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

Two new strains of Serratia marcescens were constructed by the gene manipulation method from the clinical isolate US 46, which has two kinds of pili--mannose-sensitive (MS) and mannose-resistant (MR) ones--on the cell surface. After cloning the genes of the MS and MR pili, either the MS or the MR gene was transferred to the nonpiliated Escherichia coli, and MS- or MR-piliated strains were obtained. In the experimental pyelonephritis model of rats, MS- or MR-piliated bacteria were inoculated directly to the renal parenchyma, and the following results were obtained. MS-piliated rather than MR-piliated strains stimulated severe scarring of the kidney, and this scarring was suppressed by treatment with colchicine or superoxide dismutase (SOD) during an early stage of the infection. These findings suggest that MS-piliated bacteria stimulated polymorphonuclear leukocytes, which released large amounts of superoxide resulting in renal scarring. SOD was hoped to be a drug capable of preventing renal scarring, and such a result was successfully obtained.
Nephron 1990
PMID:Suitability of colchicine and superoxide dismutase for the suppression of renal scarring following an infection with bacteria showing mannose-sensitive pili. 168 29

We have investigated anemia in patients at different stages of the evolution of three chronic renal diseases: Balkan endemic nephropathy (BEN), chronic pyelonephritis (PN) and chronic glomerulonephritis (GN). A total of 88 patients with creatinine clearances from 9 to 118 ml/min and hemoglobin concentrations from 70 to 160 g/l were studied with regard to the relationship, if any, between erythropoietin production and the type and stage of nephropathy. Anemia in BEN was a particular focus of interest since it had been stated that in BEN, anemia precedes renal failure. Our data neither prove nor disprove this statement. A significant positive correlation between creatinine clearance and hemoglobin concentration was found in all three nephropathies, indicating that in the patients studied the severity of anemia increased with the impairment of renal function regardless of the underlying disease. Serum levels of immunoreactive erythropoietin were in the normal range in 54 patients, moderately increased in 20 and slightly decreased in 14. The erythropoietin level appears to be unrelated to the stage of renal failure or the type of nephropathy. The only exception was the subgroup where the patients with glomerulonephritis and normal renal function had increased serum erythropoietin levels and significantly higher parameters of red blood cell concentration than the patients from the same subgroup with tubulointerstitial nephropathies. In patients with severe renal failure and anemia, serum erythropoietin levels were inappropriately low for the degree of anemia, indicating that erythropoietin plays a role in the pathogenesis of the anemia.
Nephron 1990
PMID:Erythropoietin and anemia in the progression of Balkan endemic nephropathy and other renal diseases. 231 25

Acute renal failure developed in a 3-year-old boy with acute pyelonephritis. Renal biopsy showed acute interstitial infiltration of neutrophils and macrophages. There were also glomerulitis and capillary tuft thrombosis. He required peritoneal dialysis, but subsequently recovered renal function. Prompt antimicrobial therapy is crucial to insure a favorable outcome. Pyelonephritis is an unusual cause of acute renal failure in infants and children.
Nephron 1990
PMID:Acute renal failure due to pyelonephritis. 231 42

The urinary excretion of alpha 1-microglobulin (alpha 1M), beta 2-microglobulin (beta 2M), retinol-binding protein (RBP) and N-acetyl-beta-D-glucosaminidase (NAG) as markers of proximal tubular dysfunction was measured in various forms of urinary tract infections (UTI) and in fever due to non-renal infections. The urinary concentration of these proteins was significantly increased in acute pyelonephritis compared with acute cystitis and asymptomatic bacteriuria. Tubular proteinuria and enzymuria could also be demonstrated in subjects with fever of non-renal origin and corresponded to the findings of pyelonephritis. It is suggested that fever per se is the most likely cause of the tubular proteinuria seen in acute pyelonephritis. In localizing an acute UTI characterization of the urinary protein profile seems to have no advantage over a carefully measured body temperature. The urinary excretion of alpha 1M,beta 2M and RBP were highly correlated, while urinary NAG activity was less correlated to these low-molecular weight proteins. Fibrin degradation product D (FDP-D) was detected in the urines in 60% of the patients with acute pyelonephritis and in one third of those with acute cystitis. The estimation of FDP in urine therefore seems to be of little value in the level diagnosis of UTI.
Nephron 1985
PMID:Fever and proximal tubular function in acute pyelonephritis. 241 42

A 16-year-old female with acro-renal-ocular syndrome complicated by ventricular septal defect is described. Renal biopsy was performed for the first time in this syndrome, and the results suggested that proteinuria and renal dysfunction were caused by chronic pyelonephritis secondary to malrotation of the kidney and anomalous pelves. Chronic renal failure and hypoplasia of the optic papillae were also observed in the patient's mother, suggesting a participation of heredity in the pathogenesis of the syndrome.
Nephron 1989
PMID:Nature of renal involvement in the acro-renal-ocular syndrome. 264 60

A man was admitted with acute pyelonephritis due to Escherichia coli. Three days prior to the onset of his symptoms his wife presented with a 7-day history of cystitis due to E. coli. Before the wife developed her symptoms the couple were having vaginal intercourse every night, and this continued for the first 3 days of her symptoms. The organisms isolated from the urine of both patients were found to have the same biotype, an identical antibiogram, and the same serotype. The temporal sequence of events and the bacteriological findings strongly suggest the sexual transmission of this organism from the wife to her husband.
Nephron 1986
PMID:Sexual acquisition of urinary tract infection in a man. 353 17

Retrograde pyelonephritis was induced in inbred Fischer rat kidneys with Proteus mirabilis (1 X 10(8) organisms/ml). Sera from pyelonephritic animals sacrificed at 4 and 6 weeks contained cytotoxic antibodies to cultured syngeneic 51Cr-labeled kidney tubular cells (p less than 0.02 and p less than 0.05, respectively) which could be absorbed with plasma membranes. Immune sera from 4- and 6-week pyelonephritic animals also displayed a granular fluorescent pattern along the surface of cultured kidney tubular cells. Quick-frozen syngeneic rat kidney sections stained positively with fluorescent antibody on the intraluminal side of kidney tubular cells. The results suggest that during chronic phases of pyelonephritis, auto-antibodies to kidney tubular cells are induced.
Nephron 1985
PMID:Auto-antibody to kidney tubular cells during retrograde chronic pyelonephritis in rats. 388 65

Two inbred strains of rat have been identified that show markedly different responses to experimentally induced renal infection. Experiments involving these two strains and their F1 progeny have shown that a genetic factor either protects the host from a tissue-destructive inflammatory response (autosomal dominant gene) or potentiates lesion formation (autosomal recessive gene). The data are the first indication that genetic factors may determine the degree of renal damage in pyelonephritis.
Nephron 1985
PMID:Genetic factor(s) influence scar formation in experimental pyelonephritis. 389 46

Bone morphological parameters of renal osteodystrophy such as abundance of osteoid surface, osteoid seam width index, calcification fronts, osteoclast activity and trabecular bone volume were studied in 71 patients on maintenance hemodialysis and compared with bone densitometry, laboratory and clinical data. Increased osteoclast activity (hyperparathyroidism) was by far the most common bone morphological finding. Patients with chronic pyelonephritis or polycystic kidney disease had more than double the amount of osteoid than patients with chronic glomerulonephritis. The trabecular bone volume seemed to be increased in most patients in contrast to the cortical bone volume which was decreased, judged from bone densitometry and previously from X-ray. Despite that patients with polycystic kidney disease were older, their trabecular volume was larger than in patients with glomerulonephritis. The bone mineral content evaluated by bone densitometry was low in most patients, and more associated with bone morphological signs of osteomalacia than with secondary hyperparathyroidism. Serum phosphate (S-PO4) and serum parathyroid hormone (S-PTH) seemed to discriminate better between osteomalacia and secondary hyperparathyroidism than serum alkaline phosphatase (S-Alk. phosph.), which was elevated in both groups. Patients who had been bilaterally nephrectomized were no more abnormal than other patients, and they had lower S-Alk. phosph. The abundance of osteoclasts was found to be a predictor of future development of clinical secondary hyperparathyroidism.
Nephron 1985
PMID:Studies of bone morphology, bone densitometry and laboratory data in patients on maintenance hemodialysis treatment. 397 74

Concentration and acidification capability was tested in 41 patients with chronic pyelonephritis (PN), 14 patients with chronic glomerulonephritis (GN), 16 patients with diabetic nephropathy (DNP) and 12 healthy controls. Significant differences appeared between PN and GN, PN and DNP comparing a quotient between percent of normal osmolarity and percent of normal creatinine clearance. Similar results were obtained using a quotient creatinine clearance/ammonia excretion, which enabled the differentiation of PN from the other groups. The tubular functions of concentration and ammonia excretion in relation to creatinine are clinically useful in the differentiation of pyelonephritis from glomerular kidney diseases.
Nephron 1985
PMID:Tubular dysfunctions in the diagnostic differentiation of glomerulonephritis, pyelonephritis, and diabetic nephropathy. 397 78


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