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 presence of tubular involvement, as a marker for the detection of urinary tract infection (UTI) site, was examined in 19 patients with pyelonephritis and in 15 patients with cystitis or asymptomatic bacteriuria. The urinary excretion of four markers of tubular proteinuria, beta 2-microglobulin (beta 2M), lysozyme (LZ), lactic dehydrogenase isoenzyme V (LAD-5) and N-acetyl-beta D-glucosaminidase (NAG), was investigated. LAD-5 appeared particularly valuable for the early detection of upper UTI. However, the overall diagnostic accuracy appeared to be further strengthened using, besides LAD-5, one additional variable. A set of simple and noninvasive biochemical tests on urine samples can reliably help to identify the site of UTI.
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PMID:Contribution of four markers of tubular proteinuria in detecting upper urinary tract infections. A multivariate analysis. 675 51

Many patients with ileal conduit urinary diversion have infected urine but far fewer have clinical pyelonephritis. A noninvasive diagnostic test to distinguish renal bacteriuria from conduit colonization in these patients would seem desirable. Urine total lactic dehydrogenase and lactic dehydrogenase isoenzymes, and serum C-reactive protein have been useful to distinguish pyelonephritis from cystitis in patients with intact urinary tracts. We used these tests in patients with ileal conduits who had urine containing more and less than 10(5) organisms per ml. All patients had elevated urine total lactic dehydrogenase-5 isoenzyme, and serum C-reactive protein. No statistically significant difference in any of these parameters existed between the groups. These results may indicate that all patients with conduits have pyelonephritis but only intermittently demonstrate bacteriuria, or that the conduit mucosa contributes lactic dehydrogenase to the urine. However, it does not appear that these tests alone can distinguish accurately renal bacteriuria from conduit colonization.
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PMID:Urinary lactic dehydrogenase and serum C-reactive protein as means of localizing the site of urinary tract infection in patients with ileal conduits. 714 96

It is shown that per os administration of galascorbin to animals with acute experimental pyelonephritis in a dose of 100 mg/1 kg of mass per day normalizes the total activity of lactate dehydrogenase (EC 1.1.1.27), malate dehydrogenase (EC 1.1.1.37) and their isoenzymic spectrum in kidney tissue and blood serum. The content of pyruvic and lactic acids in blood serum also normalizes, that promotes a favourable course of the disease.
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PMID:[Effect of galascorbin on activity of lactate and malate dehydrogenases and their isoenzymic spectrum in experimental pyelonephritis]. 728 Dec 62

The aerobactin-mediated iron uptake system is encoded by pColV-K30 and other ColV plasmids. It has been known to contribute to the ability of Escherichia coli to cause pyelonephritis and cystitis. In the present study an attempt was made to evaluate the contribution of an incomplete set of genes for aerobactin synthesis to the virulence of Escherichia coli HB101. Escherichia coli HB101 was transformed with a recombinant plasmid pJHCV-12 (Tetr and Kanr) carrying aerobactin genes (complete first two genes, iucA and iucB and part of the third gene iucC) from pColV-K30. Both HB101 and a transformant H10 grew equally well when applied to a Vero cell line. These strains were tested for their ability to invade and kill Vero cells in monolayers. Light micrographs showed cell damage by the transformant carrying pJHCV-12 plasmid and this cytotoxic effect correlated with the amount of lactate dehydrogenase (LDH) released. In contrast, strain HB101 and HB101 containing parent vector pVK102 did not produce any cytotoxic effects. When the ability of these strains to produce ascending pyelonephritis in a mouse model was compared, the transformant established itself better in renal tissue than the control strain HB101, when assessed 2h, 4 h and 5 days post-infection.
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PMID:Introduction of plasmid carrying an incomplete set of genes for aerobactin production alters virulence of Escherichia coli HB101. 771 24

Regarding the mechanisms of renal scarring in pyelonephritis, several hypotheses have been put forward, among which oxidative stress is prominent. The present study investigated the possible protective effect of melatonin treatment against Escherichia coli-induced oxidative injury and scarring in renal tissue. For this purpose, 0.1 mL E. coli (ATCC 25922; 10(10) colony-forming units/mL) or saline was injected directly into the renal parenchyma of Wistar rats. Pyelonephritic rats were treated with either saline or melatonin (10 mg/kg) intraperitoneally. Twenty-four hours or 1 wk after E. Coli injection, rats were decapitated and trunk blood samples were collected for BUN, creatinine, tumor necrosis factor-alpha (TNF-alpha) and lactate dehydrogenase (LDH) determination. In kidney samples, histological analysis was performed, and malondialdehyde (MDA), glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen contents were measured. Formation of reactive oxygen species was monitored using a chemiluminescence (CL) technique. Escherichia Coli inoculation caused a significant reduction in renal GSH levels, which was accompanied by significant increases in MDA levels, MPO activity, CL levels and collagen content of the renal tissues (P < 0.05-0.001). Similarly, serum TNF-alpha and, LDH, BUN and creatinine levels were elevated in the pyelonephritic rats when compared with control animals. Melatonin treatment reversed all these biochemical indices, as well as histopathological alterations induced by acute pyelonephritis. The protective effects of melatonin can be ascribed to its ability to inhibit neutrophil infiltration, to balance the oxidant-antioxidant status, and to regulate the generation of inflammatory mediators, suggesting a future role for melatonin in the treatment of acute pyelonephritis.
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PMID:Melatonin prevents neutrophil-mediated oxidative injury in Escherichia coli-induced pyelonephritis in rats. 1694 82

Urinary tract infections may induce severe inflammation, transient impairment in renal function and scar formation, ranging in severity from acute symptomatic pyelonephritis to chronic pyelonephritis, which have a potential to lead to renal failure and death. The present study aimed to investigate the possible protective effect of montelukast, a selective antagonist of cysteinyl leukotriene receptor 1 (leukotriene CysLT1), against Escherichia coli-induced oxidative injury and scarring in renal tissue. Wistar rats were injected 0.1 ml of E. coli (ATCC 25922 10(10) cfu/ml) or saline into left renal medullae. Six rats were assigned as the sham group and were given 0.1 ml 0.9% NaCl. Pyelonephritic rats were treated with either saline or montelukast immediately after surgery and at daily intervals. Twenty-four hours or one week after E. coli injection, rats were decapitated and the kidney samples were taken for histological examination or determination of renal malondialdehyde, glutathione (GSH) levels, myeloperoxidase (MPO) activity, and collagen contents. Formation of reactive oxygen species in renal tissue samples was monitored by using chemiluminescence technique with luminol and lucigenin probes. Creatinine, blood urea nitrogen and lactate dehydrogenase (LDH) activity were measured in the serum samples. E. coli inoculation caused significant increases in malondialdehyde level, MPO activity, chemiluminescence levels and collagen content, while GSH level was decreased in the renal tissues (p<0.05-0.001). On the other hand, serum TNF-alpha, LDH, blood urea nitrogen and serum creatinine levels were elevated in the pyelonephritic rats as compared to control group. Leukotriene CysLT1 receptor antagonist montelukast reversed all these biochemical indices, as well as histopathological alterations, that were induced by acute pyelonephritis. It seems likely that montelukast protects kidney tissue by inhibiting neutrophil infiltration, balancing oxidant-antioxidant status, and regulating the generation of inflammatory mediators suggesting a future role for leukotriene CysLT1 receptor antagonists in the treatment of pyelonephritis.
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PMID:Oxidative renal damage in pyelonephritic rats is ameliorated by montelukast, a selective leukotriene CysLT1 receptor antagonist. 1717 92

The activity of lactate dehydrogenase (LDG), malate dehydrogenase (MDG), concentrations of lactic acid and lipid peroxidation (LPO) products in the blood serum and urine were estimated in 119 patients with acute pyelonephritis (70 cases of serous and 49 cases of purulent). The results of the study showed that acute pyelonephritis patients have activated anaerobic glycolysis. Ischemia leads to accumulation of lactic acid, activation of LPO. Significant differences between the groups of patients reflect strong influence of renaltissue ischemia on activity of systemic metabolic processes and metabolism in renal parenchyma. Standard infusion therapy was given to 30 patients with acute purulent pyelonephritis. 19 patients received solution of succinic acid reamberin. On day 4 of reamberin therapy plasma and urine activity of LDG and MDG attenuated, lactic acid concentration decreased, content of dienic conjugates was close to normal. Patients on reamberin treatment exhibited earlier relief of endogenic intoxication and improvement of blood count. Thus, succinic acid drugs reduce renal ischemia, improve a course of postoperative period in patients with acute purulent pyelonephritis.
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PMID:[Succinic acid infusions for correction of renal ischemia in patients with acute purulent pyelonephritis]. 1864 57

The objective of the study is to examine the assumption that a process of hemolysis plays a role in anemia of acute infection in children. The study was comprised of febrile pediatric patients, who had a positive blood or urine culture. Complete blood count measures were compared between hospitalization and prehospitalization or posthospitalization values. Children admitted to the hospital for elective surgical procedures served as controls. Blood parameters of hemolysis were investigated in some of the patients. Of the 70 patients studied, 49 (70%) were diagnosed with pyelonephritis and 21 (30%) had bacteremia. Mean (+/-SD) hemoglobin (Hgb) on hospital admission was 10.9+/-1.27 g/L as compared with 12.1+/-1.03 g/L of the controls, P<0.0001. Compared with normal-for-age Hgb values as a standard, 42 (60%) cases were identified as anemic. Compared with hospitalization values, Hgb and hematocrit (Hct) were significantly higher in prehospitalization or posthospitalization, whereas WBC values were significantly lower. All parameters of hemolysis, namely reticulocytes, bilirubin, lactate dehydrogenase (LDH), and haptoglobin, were normal. Bacteremia and pyelonephritis are accompanied by a significant drop in Hgb level. There is no evidence of hemolytic anemia in these patients.
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PMID:Anemia of acute infection in hospitalized children-no evidence of hemolysis. 1975 24

Urinary lactic dehydrogenase, alkaline phosphatase and lysozyme determinations were performed on 70 patients with various kidney diseases such as acute and chronic pyelonephritis, acute and chronic glomerulonephritis, idiopathic nephrotic syndrome, diabetic nephropathy, nephrosclerosis, lupus nephritis, analgesic nephropathy, gouty nephropathy, renal tuberculosis, renal lithiasis, and polycystic kidneys. Fifty-three of these patients had elevated levels of urinary lactic dehydrogenase, but this was not of any value in determining the etiology of the renal disease. Similarly, the elevation of alkaline phosphatase in 23 of the 70 had no etiological significance. Neither of these determinations was significant in indicating the degree of renal functional impairment or prognosis. The urinary lysozyme was significantly elevated in only five of the 70 patients and was of no value in indicating the presence or the seriousness of the underlying renal disease.
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PMID:Urinary lactic dehydrogenase, alkaline phosphatase and lysozyme studies in renal disease. 2032 65

Urinary tract infections may induce severe inflammation, transient impairment in renal function and scar formation, ranging in severity from acute symptomatic pyelonephritis to chronic pyelonephritis, and have the potential to lead to renal failure and death. In the present study, the relationship between production of tumour necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), neutrophil recruitment, bacterial colonization and tissue damage was investigated using a mouse model of acute ascending pyelonephritis induced with planktonic and biofilm cells of Pseudomonas aeruginosa. Neutrophil influx correlated with rise in TNF-alpha and IL-1beta, indicating an association between these cytokines and neutrophil infiltration. However, biofilm cells of P aeruginosa induced higher levels of TNF-alpha and IL-1beta leading to higher neutrophil infiltration causing tissue damage, assessed in terms of malondialdehyde, lactate dehydrogenase and glutathione content, which may have contributed to bacterial persistence compared with their planktonic counterparts. The results of the present investigation suggest that exaggerated cytokine production during P aeruginosa-induced pyelonephritis causes tissue damage operative through neutrophil recruitment leading to bacterial persistence in host tissues. The findings of the present study may be relevant for the better understanding of disease pathophysiology and for the future developments of preventive strategies against pyelonephritis based on anti-inflammatory intervention.
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PMID:Evaluation of tumour necrosis factor-alpha and interleukin-1beta in an experimental pyelonephritis model induced with planktonic and biofilms cells of Pseudomonas aeruginosa. 2080 54


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