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)

Kidneys obtained by nephrectomy from 85 patients with chronic nephropathy were examined by bacterial culture and by immunofluorescence for a content of E. coli antigen. A panel of 10 E. coli 0-antisera, representing the strains most commonly causing urinary tract infection, and antiserum against common enterobacterial antigen (CA), were used. Bacteria could be cultured from the nephrectomy specimens in 24 cases, mainly in cases of obstructive chronic pyelonephritis, analgesic nephropathy and congenital renal disease. By immunofluorescence, type-specific 0-antigen was found in whole bacteria and amorphously in macrophages, CA only in whole bacteria. Whole bacteria could be visualized in 12 cases, macrophages only in two cases. Amorphous bacterial antigen was no observed outside phagocytizing cells. On the basis of these results, it seems unlikely that progression of the renal lesions in chronic renal disease is due to persistant bacterial antigen in the absence of viable bacteria. Chronic pyelonephritis, defined as an interstitial nephritis due to the effects of bacterial infection in the renal parenchyma and pelvic mucosa, appears always to be a secondary manifestation following obstruction or primary renal disease, such as analgesic nephropathy or congenital renal disease.
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PMID:Bacteria and bacterial antigen in the kidney in human chronic renal disease. Bacteriological and immunofluorescence Studies. 34 94

Sterilized and unsterilized catheters were passed into the urinary bladders of 9 clinically normal adult male dogs once daily for 5 consecutive days, and the dogs were examined for up to 30 days to determine whether urinary tract infections developed. Two dogs that were catheterized with clean unsterilized catheters (1 clinically normal dog and 1 dog given immunosuppressant drugs) developed persistent cystitis and pyelonephritis due to infection with Proteus sp. One dog given immunosuppressant drugs developed a mixed bacterial infection (Proteus sp and Escherichia coli) that resolved without treatment between 22 and 30 days later.
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PMID:Urinary tract infection induced by intermittent urethral catheterization in dogs. 42 32

Complications are the major causes of illness and death after burning and most of them stem from the burn wound. Their origin and importance are reviewed with emphasis on problems and growing points in knowledge. Fluid leakage from the circulation into the burn is the cause of hypovolemic shock, but the underlying permeability changes in the burn are only partly understood. Other nonbacterial complications include acute cardiac failure, acute anemia, hemolytic jaundice, renal failure, encephalopathy, complex hypermetabolic effects including pseudodiabetes, gastric and duodenal ulceration, deep vein thrombosis and pulmonary embolism, pulmonary and glomerular microthrombosis, hepatic jaundice, and arterial thrombosis. Involvement of the airway in conflagrations carries special hazards like glottic edema and inhalation of irritant fumes. Nowadays, bacterial causes are dominant and these remain the main challenge. Bacterial infection and invasion of the burn are usually responsible for septicemia, bronchopneumonia, and pyelonephritis although other sources also contribute. Indirect manifestations of septicemia include paralytic ileus, acute gastric dilatation, toxic myocarditis, and some cases of renal failure. Therapeutic complications like agranulocytosis, thrombocytopenia, and colitis occur at times. High concentrations of oxygen given therapeutically can produce fatal aseptic hypoxic pneumonitis.
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PMID:A review of the complications of burns, their origin and importance for illness and death. 44 73

1. Cefuroxime (CXM) was studied for absorption and excretion in 4 pediatric patients given one shot intravenous injection of 20 approximately 25 mg/kg. The following serum levels were determined: 24.5 approximately 38.0 micrograms/ml at 30 minutes (mean 33.3 +/- 6.1 micrograms/ml), 10.0 approximately 17.0 micrograms/ml at 1 hours (mean 13.9 +/- 3.3 micrograms/ml), 3.4 approximately 7.6 micrograms/ml at 2 hours (mean 5.2 +/- 1.9 micrograms/ml, 0.7 approximately 2.1 micrograms/ml at 4 hours (mean 1.3 +/- 0.6 micrograms/ml, 0.1 approximately 0.3 microgram/ml at 6 hours (mean 0.2 +/- 0.1 microgram microgram/ml). Half-life (T 1/2) was 0.65 approximately 0.88 hour (mean 0.75 +/- 0.10 hour). Urinary levels were 1,280 approximately 7,100 micrograms/ml at 0 approximately 2 hours, 96 approximately 3,400 micrograms/ml at 2 approximately 4 hours, 68 approximately 250 micrograms/ml at 4 approximately 6 hours. Urinary recovery rate at 0 approximately 6 hours was 54.1 approximately 74.4% (mean 61.8 +/- 9.4%). 2. From the study on spinal fluid concentration in pediatric patients with Haemophilus influenzae-induced meningitis, the dose of CXM 52.2 mg/kg was given to 1 pediatric case with this disease by one shot intravenous injection. Spinal fluid levels were presumed as 9.0 micrograms/ml at 30 minutes, 6.8 micrograms/ml at 1 hour, 3.8 micrograms/ml at 2 hours and 1.2 micrograms/ml at 4 hours. 3. CXM was studied in 19 pediatric patients with bacterial infection for clinical efficacy, bacteriological effect and side effect. Clinical result was found good in 1 with purulent meningitis; excellent in 9 out of 15 with acute lobar pneumonia or acute bronchopneumonia, and good in remaining 6 cases; good in 2 with acute bronchitis; excellent in 1 with acute pyelonephritis. This represents efficacy ("excellent" plus "good") rate of 100%. Of 5 strains of H. influenzae presumed as causative organisms, 4 were disappeared and 1 was reduced. Two strains of Streptococcus pneumoniae and 1 strain of Escherichia coli were disappeared. No side effect was noted in terms of clinical symptom. Laboratory examination showed elevation of GOT and GPT in 1 case, but these elevated values returned to normal after the end of the CXM treatment.
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PMID:[Study of cefuroxime in pediatric field (author's transl)]. 51 99

Morphological diagnosis and differential diagnosis of pyelonephritis are discussed particularily considering macroscopic features. A special form with radiological significance is ncrotizing "emphysematous" pyelonephritis. Chronic non-obstructive pyelonephritis is rarer than formerly thought if strict morphological criteria are applied. It should be differentiated from nephropathy caused by analgetics. In analgesic nephropathy bilateral papillary necrosis is the earliest and most characteristic alteration. Differentiation between chronic pyelonephritis and analgesic nephropathy is possible in most cases but may be difficult if analgesic nephropathy is complicated by bacterial infection. A classification of "unilateral small kidney" is presented. Unilateral acquired "renal shrinkage" should be differentiated from congenital "unilateral hypoplasia". It remains to be discussed whether the so-called "Ask-Upmark-Kidney" is a malformation or the result of chronic pyelonephritis.
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PMID:[Pathologic features in diagnosis and differential diagnosis of pyelonephritis (author's transl)]. 62 16

Whether chronic interstitial nephritis (pyelonephritis) mainly results from kidney infection is widely debated. We studies 101 patients with interstitial nephritis, selected from 320 patients with newly diagnosed chronic renal disease, for frequency of etiological factors. Eleven had no etiologic factor(s) identified; 89 had clearcut factor(s): anatomic abnormalities 31, analgesic abuse 20, hyperuricemia 11, nephrosclerosis 10, stones 9, sickle cell disease1, tuberculosis 1, multiple causes7. Bacterial infection (present in 27%) was found only with another preceding primary cause of renal damage. Analgesic abusers frequently denied drug ingestion; 15% had urinary tract infection and 20% classical papillary necrosis. Two had family histories of analgesic abuse with nephropathy. We conclude that interstitial nephritis is a common form of chronic renal disease, is seldom idiopathic, rarely results from bacterial infection alone in adults, and frequently results from analgesic abuse in the United States.
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PMID:Chronic interstitial nephritis: etiologic factors. 111 62

The reasons for the initiation and the basic structure of the Bristol Pyelonephritis Registry have been discussed. The detailed follow-up data on those patients clinically at "renal risk" has been noted, with a demonstrably low incidence of proven bacterial infection, no radiological progression and minimal interference with pregnancy. Satisfactory and reassuring information has thus accrued for the first time in a particular group of patients with often severe recurrent symptoms.
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PMID:The Bristol Pyelonephritis Registry: 10 years on. 122 36

P-fimbriated Escherichia coli, which cause nonobstructive pyelonephritis, adhere to a specific urothelial glycolipid receptor. In either the presence or absence of reflux (in the area of turbulent urine flow) these bacteria ascend the ureter and cause a decrease in ureteral motility. Endotoxin causes peristalsis to cease, leading to ureteral dilatation and change in papillary shape, thus allowing intrarenal reflux and adherence of the bacteria to renal tubules. Bacterial infection of a refluxing ureter may cause reflux to persist. Once the bacteria reach the kidney rapid effects occur at the cellular level with activation of complement followed by granulocytic aggregation and capillary obstruction, causing renal ischemia and damage during reperfusion. In addition, during phagocytosis the respiratory burst occurs, releasing toxic oxygen molecules, which leads to renal tubular death, invasion of the interstitium, microabscess and renal scar formation, that is chronic pyelonephritis, which equates with reflux nephropathy.
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PMID:Vesicoureteral reflux and pyelonephritis in the monkey: a review. 143 97

The role of superoxide in scar formation following renal infection caused by mannose-sensitive (MS) piliated strains of bacteria was studied in the experimental pyelonephritis model using female Sprague-Dawley rats. The MS piliated strain stimulated renal scarring to a significantly greater extent than either the non-piliated or MR-piliated strain. Modulation of leukocytes by administering cyclophosphamide to induce neutropenia and colchicine to inhibit leukocyte migration was effective in preventing renal scarring. Treatment with superoxide dismutase during the early stage of infection was also effective in preventing scar formation. Finally, the production of superoxide by rat leukocytes was significantly larger following stimulation by MS piliated than either the non-piliated or MR piliated strains. These observations suggest that superoxide released from leukocytes plays a critical role in the development of renal scarring following a bacterial infection, especially by MS piliated strains.
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PMID:Role of superoxide in renal scarring following infection by mannose-sensitive piliated bacteria. 168 8

We reported the prophylactic and therapeutic effect of human granulocyte-colony stimulating factor (G-CSF) on mice with ascending pyelonephritis induced by Pseudomonas aeruginosa (G-group). In the cyclophosphamide-treated neutropenic mice, the prophylactic administration of G-CSF (2 micrograms/day/mouse) yielded a lower incidence of infection than that of saline alone. However, the therapeutic administration of G-CSF (2 micrograms/day/mouse) did not produce decreases of the rate, suggesting that this type of administration had no effect on infection. Thus, we investigated the effect of the combination therapy of G-CSF and Amikacin. In neutropenic mice, the therapeutic administration of G-CSF alone and Amikacin (20 mg/kg) alone did not produce decreases of incidence of infection. But, combination administration of these yielded a lower incidence of infection. These results suggest that synergy of bactericidal effects of neutrophils accelerated by G-CSF with Amikacin, and a combination of these have a therapeutic effect on bacterial infection in neutropenic mice.
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PMID:[Study of the effect of combination therapy of human granulocyte-colony stimulating factor (G-CSF) and amikacin on experimental pyelonephritis induced by Pseudomonas aeruginosa in neutropenic mice]. 169 97


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