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 frequency of chronic pyelonephritis is often overestimated. Chronic pyelonephritis is probably always a secondary disease in cases with obstructive changes in the ureters or other primary renal damage. The influence of chronic infection on the progression of renal insufficiency is still not well understood today. Underlying disease and infection should always be taken into consideration in the treatment of chronic pyelonephritis.
Infection 1979
PMID:[Chronic pyelonephritis in adults (author's transl)]. 55 Oct 81

Twelve normal volunteers in the fasting state were given 1000 mg cefaclor, and the serum and urine concentrations over 8 h and 24 h respectively were measured. The average peak serum concentration was 34.6 +/- 7.8 mg/l, this value being reached after 65.2 +/- 11.1 min; the half-life was 42.5 +/- 8.3 min. In another six volunteers the absorption of 500 mg of 'cefaclor following administration in the fasting state and after a test breakfast was studied. The peak serum concentrations after administration in the fasting state were 16.1 +/- 3.2 mg/l, and after a meal 12.5 +/- 1.9 mg/l; the areas under the curve did not differ. The low recovery rate of cefaclor in urine observed in this series of investigations could be partly explained by the inactivation of the substance in urine. Cefaclor was administered therapeutically to 23 patients, most of whom were suffering from bronchopulmonary infections and chronic pyelonephritis. The results of therapy were good in four patients, satisfactory in 13 patients and unsatisfactory in three patients. Intolerance was rare.
Infection 1979
PMID:[Pharmacokinetics of cefaclor and initial therapeutical experience (author's transl)]. 55 Oct 86

Sera from 103 fasting individuals 3 to 76 years of age and free of clinical infectious disease and sera from 183 patients with infectious disease were assayed for serum total non-esterfied fatty acids (tNEFA) and compared. Data were also separated into five groups according to age of donor: 3--7, 8--19, 20--35, 36--60, and 61--76 years. The mean group serum levels of tNEFA increased with age. Among patients with infectious diseases sixty-five were diagnosed as having hepatitis, 41 with infectious mononucleosis, 18 with cellulitis, 12 with pulmonary tuberculosis, 11 with non-pneumococcal pneumonia, 9 with pneumococcal pneumonia, 8 with pharyngitis, 6 with pyelonephritis, 6 with aseptic meningitis, 4 with Gram-negative sepsis, and 3 with encephalitis. The sera from 23 non-fasting patients with gonorrhea were also tested. The serum tNEFA levels were found to be altered, in fact depressed from normal group values, only in patients with pneumonia or tuberculosis. This depression may be related to aberrant pulmonary metabolism during pneumonia.
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PMID:Reduced level of non-esterified fatty acids in sera from patients with infectious respiratory disease. 69 41

Chronic atrophic pyelonephritis is associated with vesicoureteric reflux in infancy. Reflux disappears during childhood in 50% of cases. It is more commonly detected in infants (49%) and children (26%) with infection than in adults (4.4%). Severe reflux may persist in adults and is usually (94%) associated with scarring. Patients with end-stage renal failure due to pyelonephritis are much younger than patients with end-stage renal failure due to other causes. The incidence of reflux according to sex is equal in infancy, but after infancy both pyelonephritic scarring and reflux are far more common in females. Infection is the likely cause of progressive scarring in females. Hypertension is associated with chronic atrophic pyelonephritis. Proteinuria is the worst prognostic feature in patients with reflux nephropathy and pyelonephritic scarring. Intrarenal reflux determines the site of scarring. The role of surgical correction of vesicoureteric reflux remains uncertain, but meticulous control of infection appears to prevent progressive scarring.
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PMID:Reflux nephropathy and chronic atrophic pyelonephritis: a review. 73 56

The relationship between vesico-ureteric reflux and coarse renal scarring (atrophic pyelonephritis) has been studied in swine. Scars were observed to develop where reflux took place into the kidney substance via the renal papillae (intrarenal reflux). They were confined to these regions and were similar in size, distribution and other features peculiar to those found in the human from early childhood onwards. Intrarenal reflux was found to be related to the pressure within the urinary tract as well as to vesico-ureteric reflux. Infection was not an essential factor in scar-formation, but it appeared to intensify the scarring process. The histological findings were a progressive focal interstitial fibrosis confined to the zones of intrarenal reflux, extending from the capsule to the papillary tip, and varying in severity with pressure, time and the extent of intrarenal reflux. Nephron and tubular damage accompanied all grades of fibrosis, with the possible exception of the earliest. In many respects the histological changes closely resemble those due to obstruction, except they are focal in distribution. Added features are the early peripheral lymphocytic aggregations and interstitial fibrosis which appear to suggest that some "irritant"--possibly urine--reaches the interstitium and drains away via the lymphatic system. Many of the phenomena observed were strikingly similar to those present in children with the more severe grades of vesico-ureteric reflux. In some cases a mixture of generalized obstructive nephropathy and focal scarring developed; in others focal scarring took place with normal papillae elsewhere. The results are readily reproducible. The basic questions as to whether it is bladder pressure, or infection, or a mixture of the two which is responsible for scar-formation are discussed.
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PMID:The pathogenesis of reflux nephropathy (chronic atrophic pyelonephritis). 76 85

In these experiments, renal function in chronic active pyelonephritis was investigated and the effect of antibiotic treatment and elimination of infection on the gross pathology, histopathology and renal function in animals with chronic pyelonephritis was determined. A severe loss of urine concentrating capacity was demonstrable when the maximum urinary osmolality of a group of animals with pyelonephritis was compared with control animals. Concentrating capacity decreased sharply over the first month but further loss over an eight-month period was minimal. A compensatory increase in the glomerular filtration rate (GFR) in the control, nonchallenged, group occurred after nephrectomy but no comparable compensation in the infected group was found. Antibiotic therapy had a marked effect on the urinary concentrating capacity and the defect in concentrating ability was significantly less in the treated animals during the first 30 days after challenge. Infection again prevented a compensatory increase in the GFR of pyelonephritic animals which was not reversed by antibiotic therapy. Blood urea concentrations in treated and nontreated animals were not significantly different nor did the eradication of infection affect the gross pathologic and histopathologic changes found at autopsy.
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PMID:Experimental pyelonephritis: the effect of chronic active pyelonephritis on renal function. 78 79

Using the direct immunofluorescence technique antibody-coated bacteria were demonstrated in urine samples from 49 of 57 patients with the clinical diagnosis of chronic pyelonephritis, but were not observed in urines from 11 patients with cystitis. A correlation rate was found between the presence of antibody-coated bacteria in the urine seidment and elevated serum antibody titers in the pyelonephritis group as determined by the indirect immunofluorescence technique. Patients with elevated serum antibody titers without antibody-coated bacteria in the urine, and vice versa, were also found. Patients with cystitis did not have elevated serum antibody titers against the homologous strain isolated from the urine. The clinical diagnosis of chronic pyelonephritis could be confirmed in 86.5% of patients taking into account the presence of antibody-coated bacteria and/or elevated serum antibody titers.
Infection 1976
PMID:[Antibody binding bacteria in the urine in chronic pyelonephritis]. 78 52

Vesicoureteric reflux was found unexpectedly during routine investigations before renal transplantation in 12 patients with chronic glomerulonephritis and in one with hypertensive nephrosclerosis. They had all received long term hemodialysis treatment for nine to 106 months (mean 47 months) at the time of micturating cystourethrography (MCU). Four of the patients had previously had a normal MCU indicating that reflux developed after onset of end stage renal failure. The cause of reflux is obscure. It was not related directly to defunctioning of the urinary tract as several patients had daily urine volumes in excess of 300 ml. Infection, another potential cause, was uncommon in patients with reflux. Histology of the excised ureters showed abnormality in most cases with loss of the normal mucosal folds and submucosal cellular infiltrate and fibrosis. These changes are also unexplained. In this group of patients nephroureterectomy for reflux in anticipation of renal transplantation was associated with considerable morbidity. A minimal estimate of the incidence of reflux in chronic glomerulonephritis was 11%. We suggest that in this group and in patients with renal diseases other than chronic pyelonephritis reflux alone does not constitute sufficient indication for nephroureterectomy before transplantation to warrant the risks of major surgery.
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PMID:The significance of vesicoureteric reflux in non-pyelonephritic patients supported by long term hemodialysis. 89 Oct 48

Lipid A antibody titers were measured by the passive hemolysis test in 349 humans. In two out of 20 healthy adults and 16 out of 18 children with recurrent urinary tract infection (UTI) in the presence of anomalies anti-lipid A antibodies were present. In contrast, no titers were found in 23 newborn babies. In a group of 156 patients with acute UTI, 28% revealed positive titers, whereas in a group of 132 patients with recurrent UTI titers occurred in 81%. In a selected group of 132 patients with recurrent infections of the upper tract 59 (=96%) showed definite titers. There was no difference in the development of anti-lipid A antibodies between men and women and the height of the titers did not correlate with the clinical picture of the disease (acute or chronic). The combination of proteinuria and anti-lipid A antibodies indicates the presence of recurrent UTI or chronic pyelonephritis with about 90% accuracy. The titers are caused by immunogenically active lipid A in the body. Since lipid A has the ability to remain in the renal tissue for a long period of time and thereby to maintain the inflamatory response, long-term antimicrobial prophylaxis (six months) should be given to patients with a high risk of recurrent UTI.
Infection 1977
PMID:[Occurence, significance and clinical consequences of lipid A antibody titers in patients with urinary tract infection (author's transl)]. 91 62

Prostaglandin concentrations of cerebrospinal fluid (CSF) of 38 febrile patients (from infants up to adults) were compared with those of 19 afebrile adult control persons. CSF samples were extracted and the prostaglandins groups of the extract separated by column chromatography. Concentrations of prostaglandins of the E and F series were estimated by radioimmunoassay. In CSF of all feverish patients with meningitis, pneumonia, or pyelonephritis about 2-fold higher concentrations of prostaglandin E (PGE) were found that in those of the afebrile control persons. In contrast, concentrations of prostaglandin F (PGF) in adults and infants remained largely unchanged during fever; Solely, in 4 of the 8 babies examined, concentrations of PGF were also increased besides those of PGE. Repeated estimations of prostaglandin concentrations in CSF from the same patients showed, that concentrations of PGE, which had been elevated during fever, normalized after defervescence. The height of fever and the concentrations of PGE in CSF tended to correlate in a dose related manner. In correspondence with the results of animal experiments prostaglandins of the E series seem to act as mediators of fever during infectious diseases also in man.
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PMID:Prostaglandins as possible mediators of fever genesis in man. 101 27


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