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

Excretory urograms of 40 patients with a clinical and laboratory diagnosis of acute pyelonephritis were reviewed. Eleven (28%) had abnormal urograms attributable to the acute disease process. Of the 11 abnormal patients, 7 had obvious urographic abnormalities, while in 4 the findings were few and subtle. The most common findings were renal enlargement, decreased density of contrast material, delayed calyceal appearance time, and dilatation of the collecting system; of these, the last two most frequently correlated with the clinically abnormal side.
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PMID:The radiological spectrum of acute pyelonephritis in adults and adolescents. 124 76

Escherichia coli is the most frequent cause of pyelonephritis. Its possible virulence factors include the ability to adhere and colonize the urinary tract, an important initiating factor in all urinary tract infections (UTIs). The importance of P fimbriae in this adhesion is stressed and the evidence for its importance in pyelonephritis is presented in epidemiologic studies of patients, as well as in animal studies. It appears that both host receptor density and the nonsecretor state is responsible for susceptibility to urinary tract infection. Vesicoureteral reflux can be responsible for ascending upper tract infection, but infection with P-fimbriated E coli may lead to ascending pyelonephritis without reflux because of the paralytic effect of lipid A on ureteral peristaltic activity. Renal ischemia leads to renal damage following infection by reperfusion damage due to the release of superoxide. Experimentally, this ischemic damage can be prevented by allopurinol, a xanthine oxidase inhibitor. The acute inflammatory response can produce renal damage because of the respiratory burst of phagocytosis, which while killing phagocytosed bacteria also damages renal tubules. An amelioration of the inflammatory response by treatment with superoxide dismutase or corticosteroids has been shown to modulate renal damage. Vaccination with P fimbriae has been shown experimentally to prevent the initiation of the disease. However, since vaccines are not clinically available, the clinical and animal studies on therapy of acute disease are stressed. Acute pyelonephritis during the first 3 years of life more often produced the renal damage that could lead to end-stage renal disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Etiology and pathophysiology of pyelonephritis. 167 Sep 5

While acute pyelonephritis is known to elicit an antibody response, it is also known that a patient who has had pyelonephritis once is susceptible to recurrent renal infection. Using our experimental model of pyelonephritis in the monkey, we tested whether antibiotic therapy of the acute disease would affect the antibody response. We found that it did, because antibiotic therapy beginning 72 h after bacterial inoculation attenuated the antibody response so that rechallenge 3 months later produced acute pyelonephritis and prolonged bacteriuria. The animals with untreated infection had an antibody response that lasted a sufficient period of time to prevent acute pyelonephritis after renal challenge. We have confirmed that antibody titers against P fimbriae are protective, and to a degree, this protective effect may be abrogated by antibiotic therapy.
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PMID:Attenuation of antibody response to acute pyelonephritis by treatment with antibiotics. 180 7

Insights into the pathogenesis of urinary tract infections warrant reflections on new therapeutic strategies. Of particular interest is the phenomenon of bacterial adherence to cells, as the adhesion of microorganisms to uroepithelial cells plays an important role in the development of the disease. In 21 women with an acute episode of lower urinary tract infection who were known of having chronic pyelonephritis, we studied the influence of a one-day (n = 7) and a seven-day treatment by administering the regular sulfamerazine/trimethoprime (Berlocombin) dose (2 X 2 tablets from the 2nd day, n = 7) or a reduced amount (2 X 1 tablet from the 2nd day, n = 7). All treatment regimes led to a disappearance of the clinical symptoms; however, in one case of the group receiving one-day treatment, dysuric complaints recurred as early as on day 3 after therapy. Only when employing the regular schedule of therapy, the controls of the urine cultures revealed sterility of the urine for all cases still on the 21st day after treatment. This treatment regimen most clearly influenced the ability of the microorganisms to adhere to the uroepithelial cells of the probands (in-vivo adherence). The one-day treatment was not able to reduce the rates of bacterial adherence to the cells. In all patients, the acute disease resulted in an increase in microorganisms coated with antibodies; on day 21 following therapy, however, the findings registered were as before onset of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Comparative studies of the effectiveness of 1-day treatment and 7-day treatment with sulfamerazine/trimethoprim (Berlocombin) of patients with urinary tract infection]. 233 Jul 31

This review summarizes recent work examining the interaction between host and parasite in recurrent urinary tract infection (UTI) and renal scarring. Virulence in uropathogenic E. coli has been defined by the severity of acute disease. Isolates from patients with acute pyelonephritic strains differ from those causing asymptomatic bacteriuria by multiple traits which contribute to virulence, and which are coexpressed in a non-random manner. The single marker most characteristic for the pyelonephritogenic clones is bacterial adherence to uroepithelial cells binding specifically to the disaccaride Gal alpha 1-4 Gal beta within the globoseries of glycolipids. The notion that the most severe consequence of acute pyelonephritis, i.e. renal scarring, was caused by the most virulent clones, was contradicted by comparison of pyelonephritic strains isolated from children with and without scarring. The virulent clones were significantly less frequent in patients with renal scarring (22%) than in patients with recurrent pyelonephritis not developing renal scars (62%). In view of the unexpected inverse association of bacterial virulence with renal scarring lack of Gal alpha 1-4 Gal beta binding capacity of E. coli strains was found to predict the risk for renal scarring among boys with first-time acute pyelonephritis. Vesicoureteric reflux (VUR) is widely accepted as a host determinant of susceptibility to pyelonephritis and renal scarring. In our study the frequency of renal scarring was 57% among girls with VUR as compared to 8% of those without. The reflux alone did however, not explain the selection of bacteria of low virulence. Individuals prone to UTI and renal scarring were found to be a genetically selected subgroup of the general population. A correlation between P1 blood group phenotype and susceptibility to UTI and between blood group non-secretor state and renal scarring was found. The mechanisms behind these relationships need to be defined. The bacterial and host parameters combined indicate that host parameters are essential for the tendency to develop renal scarring after acute pyelonephritis.
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PMID:Bacterial and host determinants of renal scarring. 265 83

On the assumption that increased urinary lysozyme concentration (;lysozymuria') indicates tubular proteinuria and therefore impaired tubular function, urinary lysozyme has been estimated in acute disorders where transient disturbances of renal function might be expected, in cases diagnosed clinically as extrarenal uraemia, and in a few examples of acute renal disease. Reversible lysozymuria occurred with hypokalaemia, postoperative ;collapse', electrolyte depletion, severe extrarenal infection, acute pyelonephritis, the nephrotic syndrome, after a few apparently uncomplicated surgical operations, and very transiently after ventricular fibrillation abolished by DC shock. There was no lysozymuria with severe uraemic heart failure, aspirin and paracetamol poisoning, or severe jaundice, nor in two cases of acute glomerulonephritis. Although lysozymuria may occasionally be useful in the clinical diagnosis of acutely disordered renal function, the results suggest that its value is limited; on the other hand, they have provided information on renal pathophysiology in acute disease.
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PMID:Lysozymuria and acute disorders of renal function. 470 97

Bacteremia develops in a subgroup of patients with acute pyelonephritis. This study examined isolates of Escherichia coli from the urine and the blood of 25 bacteremic and 67 nonbacteremic women with this acute disease. P-fimbriated strains were found in 100% of bacteremic patients without complicating factors but in only 71% of nonbacteremic patients without complications (P < .05). Non-P-fimbriated strains were only found to cause bacteremia in three patients with compromising host factors. Strains from the bacteremic group and those from the nonbacteremic group did not differ significantly in terms of hemolysin or aerobactin production or of serum resistance. The P-fimbriated strains from both groups of patients carried pap DNA sequences of the papGIA2 adhesin type; prsGJ96 homologous DNA sequences were rare. The results suggested that P fimbriae and compromising host conditions independently increase the risk for bacteremia during acute pyelonephritis.
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PMID:Virulence factors and pap genotype in Escherichia coli isolates from women with acute pyelonephritis, with or without bacteremia. 808 34

Neutrophil migration to infected mucosal sites involves a series of complex interactions with molecules in the lamina propria and at the epithelial barrier. Much attention has focussed on the vascular compartment and endothelial cells, but less is known about the molecular determinants of neutrophil behavior in the periphery. We have studied urinary tract infections (UTIs) to determine the events that initiate neutrophil recruitment and interactions of the recruited neutrophils with the mucosal barrier. Bacteria activate a chemokine response in uroepithelial cells, and the chemokine repertoire depends on the bacterial virulence factors and on the specific signaling pathways that they activate. In addition, epithelial chemokine receptor expression is enhanced. Interleukin (IL)-8 and CXCR1 direct neutrophil migration across the epithelial barrier into the lumen. Indeed, mIL-8Rh knockout mice showed impaired transepithelial neutrophil migration, with tissue accumulation of neutrophils, and these mice developed renal scarring. They had a defective antibacterial defense and developed acute pyelonephritis with bacteremia. Low CXCR1 expression was also detected in children with acute pyelonephritis. These results demonstrate that chemokines and chemokine receptors are essential to orchestrate a functional antimicrobial defense of the urinary tract mucosa. Mutational inactivation of the IL-8R caused both acute disease and chronic tissue damage.
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PMID:Neutrophil recruitment, chemokine receptors, and resistance to mucosal infection. 1140 74

Our knowledge of the molecular mechanisms of urinary tract infection (UTI) pathogenesis has advanced greatly in recent years. In this review, we provide a general background of UTI pathogenesis, followed by an update on the mechanisms of UTI susceptibility, with a particular focus on genetic variation affecting innate immunity. The innate immune response of the host is critically important in the antibacterial defence mechanisms of the urinary tract, and bacterial clearance normally proceeds without sequelae. However, slight dysfunctions in these mechanisms may result in acute disease and tissue destruction. The symptoms of acute pyelonephritis are caused by the innate immune response, and inflammation in the urinary tract decreases renal tubular function and may give rise to renal scarring, especially in paediatric patients. In contrast, in children with asymptomatic bacteriuria (ABU), bacteria persist without causing symptoms or pathology. Pathogenic agents trigger a response determined by their virulence factors, mediating adherence to the urinary tract mucosa, signalling through Toll-like receptors (TLRs) and activating the defence mechanisms. In ABU strains, such virulence factors are mostly not expressed. However, the influence of the host on UTI severity cannot be overestimated, and rapid progress is being made in clarifying host susceptibility mechanisms. For example, genetic alterations that reduce TLR4 function are associated with ABU, while polymorphisms reducing IRF3 or CXCR1 expression are associated with acute pyelonephritis and an increased risk for renal scarring. It should be plausible to "individualize" diagnosis and therapy by combining information on bacterial virulence and the host response.
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PMID:Susceptibility to acute pyelonephritis or asymptomatic bacteriuria: host-pathogen interaction in urinary tract infections. 2232 87