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

The ultrastructure of the ureter in the nonhuman primate is described. In experimentally produced chronic pyelonephritis, the ureter shows extensive ultrastructural changes throughout the wall. The epithelium has cellular damage progressing from the basal cells to the superficial cells. There is an invasion of leukocytes into the intercellular spaces at all levels. The connective tissue layer seems thickened with an increase in active fibroblasts, leukocytes, collagen, and elastic fibers. There are various stages of damage in the smooth muscle layer and an abnormal increase of connective tissues between bundles and smooth muscle cells. The interdigitating nexuses seem stretched and altered. The changes are similar to those seen in ureteral obstruction and are assumed to be reparative.
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PMID:Chronic pyelonephritis. Electron microscopic study. III. The ureter. 11 82

To determine the role of hypoxia in the evolution of tubular damage in acute pyelonephritis (PN), the blockage of blood flow and injury to peritubular capillaries and tubules were studied morphologically in hematogenous acute E. coli PN of rats. Renal microvessels were stained by in situ intraarterial administration of Alcian blue. The non-occurrence of staining indicated blockage of perfusion. Injury to cortical capillaries and tubules was examined by electron microscope. In areas of inflammation, binding of Alcian blue did not occur in capillaries plugged by polymorphonuclear leukocytes (PMNL-s) and in the majority of glomerules. Ultrastructurally, severe injury to capillaries was found around endothelium-adhered, degranulated PMNL-s containing bacteria: the vessel wall was fragmented, the capillary basement membrane perivascular connective tissue matrix and collagen fibrils had disappeared, and fibrin had deposited intra- and extravascularly. Tubular changes varied from swelling to ischemic necrosis. The observations suggest that tubular damage was related to hypoxia due to preglomerular and capillary perfusion defects, and that PMNL-s injure capillaries via lysosomal enzymes discharged into the capillary fluid during the phagocytosis of bacteria. Since leukocyte plugs in capillaries, PMNL-dependent lytic injury to capillaries and mild ischemic tubular changes, but not ischemic necrosis, have been found in human acute PN previously, the preglomerular vasospasm may cause the tubular necrosis in experimental acute PN.
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PMID:Hypoxic damage to tubules due to blockage of perfusion in acute hematogenous E. coli pyelonephritis of rats. 181 80

Overall 162 patients with chronic pyelonephritis (CPN) were examined. The control group was made up of 47 practically healthy subjects. Conventional research methods were employed in the diagnosis of CPN. The status of the main substance of connective tissues and collagen structures was estimated by measurements of the content of glycosaminoglycans, hydroxyproline and their fractions in the blood serum and urine. Cellular and humoral immunity was also investigated. It has been established that in the presence of a clinical remission, the lack of the urinary syndrome, bacteriuria and acute-phase inflammation tests, glycoaminoglycanuria, hyperhexosemia, abnormal metabolism of collagen structures, and high concentration of IgA and IgM remained unchanged. The data obtained indicate that in patients with CPN, the changes of connective tissue metabolism, cellular and humoral immunity are of unidirectional nature, which can serve an objective enough criterion for the efficacy and duration of the treatment.
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PMID:[The clinical significance of connective tissue metabolism and of cellular and humoral factors in chronic pyelonephritis]. 194 45

Acute inflammatory cell-capillary endothelial cell interactions, related to injury and repair, were investigated light and electron microscopically in acute human bacterial pyelonephritis. In inflammatory infiltrate-adjacent microvessels, the small capillaries were completely occluded by leukocyte plugs and the large capillaries were densely filled with acute inflammatory cells adhering to the endothelium. Severe damage to small and large capillaries was observed around endothelium adherent, degranulated neutrophil granulocytes containing phagocytosed bacteria. There were spaces in the endothelium, degradation of the vascular basement membrane, of the perivascular interstitial matrix and of collagen fibrils, with fibrin deposition and vessel wall fragmentation. In the small capillaries relatively distant from the interstitial infiltrates, emigration of leukocytes was frequently seen. Around the escaping cells the endothelial lining displayed occasional discontinuities, allowing leakage of vascular fluid into the interstitial space. Some small capillaries not related to the infiltrate were occluded by fibrin thrombi with apparent damage to the endothelial cells and disruption of the capillary wall. Various reparative changes were noticed in association with this change including capillary neovascularization. The findings confirm the existence of polymorphonuclear leukocyte-mediated injury of capillaries during the development of inflammatory responses in acute pyelonephritis.
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PMID:Microvascular injury and repair in acute human bacterial pyelonephritis. 244 17

A hospital-based case-control study of 153 multiple myeloma (MM) cases and 459 controls was conducted to evaluate the hypothesis that chronic or frequent infections or allergic and autoimmune diseases might be of higher prevalence in individuals who develop MM. Information was obtained by direct interviews of subjects. Controls were matched to cases on age, sex, race, and hospital. "Immune-stimulating conditions" included chronic infections such as pyelonephritis, urinary tract infections (UTIs), prostatitis, rheumatoid arthritis and other collagen vascular diseases, allergies, bronchitis, tuberculosis, cholecystitis, diverticulitis, and osteomyelitis. The overall odds ratio (OR) (odds of history of immune-stimulating conditions in cases versus controls) was 0.4 (95% confidence interval = 0.3-0.7) which suggested that cases had significantly less immune-stimulating conditions than did controls. The exposure rate for these conditions was high for cases (0.7) as well as for all control groups (0.8). These findings suggest that immune-stimulating conditions alone are not the causative factor in the etiology of MM, though they may play a role in the predisposed individual.
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PMID:Role of immune stimulation in the etiology of multiple myeloma: a case control study. 381 65

The use of stemmed patches and tubes from the seromuscular layer of the colon wall to replace part of the ureter has proven unreliable because of complications such as urinary leakage and invagination, fibrosis, bone formation, shrinkage and disappearance of the intestinal wall due to ischemia and necrosis, causing hydronephrosis and pyelonephritis. The use of tubes and patches of tanned and untanned collagen, implanted in order to study the ingrowth of urothelium and possibly muscle cells, resulted in fibrosis, bone formation, rejection of the material and, in the case of the tubes, complete obstruction with hydronephrosis and destruction of the kidney.
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PMID:Ureter replacement by collagen and seromuscular parts of the large bowel in dogs. 647 2

Chronic pyelonephritis was induced in young adult cats by the intravenous injection of a human or a feline strain of Escherichia coli after ligation of one ureter for 24 or 48 h. In the 3 cats infected with the feline strain, scarred kidneys from the obstructed side were removed at necropsy 3, 4 and 5 months later. Collagen was extracted from pyelonephritic and normal kidney tissue with dilute acetic acid and limited proteolysis with pepsin. Scarred kidneys gave higher yields of both acid-soluble collagen (normal = 0.57 +/- 0.12 mg per g tissue; scarred = 0.88 +/- 0.10 mg per g tissue) and pepsin-solubilized collagen (normal = 9.69 +/- 1.79 mg per g tissue; scarred = 20.02 +/- 2.84 mg per g tissue). There was no significant increase in the collagen yield from the kidneys of the 2 cats in which mild focal lesions were found 14 and 16 months after infection with the human strain of E. coli. Pepsin released collagens were separated by fractional salt precipitation and identified by agarose gel chromatography and polyacrylamide gel electrophoresis. Normal kidney was shown to contain collagen of Types I, IV and V (AB). The Type IV collagen extracted consisted of a mixture of 4 major pepsin-resistant chains of apparent molecular weights of 150 000, 115 000, 85 000 and 60 000. The collagen extracted from scarred kidneys was predominantly Type I, only trace amounts of Type IV and V components being present. These findings suggest that basement membrane collagens of the kidney are selectively degraded during the atrophy and scarring of chronic feline pyelonephritis and are preferentially replaced by interstitial Type I collagen.
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PMID:Experimental pyelonephritis in the cat: 3. Collagen alterations in renal fibrosis. 684 96

Adult male rats were subjected to pyelonephritis by direct kidney intramedullary injection of 0.1 ml saline suspension of 10(5) E. coli. Animals were killed at intervals of 4, 10, 15, 30 and 60 days. Half of each kidney and bladder were cultured in proper bacteriologic media to demonstrate the existence of infection. The other halves were submitted to light microscopy and ultrastructural studies. Immunofluorescence methods were used for the study of connective matrix components, at the initial stage of the inflammatory process (4, 10 and 15 days). Infection was documented by bacteriologic, gross and microscopic findings in all groups following inoculation, and it lasted up to two months. Following the acute inflammatory reaction, fibronectin and type III collagen were deposited in the interstitium of kidneys. Small amounts of type I collagen were found later. Type IV collagen appeared in small quantities, associated with collapse of structures containing basement membranes. Fibronectin became concentrated in re-activated foci. The subsequent scarring and associated focal renal atrophy depended upon the extension of the acute lesion.
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PMID:Dynamics of connective matrix deposition in acute experimental E. coli pyelonephritis in rats. 808 88

In the pathogenesis of glomerulonephritis, acute renal failure, pyelonephritis and other diseases of the kidneys oxygen radicals are involved. Some types of glomerulonephritis are characterized by infiltration of the glomeruli by neutrophils and monocytes which can form oxygen radicals (superoxide, hydrogen peroxide). The increased amount of cAMP in glomeruli can be due to oxygen radicals. Cyclic nucleotides modulate the inflammatory or immune response in glomerular disease and play a part in the action of local mediators of the inflammation. Oxygen radicals act as second messenger for the activation of cytokines via NF-kappaB transcription factor, they stimulate the formation of TNF-alpha, IL-1, IL-6 and influence the expression of monocyte-specific cytokines (CSF-1 and MCP-1). Radicals formed by the system myeloperoxidase--hydrogen peroxide--halogen derivatives activate proteolytic enzymes (proteinases) which break down collagen and other components of the extracellular matrix present in the basal membrane of glomeruli and in the mesangium. Oxygen radicals and proteinases can cause and amplify glomerular damage. Glucocorticoid administration leads to an increased activity of endogenous antioxidant enzymes in the glomerulus and reduced the of lipid peroxidation.
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PMID:[The role of oxygen radicals in the pathogenesis of glomerulonephritis]. 859 8

A 41-year-old male with myelomenigocele underwent a bladder auto-augmentation and endoscopic collagen injections. He has been performing self intermittent catheterization for 10 years but urinary incontinence remained unchanged. Furthermore, he suffered from recurrent pyelonephritis due to the left vesicoureteral reflux. A preoperative fluoroscopic urodynamic study showed a poorly compliant bladder with the maximal bladder capacity of 200 ml at 60 cmH2O. The left vesicoureteral reflux was observed at 10 cmH2O. The low compliant bladder was treated with the bladder autoaugmentation and the left vesicoureteral reflux was treated with the endoscopic subureteral injection of collagen 5 months after the previous operation. A fluoroscopic urodynamic study 6 months postoperatively showed the increase of the maximal bladder capacity of 300 ml at 18 cmH2O and the reflux disappeared completely. The endoscopic periurethral injections of collagen improved his persisting urinary incontinence. In patient with neurogenic bladder having a lot of clinical problems, bladder auto-augmentation is less invasive and offers many advantages over enterocystoplasy.
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PMID:[Usefulness of bladder auto-augmentation in neurogenic bladder: a case report]. 869 4


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