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 medical records of 32 dogs with microscopically proven renal parenchymal disease were evaluated to characterize the associated ultrasonographic patterns and to assess the contribution of ultrasonography to the diagnosis and management in each case. Ultrasonography provided additional information on internal renal architecture in 18 dogs with radiographic evidence of structural abnormality. Ultrasonography determined the renal origin of 2 abdominal masses, defined the extent and distribution of neoplastic disease in 6 dogs, and identified kidneys not seen on survey radiographs or excretory urograms in 5 dogs because of decreased abdominal contrast or poor function. The ultrasonographic patterns were most specific for focal and multifocal or diffuse neoplasia. Ultrasonographic findings were least specific for diffuse parenchymal disease without architectural disruption such as glomerulo/interstitial nephritis, renal tubular necrosis, and nephrocalcinosis. In these cases, biopsy was recommended. Six interpretive errors were made. Four of these errors were related to the overestimation of renal pelvic and diverticular size because of confusion with medullary papilla. Two errors occurred in the diagnosis of renal lymphosarcoma, one of which was interpreted to be pyelonephritis. The other was an interpretive dilemma because of absence of hypoechoic multifocal nodules. Renal tubular necrosis was confirmed in this case.
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PMID:Ultrasonographic evaluation of renal parenchymal diseases in dogs: 32 cases (1981-1986). 331 41

Increase in renal volume and asymmetry in kidney size determined by sonography proved to be a valuable diagnostic criterion for differentiation between infections of the upper and lower urinary tract in 175 children: acute bacterial interstitial nephritis (79) and lower urinary tract infection (96). Kidney volume in acute pyelonephritis increased to an average of 175% of normal. In 71% of cases, affected kidneys showed an enlargement of at least 2 SD when compared with a group of 325 children without kidney pathology. Most impressive kidney enlargement was seen during the first year of life. In 50% of cases, acute pyelonephritis caused a bilateral increase in renal size and/or distinct volume asymmetry. Kidneys of patients with lower urinary tract infections had a mean volume of 99.68% and a physiologic volume asymmetry comparable to normal kidneys.
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PMID:Renal sonography in the differentiation of upper from lower urinary tract infection. 351 90

The diagnostic value of ultrasound kidney biometry in the diagnosis of parenchymatous kidney disease was evaluated in 277 children. Kidney enlargement of more than 140% of normal volume proved to be a sensitive criterion for differentiation of acute bacterial interstitial nephritis (pyelonephritis) and isolated lower urinary tract infection. Mean kidney volume in acute pyelonephritis was 175%. Normalization of kidney volume under antibiotic treatment required 4-6 days. Kidneys with non-bacterial nephritis and glomerulonephritis showed a 63% pathological size increase at biopsy; the kinetics of kidney volume in the acute phase of the disease paralleled the clinical course.
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PMID:[Bacterial and abacterial inflammatory kidney diseases. Diagnostic value of the sonographic determination of kidney volume]. 352 34

Analgesic nephropathy, its morphology, development and pathogenesis are described. The earliest analgesic-caused lesion is capillary sclerosis of the urinary tract mucosa. Later focal necroses can be found in the papillae surrounding the collecting ducts. Foci of necrosis progress and become confluent, resulting in complete papillary necrosis. Later renal cortical lesions develop due to retained areas of papillary necrosis. The cortical changes include chronic interstitial nephritis with cortical atrophy in the suprapapillary region as well as hypertrophy of the columnae Bertini with segmental, focal glomerulosclerosis. The analgesic-related lesions are the result of toxic damage to endothelial, tubular and interstitial cells. Analgesic-induced kidney and urinary tract changes are quite specific. Frequent complications include hypertension, pyelonephritis, hydro- or pyonephrosis and urinary tract tumors. The clinical picture is characterized by the consequences of distal tubular damage: impairment of urine concentrating capacity, acidosis, electrolyte loss. Analgesic nephropathy is an example of an absolutely preventable drug induced nephropathy. It is the most important single manifestation of the analgesic syndrome. It is recommended that prescriptions for mixed analgesics (multi-component analgesics) should be made obligatory. Monocomponent analgesics could be sold over-the-counter.
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PMID:[Analgesic nephropathy]. 355 93

Basing on the data obtained at 10433 autopsies performed from 1972 to 1981, cases of secondary kidney cirrhosis (chronic pyelonephritis, glomerulonephritis and interstitial nephritis) and renal pelvis cancer were thoroughly analysed. Analgetic nephropathy was found in 13.5% of all chronic interstitial and tubulo-interstitial inflammatory renal diseases, and in cases of bilateral lesions--in 17.2%. The conclusion was made on the basis of morphologic criteria ("chronic" papillary necroses and capillarosclerosis of renal pelvis). There was 41 patient with analgetic nephropathy, who died of chronic renal insufficiency, i.e. 10.6% out of the total number of patients deceased of the same reason for the period mentioned. In the biopsy material reviewed for the same period, that mainly consisted of cases with renal pelvis cancer, analgetic nephropathy was found in 15.7%.
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PMID:[Morphology of analgesic nephropathy and its incidence in Czechoslovakia]. 356 46

Repetitive topical applications of 2 micrograms 12-O-tetradecanoylphorbol-13-acetate (TPA) twice weekly for 37 to 52 weeks induced a sustained epidermal hyperplasia, hyperplasia of hair follicles, and increased dermal cellularity in SENCAR mice. In addition, after 52 weeks of protracted promoter treatment most animals developed generalized amyloidosis involving liver and spleen, as well as interstitial nephritis. Severe pyelonephritis and papillary necrosis were also frequently seen. Reactive lymphoid hyperplasia was also a frequent finding. Chronic administration of TPA is not an innocuous treatment affecting only the interfollicular epidermis. The general effect of the promoter on the animals was a marked decrease in their longevity, probably through impairment of the immune system.
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PMID:Effects of chronic topical application of 12-O-tetradecanoylphorbol-13-acetate on the skin and internal organs of SENCAR mice. 378 Jun 35

The case is reported of a 10-yr-old girl who developed intractable hematuria from hemorrhagic cystitis following chemotherapy for a malignant lymphoma. Following the intravesical instillation of formalin, which controlled the hematuria, she developed oliguria attributable to ureteric stenosis and fibrotic contraction of the renal pelves. Bilateral nephrostomies were constructed, but recurrent pyelonephritis and further renal pelvic obstruction developed. A series of renal biopsies and ultimately bilateral nephrectomy revealed severe, chronic interstitial nephritis, massive renal interstitial accumulation of deposits probably containing Tamm-Horsfall protein and, in the left nephrectomy specimen, a florid interstitial chronic granulomatous inflammatory reaction. Although ureterohydronephrosis has been described by others as a complication of the intravesical instillation of formalin, fibrotic contraction of the upper urinary tract and the florid interstitial nephritis with granulomata as described herein have not previously been reported. It is proposed that vesicoureteric reflux of formalin, perhaps accompanied by intrarenal reflux, caused or contributed to these pathological changes.
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PMID:Renal and urinary tract complications following the intravesical instillation of formalin. 382 22

The plasma levels of tocainide have been followed after oral administration of 600 mg p.o. to 20 patients with renal failure due to various causes, and to 8 healthy controls. The peak plasma concentrations in the patients with pyelonephritis (3.80 micrograms/ml) and interstitial nephritis (3.74 micrograms/ml) but not in those with glomerulonephritis (3.17 micrograms/ml) differed from that in healthy volunteers (3.24 micrograms/ml). The renal clearance of tocainide was well correlated with the endogenous creatinine clearance and was dependent on urine pH. No difference in renal clearance was observed between the patients groups. It is suggested that the changes in plasma levels are a consequence of decreased renal clearance. Creatinine clearance was shown to be a poor estimator of tocainide clearance, which suggests that extrarenal clearance plays an important role in the handling of the drug in the body. The findings are used to suggest a safe dosage regimen.
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PMID:Pharmacokinetics of tocainide in patients with severe renal failure. 393 83

On the basis of a specific definition a summarizing description of the inflammatory diseases of the kidney and the efferent urinary tract is given. Apart from the description of the bacteriology of the infections of the urinary tract the author particularly deals with the significance of the asymptomatic bacteriuria, the acute bacterial cystitis, the acute pyelonephritis as well as the reflux nephropathy. Besides proposals for therapy references are given to the conduction of the patients after treatment. In the description of the chronic interstitial nephritis the nephropathy by analgesics is emphasized as most common disease.
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PMID:[Inflammatory diseases of the kidney and efferent urinary tract]. 403 80

The histologic picture in the kidney in Alport syndrome varies (later lesions resemble glomerulonephritis, pyelonephritis, or interstitial nephritis), and the site of the initial renal lesion is uncertain. We have observed marked characteristic ultrastructural changes in the basement membranes of glomerular capillaries, even when few abnormalities were seen in the kidney by light microscopy. Their cause is unknown. There was no significant evidence that immune complexes, fibrin, or viruses were factors in their pathogenesis.
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PMID:The pathology of the kidney in the Alport syndrome. 447 Aug 85


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