidant injury. When antioxidant defense mechanisms are decreased, or when the generation of reactive oxygen molecules is increased, oxidant injury results from the shift in the oxidant/antioxidant balance. Oxidant-induced alterations of proteins, membranes, DNA, and basement membranes leads to cell and organ dysfunction. Several renal diseases including glomerulonephritis, vasculitis, toxic nephropathies, pyelonephritis, acute renal failure, and others are likely to be mediated at least in part by oxidant injury. In the future, mechanisms to decrease the generation of reactive oxygen molecules and/or antioxidant therapy may develop into new avenues of therapeutic intervention.
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PMID:Reactive oxygen molecules, oxidant injury and renal disease. 166 82

The production of reactive oxygen metabolites by neutrophils plays a key role in the host defense against invading microorganisms and in tissue damage resulting from infection. In the present study we measured the ability of different uropathogenic Escherichia coli strains to induce generation of oxygen metabolites upon interaction with human neutrophils. The strains were selected to represent two groups of patients with recurrent episodes of acute pyelonephritis: one with renal scars (12 strains) and one without renal scarring (11 strains). The majority of strains (from both groups) induced a pronounced neutrophil respiratory burst activity. When the intracellular and extracellular oxidative responses were measured separately, it was found that the response induced by nonscarring strains was primarily of intracellular (intraphagosomal) origin, whereas a proportionally larger fraction of the response induced by the scarring strains was extracellular. Since reactive oxygen products are toxic to the renal tissue, this release can be of importance in the development of renal scars.
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PMID:Extracellular release of reactive oxygen species from human neutrophils upon interaction with Escherichia coli strains causing renal scarring. 193 73

Acute gestational pyelonephritis infrequently leads to nonhydrostatic permeability pulmonary edema known clinically as acute respiratory distress syndrome (ARDS). In this form of ARDS, sepsis is considered the primary cause of pulmonary dysfunction. Decreases in colloid osmotic pressure, plasma fibronectin, and arterial oxygen saturation are associated with a worsening prognosis in septic conditions. We sought to investigate the changes in these parameters with acute gestational pyelonephritis to gain insight into the factors that may place the patient at risk for sepsis-related morbidity. Colloid osmotic pressure, plasma fibronectin, and arterial oxygen saturation via pulse oximetry were prospectively measured during the inpatient treatment of 17 pregnant patients with acute gestational pyelonephritis. All three parameters achieved their nadir within 24 hours of hospitalization and the initiation of therapy. Although no patient developed significant pulmonary dysfunction, we believe that patient susceptibility for pulmonary edema and general morbidity could be maximal in the first 24 hours after therapy. Future studies using a larger number of patients may identify one or more of these laboratory parameters as helpful in identifying gravid patients who are at risk of developing gestational ARDS.
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PMID:Acute gestational pyelonephritis: the impact on colloid osmotic pressure, plasma fibronectin, and arterial oxygen saturation. 202 86

Emphysematous pyelonephritis is a severe necrotizing infection that usually occurs in patients with diabetes mellitus or obstructive uropathy. Although glucose fermentation has been considered as the main cause of gas production the actual mechanism remains controversial. Compositions of gas samples from 2 patients with emphysematous pyelonephritis recently encountered were analyzed, and showed 15% hydrogen, 4.8% carbon dioxide, 60% nitrogen, 6.7% oxygen and some unknown gases in case 1, and 3.4% hydrogen, 22% carbon dioxide, 66% nitrogen and 9.8% oxygen in case 2. These results tend to implicate mixed acid fermentation of glucose as the pathway by which emphysematous urinary tract infections develop.
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PMID:Mixed acid fermentation of glucose as a mechanism of emphysematous urinary tract infection. 205 76

It was established during the study of blood serum and urine chemiluminescence in 57 children with pyelonephritis and in 38 children with glomerulonephritis that in the active disease stage, the intensity of overfaint luminescence rises as a result of lipid peroxidation (LPO) activation, accumulation of lipid hydroperoxides and oxygen-containing radicals. Four types of the kinetic curves of urine chemiluminescence were identified. They characterize the correlation between LPO activation and the level of antiradical defence in patients suffering from pyelo- and glomerulonephritis. The measurement of urine chemiluminescence in patients afflicted with pyelonephritis and glomerulonephritis may be one of the criteria for administering drugs possessing antiradical and antioxidant activity and can also be used in the control over the treatment efficacy.
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PMID:[Chemiluminescence of blood and urine in children with pyelonephritis and glomerulonephritis]. 262 9

Alpha-hemolysin (AH) is a 110,000-dalton protein secreted extracellularly by certain Escherichia coli. This protein is an acknowledged virulence factor for E coli and recently has been implicated as an important determinant in the pathogenesis of E coli pyelonephritis. Recombinant engineered strains of E coli were used that varied only in their ability to secrete AH extracellularly. The effect of AH on vital dye exclusion, oxygen consumption rate (QO2) adenosine triphosphate (ATP) levels, superoxide (O2-) and hydrogen peroxide (H2O2) production in preparations of isolated rat cortical renal tubular cells (RTCs) was assessed. Approximately 5-10 pg of AH dramatically stimulated QO2 by nearly 150%. This was associated with a marked increase in production of O2- and H2O2, to 13.9 +/- 1.7 and 13.2 +/- 2.1 nM/mg cell protein, respectively (P less than 0.05), as well as a 38% decrease in cellular ATP. These biochemical effects were all seen after a 30-minute exposure to AH and by 120 minutes were associated with 15.7% +/- 1.1% of RTCs that were unable to exclude vital dye. The effect of AH on QO2 and O2- formation was prevented by pretreatment of RTCs with ouabain, which indicates that the effect of AH on oxygen metabolism is linked to Na-K ATPase activity. However, when ouabain-treated RTCs were exposed to AH, ATP remained depressed despite the inhibition of QO2 and O2- production. In contrast, in ouabain-pretreated RTCs, cell membrane integrity was dramatically protected, because only 2.4% +/- 0.4% of RTCs were not unable to exclude vital dye. Thus, the data demonstrate that E coli AH provokes at least two biochemical events that may be injurious to RTC: increased oxygen intermediates (O2- and H2O2 and ATP depletion. These findings with ouabain suggest that the first mechanism of injury may be a more proximate cause of cell death. Moreover, the data suggest that endogenous production of reactive oxygen molecules may be critical modulators of RTC membrane injury.
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PMID:Mechanism of Escherichia coli alpha-hemolysin-induced injury to isolated renal tubular cells. 303 Jan 15


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