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)

The authors analyze the status of cationic transmembranous transport in leukocytes in patients with chronic secondary pyelonephritis (CPN) as related to the clinical manifestations of pathology and immune response. 117 patients with CPN were examined. In 58 patients, pyelonephritis was associated with nephrolithiasis, in 59 with different abnormalities of the kidneys and urinary tract. The immunity status was examined according to the content of IgA, IgG, IgM, T and B lymphocytes, complement (CH50), the phagocytic neutrophil test and secretory IgA in the urine. In white blood cells, a study was made of the activity of Mg(2+)-, Na(+)-K(+)-, Ca(2+)-ATPases. As a result of the studies the patients were found to have low functional activity of Ca(2+)-ATPase, Na(+)-K(+)-ATPase during the clinical manifestations of pyelonephritis. Analysis of the frequency of enzymatic activity values showed their nonuniformity. In some patients, it was lowered (less than X--1), whereas in others, it appeared increased (over X+1). Patients with an enzymatic activity below X--1 manifested a decrease of the content of IgA, IgG, IgM, T and B lymphocytes, and of phagocytic activity of neutrophils as compared to patients exhibiting a high enzymatic activity. The conclusion is made about the relationship between enzymatic function and immune response. It is recommended that drugs possessing membrane-protective and reparative pharmacological effects be included into multimodality therapy.
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PMID:[Role of structuro-functional changes in cell membranes in the formation of the immune response in patients with chronic pyelonephritis]. 164 87

The paper examines the relationship between the clinical manifestations of pyelonephritis and the functional activity of enzymes of cation transmembrane erythrocyte transport (Mg(2+)-, N(+)-K(+)-, Ca(2+)-ATPases). An individual analysis ascertained that the patients who showed a low Ca(2+)-ATPase activity had marked signs of inflammation in the body, as evidenced by ESR, seromucoid and fibrinogen concentrations. These patients had more significantly depressed immune defense mechanisms as reflected by the levels of immunoglobulins, T-lymphocytes, complement, the neutrophil phagocytosis, and urinary IgA concentrations). Variations were also found in examining the excretion of a number of metabolites. There was a substantial decrease in urea, creatinine, titrated acid, phosphorus excretions in patients with deficient Ca(2+)-ATPase activity than in those with its high activity. It was concluded that there was a relationship between some clinical manifestations of pyelonephritis and the functional activity of enzymes of cation transmembrane transport. To treat metabolic disorders, membrane-protective agents are recommended to include into combined therapy.
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PMID:[The enzyme function of cationic transmembrane transport and its relationship to the homeostatic indices of patients with chronic pyelonephritis]. 183 Apr 30

Lipid peroxidation (LPO) and transmembranous transportation were analysed in the red cells of 56 patients with chronic pyelonephritis with regard to the pathologic changes in the membranes. LPO registration was made on the basis of the levels of diene conjugates and Schiff's bases. The activity of enzymes of transmembranous transportation-calcium, magnesium, sodium/potassium pump--was studied. The levels of the LPO markers were found to be tending to an increase in the active stage of the disease and to a decrease in its remission. Though the initial control levels of the markers were not reached. In the active stage of the disease the levels of diene conjugates were 59.66 +/- 6.43 nmol (42.6 +/- 94 nmol/litre in the control) while in the remission they were 22.16 +/- 3.22 a. u. (14.80 +/- 1.06 in the control). The results obtained are indicative of the polymorphism of clinically manifest metabolic changes. In the patients with higher levels of Ca2-ATPase the disease ran more silent than in those in whom the enzymic functional activity were lower. Inadequate activity of enzyme transmembranous transportation revealed in some patients in the course of manifest inflammation was a direct reflection of the failure in the mechanism of adaptation and an evidence of the initially heterogeneous activity (individuality) the enzymes of transmembranous cation transportation. The revealed phenomena contributed to the clinical course of pyelonephritis in a particular person and with regard to pathogenetic mechanisms required an approach to the therapy on an individual basis.
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PMID:[Lipid peroxidation and transmembrane transport in patients with chronic pyelonephritis]. 261 35

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

It is established that active pyelonephritis and operative stress are accompanied with structural and functional changes in erythrocytic membranes: cholesterol and its ethers rose in quantity as well as difficulty oxidized phospholipids, cation adenosine triphosphatase activity changed. Being nonspecific, these changes seemed more pronounced in the active phase of chronic pyelonephritis. Minor structural rearrangement of membrane lipids in surgical patients indicated uneventful postoperative period. It is suggested that bacterial inflammation in the kidneys and urinary tracts may be related to the above shifts. The adjuvant use of dimephosphone produced a clear-cut membrane-stabilizing effect clinically reflected by reduced inflammation and improved renal function.
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PMID:[Membrane-destabilizing processes as the universal basis of inflammation]. 801 97

The contribution of pyelonephritis activity to calcium reabsorption defects was investigated in 176 patients with chronic pyelonephritis (CP) aged 18-54 with normal tubular filtration and calcium serum concentrations under calcium reabsorption above 98%. 86 of these patients had CP complicated by nonocclusive pelvic stones. Ca-excretory capacity of the kidneys was evaluated with estimation of the excreted calcium by activity phases considering individual deviations or without them. Measurements were also made of CP activity and severity by the inhibition of Ca-ATPase activity of the microsomes isolated from rat intact kidneys. The findings indicate that in active CP calcium-reabsorption impairments related to the inflammation are combined with the preexisting ones, the changes being more pronounced with growing activity of the inflammation, irrespective of the presence of nephrolithiasis. The relationship established between the shifts in excreted calcium induced by inflammation and plasma ability of CP patients to inhibit Ca-ATPase activity of rat renal microsomes in single tests in the same patients allows assessment of calcium reabsorption changes due to CP activity in patients when analysing their blood inhibitory effect on the test enzyme system. Simultaneous one-stage determination in CP patients of their blood inhibition in response to the test enzyme system and excreted calcium helps prognosticate calcium reabsorption expected in remission.
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PMID:[The importance of studies of calcium reabsorption and of the capacity of the blood plasma to inhibit Ca-ATPase activity for the diagnosis of the activity of the inflammatory process and for the prognosis of tubular function in patients with chronic pyelonephritis]. 801 98

Whether blood plasma from 63 pyelonephritis patients can inhibit Ca-ATPase activity when compared to known toxicity marker (middle-sized molecule number) was studied. This was done to assess diagnostic potentialities of the test based on the ability of plasma from pyelonephritis patients to inhibit the test enzymatic system, i. e. Ca-ATPase activity of the microsome fraction from renal cortex in intact rats. The inhibition of Ca-ATPase activity by the plasma is shown to correlate with inflammation activity and the patients condition. In pyodestructive acute pyelonephritis this inhibition reached 60.6 +/- 3.86%, in acute serous pyelonephritis 36.02 +/- 1.54%. It follows, that the above parameter is more informative than the number of middle-sized molecules and can be introduced as one of the criteria of the patients' condition and for choice of treatment.
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PMID:[The suppression of the Ca ATpase activity of rat kidney microsomes under the action of blood plasma as an index of the severity of the status of pyelonephritis patients]. 820 66

The author has estimated levels of malonic dialdehyde (MDA) indicative of activity of membrane phospholipid peroxidation activity, basal and true (in incubation in the culture containing glomeruloform antibiotic alameticin) Ca-ATPase activity in microsomal fraction isolated from cortical tissue of functioning kidneys obtained intraoperatively from 26 patients. 12 samples of cortical tissue obtained from uninvolved parts of the kidneys affected with carcinoma served as control. 14 samples were obtained from the tissue of functioning kidneys affected with nephrolithiasis and active chronic pyelonephritis. The investigations show elevated MDA levels, enhanced basal in reduced true Ca-ATPase activity of microsomes from the kidneys of patients with nephrolithiasis and active chronic pyelonephritis compared to control. It is suggested that high basal against low true Ca-ATPase activity of renal microsomes may be explained by increased permeability of renal membranes for Ca2+ under activation of lipid peroxidation in active chronic pyelonephritis and nephrolithiasis.
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PMID:[Lipid peroxidation and Ca-dependent ATPase activity in the microsomal fraction of renal tissue in patients with nephrolithiasis and chronic pyelonephritis]. 905 96

Ion transport is essential for maintenance of transmembranous and transcellular electric potential, fluid transport and cellular volume. Disturbance of ion transport has been associated with cellular dysfunction, intra and extracellular edema and abnormalities of epithelial surface liquid volume. There is increasing evidence that conditions characterized by an intense local or systemic inflammatory response are associated with abnormal ion transport. This abnormal ion transport has been involved in the pathogenesis of conditions like hypovolemia due to fluid losses, hyponatremia and hypokalemia in diarrhoeal diseases, electrolyte abnormalities in pyelonephritis of early infancy, septicemia induced pulmonary edema, and in hypersecretion and edema induced by inflammatory reactions of the mucosa of the upper respiratory tract. Components of membranous ion transport systems, which have been shown to undergo a change in function during an inflammatory response include the sodium potassium ATPase, the epithelial sodium channel, the Cystic Fibrosis Transmembrane Conductance Regulator and calcium activated chloride channels and the sodium potassium chloride co-transporter. Inflammatory mediators, which influence ion transport are tumor necrosis factor, gamma interferon, interleukins, transforming growth factor, leukotrienes and bradykinin. They trigger the release of specific messengers like prostaglandins, nitric oxide and histamine which alter ion transport system function through specific receptors, intracellular second messengers and protein kinases. This review summarizes data on in vivo measurements of changes in ion transport in acute inflammatory conditions and in vitro studies, which have explored the underlying mechanisms. Potential interventions directed at a correction of the observed abnormalities are discussed.
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PMID:Changes in ion transport in inflammatory disease. 1657 Nov 16