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)

Although there is a marked variability in the development of renal lesions among individual animal models of schistosomal infections, much has been learned about the mechanisms leading to renal injury. The lesions in S. mansoni and S. japonicum infections correspond quite closely to the immune complex type of lesions, with complement involvement. The main antigens involved seem to be polysacharides of worm-gut origin, but participation of other antigens (including soluble egg antigens) cannot be excluded. Many observations testify to the localization of immune complexes, preformed in circulation, but the possibility that antigens, filtered through glomeruli, deposit incapillary walls first and bind with corresponding antibodies later on should be considered also. Deoxyribonucleic acids also may play a role in the pathogenesis. The perpetuation of the lesions is probably due to constant supply of antigens. In some models, renal pathology was related to the dose of infection, but in others there was no relation to worm burden. Renal pathology in S. haematobium infections is different, being related to the lower urinary tract, with obstructive lesions causing pyelonephritis and hydronephrosis.
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PMID:Experimental renal disease due to schistosomiasis. 11 88

The antibody amounts and avidities were analyzed in 13 patients with acute primary pyelonephritis, 11 patients with acute primary cystitis, and one with ureterocele and recurrent infections, using the ammonium sulphate precipitation (ASP) technique. The ASP titrations did not discriminate as well between pyelonephritis and cystitis as do the determinations with the indirect hemagglutination technique. The increase of antibody titer and avidity detected by the ASP method in some of the cystitis patients suggested a deeper tissue involvement in some cases resulting in antibodies demonstrable with this technique. Since control patients also showed a somewhat heterogenous antibody response regarding titer and avidity it cannot be excluded that stimulation by Escherichia coli antigens in the gut is detected by the ASP method.
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PMID:Amount and avidity of antibody to Escherichia coli O antigen measured with the ammonium sulphate precipitation technique in children with urinary tract infections. 110 May 27

It is a description of a new technique of putting a removable purse-string hemostatic stitch on the prostatic adenoma bed. Four stitches are made with a double catgut thread. The loop of the thread encircles the ureteral catheter introduced into the urethral tube. Upon tightening the purse, loose thread ends are connected with the urethral tube and fastened, the tube is tracted. Postoperative drop irrigation of the bladder with antiseptic drugs proceeds through the ureteral catheter. The purse-string suture is taken out when the catheter is removed from the urethral drainage at postoperative hour 20-24. The bladder is sutured tightly using double-row buried purse-string gut stitches. A total of 143 patients underwent surgery according to the technique of whom 70% had aggravating chronic cysto-pyelonephritis, 17.5% suffered from urolithiasis, 72% from cardiac diseases and 30% of respiratory disorders. 28% of the patients combined prostatic adenoma with chronic prostatis. 38 patients (26.5%) needed blood transfusions. Mean stay in hospital after one-stage adenomectomy made up 16.4 days at stage I-II of the disease, after delayed adenomectomy 19 days, after two-stage adenomectomy 21.8 days. Two patients died (1.37%).
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PMID:[The hemostatic pursestring suture in adenomectomy of the prostate]. 175 21

Human urinary tract infection is an infectious disease that depends on a series of host-microbial interactions. The bacteria first colonize the colon and then the periurethral/vaginal areas; they ascend to and infect first the bladder and then the kidneys. Expression of Escherichia coli P-fimbriae constitutes the strongest correlation to renal pathogenicity, but is also related to first-time cystitis in children. The role of P-fimbriae in the preceding steps in the infectious process is unknown. To examine this, we constructed, from a P-fimbriated E. coli strain with a class II G-adhesin preferentially binding to globoside, one isogenic mutant lacking the G-adhesin and another isogenic mutant in which we replaced the papG class II allele with a class III adhesin preferentially binding to the Forssman antigen. We report here the comparison of the adhesin knockout mutant (DS17-8) and the class-switch mutant (DS17-1) with the wild-type (DS17) for in vivo colonization of the gut, vagina, and bladder of cynomolgus monkeys. It was recently shown that the class II tip G-adhesin is a prerequisite for acute pyelonephritis to occur in the monkey model in the absence of other kidney-specific adhesins or obstruction of the urinary flow. Here we show that it is not required for bladder infection but gives a competitive advantage in mixed infections. In the vagina and colon, the G-adhesin gives no competitive advantage.
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PMID:The PapG-adhesin at the tip of P-fimbriae provides Escherichia coli with a competitive edge in experimental bladder infections of cynomolgus monkeys. 750 14

We report the case of a girl with Hardikar syndrome who underwent living-donor liver transplantation at 2 years of age. This disease, described in 1992, includes a constellation of abnormalities, such as cleft lip and palate, pigmentary retinopathy, and multiple tubular stenoses (e.g., bile ducts, ureters). Other system involvement is variable. Rotation anomalies of the gut and cardiac abnormalities are frequently present. Pathogenesis remains obscure. Our patient was delivered at 33 weeks of gestation by cesarean section, and was jaundiced, with low birth weight and height. On day 5 after birth, the patient underwent Ladd's surgery for intestinal malrotation. One month later, she developed pyelonephritis and urosepsis. She remained jaundiced and a liver biopsy revealed cirrhosis with regenerating nodules, portal chronic inflammation with bile duct proliferation, and lobular cholestasis. The patient underwent several corrective operations, and at 12 months of age she was diagnosed with Hardikar syndrome. She failed to thrive and had progressive cholestasis and jaundice, coagulation disorders, bilateral ureterostomies, repetitive urinary tract infections, bilateral cleft lip and palate, retinopathy, and gut malrotation. She received a liver transplant at 24 months of age from a living donor. She has had an excellent clinical outcome in liver function without further decline of growth and development.
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PMID:Hardikar syndrome: a case requiring liver transplantation. 1239 56

Bone morphogenetic protein 7 (BMP 7) is a member of the transforming growth factor (TGF) beta superfamily and is involved in regeneration, repair, and development of specific tissues, for example kidney, gut, lens, and skeleton. BMP 7 has emerged as a renotrophic factor and experimental studies have shown its protective role against fibrotic processes. Tubulointerstitial changes are present in the pyelonephritic kidney which progresses to fibrosis. Renal fibrosis may lead to significant morbidity in the form of hypertension, proteinuria, and loss of renal function. The objective of this study was to investigate BMP 7 expression in experimental acute and chronic pyelonephritis models. Eighteen Wistar rats were injected with 0.1 mL solution containing E. coli ATCC 25922 10(10) cfu mL(-1) into left renal medullae. Six rats were used as a sham group and were given 0.1 mL 0.9% NaCl. Pyelonephritic rats were sacrificed 24 h (group I, n=6), 1 week (group II, n=6), and 6 weeks (group III, n=6) after E. coli injection. Serum creatinine levels were analyzed. Renal tissues were studied histopathologically by use of hematoxylin and eosin and scored for diagnosis of pyelonephritis. BMP 7 expression was studied semiquantitatively by immunohistochemical staining. Acute (group I) and chronic (group II and group III) pyelonephritic histopathological changes were observed in experimental pyelonephritic groups. A gradual decrease in BMP 7 expression was observed in the tubulointerstitial and tubular area of the pyelonephritic kidneys, mildest in the acute pyelonephritic group and most severe in the chronic pyelonephritic 6th week group. A statistically significant difference was observed between tubulointerstitial BMP 7 expression by groups I and III (P=0.017) and by groups III and IV (P=0.000). Tubular BMP 7 expression was statistically significantly different between groups II and IV (P=0.009) and between groups III and IV (P=0.002). The data imply that BMP 7 has a major role in chronic pyelonephritis. Tubulointerstitial and tubular BMP 7 expression also had a significant negative correlation with fibrosis, tubular, atrophy, and vascular changes. Serum creatinine levels of the study group were all normal. We conclude that the decrease in renal BMP 7 expression in experimental chronic pyelonephritis is one of the factors responsible for fibrotic changes in persistent renal damage.
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PMID:Downregulation of the expression of bone morphogenetic protein 7 in experimental pyelonephritis. 1603 30

In contrast to other mucosal sites, information on migration/homing of lymphocytes activated in the human urinary tract is lacking. The expression of lymphocyte homing receptors (HR) on pathogen-specific antibody-secreting cells (ASC) originating from the urinary tract (patients with pyelonephritis, PN) was compared to that on antigen-specific ASC originating from the intestine (patients with gastroenteritis) or from a parenteral site (tetanus toxoid-immunized volunteers). In the PN group, 61% of ASC expressed the gut HR, alpha(4)beta(7,) 52% the peripheral lymph node HR, L-selectin, and 13% the skin HR, CLA. This homing profile of urinary tract-originating lymphocytes was found to differ from both of the two major vaccination routes, intestinal (less gut-targeting) or parenteral (more gut-targeting, less targeting to parenteral sites). This information on targeting of the immune response may prove useful when developing vaccines against urinary tract infection (UTI).
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PMID:Distinctive homing profile of pathogen-specific activated lymphocytes in human urinary tract infection. 1858 60

Hyponatremia is the most common electrolyte abnormality in children and underlying causes are many. It is most often caused by excessive salt loss from the gut but is also associated with severe systemic disorders in which there is actual or apparent aldosterone deficiency, such as congenital adrenal hyperplasia (CAH), which is the most common inherited disorder of aldosterone synthesis, and pseudohypoaldosteronism (PHA). Abscent aldosterone activity also leads to hyperkalemia which is characteristic for PHA and can result in life threatening arrythmias. This is a case report about a boy presenting with life threatening electrolyte disturbances in conjunction with PHA resulting from pyelonephritis and vesicoureteral reflux.
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PMID:[A case report - Severe electrolyte disturbances in an eight week old boy]. 2044 21

Numerous studies in recent years had proved pathogenetic correlation of the intestinal ecological community, not only with diseases of the gastrointestinal tract but also with diseases such as atherosclerosis and hypertension, urolithiasis and pyelonephritis, gallstones and hepatitis. In its role in maintaining homeostasis an intestinal microflora isn't inferior to any other vital organs. All this allowed to distinguish it as an independent body. Recently, as one of the most important factors for the development of dyslipidemia scientists consider breaking the functional state of the liver, as well as changes in blood lipid spectrum and disturbance of cholesterol metabolism begins at the level of the hepatocyte. However, in 2001, Carneiro de Moura proposed a theory of violation of the microbial community in the colon as one of the ways to lipid metabolism. By reducing the detoxification function of intestinal microflora associated with Microecological disorders of various origins, the first "hit" is to the host liver--is on one side. On the other--the vast majority of microorganisms are characterized by a pronounced ability of bile acids deconjugation, and therefore the increased reproduction in the ileum of bacteria (especially anaerobic, with enhanced activity against deconjugation activity to related bile acids) and the formation of toxic endogenous bile salts, acids are important prerequisites for the occurrence of violations of all functions of the liver, including the activities of Kupffer cells and the whole system of mononuclear macrophages. In this regard, the formation and progression of dyslipidemia, regardless of the target organ must be closely linked with the digestive tract by micro. Schematically it can be represented as follows: violation of microecology intestine --> accumulation of endotoxin in the gut --> entry of endotoxins in portal vein to the liver --> RES of liver cell damage --> strengthening the pathological effects of toxicants other (non-microbial) origin --> dysfunction of hepatocytes --> dislipoproteidemiya.
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PMID:[Intestinal dysbiosis and atherogenic dyslipidemia]. 2049 50

Uropathogenic Escherichia coli (UPEC) strains are a leading cause of infections in humans, but the mechanisms governing host colonization by this bacterium remain poorly understood. Previous studies have identified numerous gene clusters encoding proteins involved in sugar transport, in pathogen-specific islands. We investigated the role in fitness and virulence of the vpe operon encoding an EII complex of the phosphotransferase (PTS) system, which is found more frequently in human strains from infected urine and blood (45%) than in E. coli isolated from healthy humans (15%). We studied the role of this locus in vivo, using the UPEC E. coli strain AL511, mutants, and complemented derivatives in two experimental mouse models of infection. Mutant strains displayed attenuated virulence in a mouse model of sepsis. A role in kidney colonization was also demonstrated by coinfection experiments in a mouse model of pyelonephritis. Electron microscopy examinations showed that the vpeBC mutant produced much smaller amounts of a capsule-like surface material than the wild type, particularly when growing in human urine. Complementation of the vpeBC mutation led to an increase in the amount of exopolysaccharide, resistance to serum killing, and virulence. It was therefore clear that the loss of vpe genes was responsible for all the observed phenotypes. We also demonstrated the involvement of the vpe locus in gut colonization in the streptomycin-treated mouse model of intestinal colonization. These findings confirm that carbohydrate transport and metabolism underlie the ability of UPEC strains to colonize the host intestine and to infect various host sites.
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PMID:Role of the vpe carbohydrate permease in Escherichia coli urovirulence and fitness in vivo. 2261 42


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