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

Study of case-notes and autopsy reports of patients with renal disease suggests that analgesic nephropathy is responsible for at least 12 per cent of cases of chronic renal failure, Between 1970 and 1975 eight new cases of analgesic nephropathy were seen annually in a population of three-quarters of a million. This is equivalent to an incidence of 490 new cases per year in England and Wales. Fifty-five patients with analgesic nephropathy were followed from one to 84 months for a total of 190 patient years. Changes in renal function were correlated with bacteriuria, hypertension and analgesic consumption. One-third of the cases had been misdiagnosed and analgesic abuse was only revealed by thorough examination of case-notes and autopsy records, together with careful questioning of patients and relatives. A number of cases had been classified as chronic pyelonephritis. The calculated survival rate at five years was 44 per cent. Mortality was related to the level of analgesic consumption and the degree of renal failure at the time of diagnosis. The prognosis was poor if serum creatinine at presentation was greater than 400 mumol/l. There was no significant correlation between deterioration in renal function and bacteriuria or hypertension. Forty-two per cent of the patients were taking analgesics for arthritis; 27 per cent had rheumatoid arthritis. Most had been taking large quantities of analgesic mixtures containing phenacetin. Renal papillary necrosis was present in only 26 per cent on intravenous urography but was found in all those examined at autopsy. Twenty thousand, two hundred and twenty-nine autopsy reports were examined for the presence of renal disease. Renal papillary necrosis was found in 0.41 per cent, and could be attributed to analgesic nephropathy in 24 per cent. In patients under 65 years of age analgesic nephropathy appeared to be a more frequent cause of death than chronic pyelonephritis. The report indicates the need for careful enquiry about analgesic consumption in all patients with renal disease, and emphasizes the importance of early diagnosis and cessation of analgesics in suspected cases of analgesic nephropathy.
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PMID:Analgesic nephropathy: an important cause of chronic renal failure. 67 50

Diabetes mellitus is a prevalent disorder, well controlled in many persons with prolongation of life. Several radiologic manifestations are sufficiently specific to suggest a diagnosis in the unidentified patient, but even more important is an awareness of the sometimes life-threatening complications of diabetes which can be diagnosed from uroradiologic studies. We review the following urinary tract manifestations and complications of diabetes: pyelonephritis, perinephric abscess, renal papillary necrosis, emphysematous pyelonephritis, emphysematous cystitis, fungus infections, calcification of the vas deferens, seminal vesicle, and intrarenal branches of the renal artery, neuropathic bladder, and renal failure.
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PMID:Uroradiology of diabetes mellitus. 97 1

In studies primarily designed to evaluate the effectiveness of chitosan as a treatment for cyclophosphamide-induced hemorrhagic cystitis in the rat, renal papillary necrosis and pyelonephritis were observed. Cyclophosphamide alone produced relatively mild renal changes. The combination of cyclophosphamide and intravesical instillation of acetic acid induced renal papillary necrosis (38 to 83% incidence) along with pyelonephritis, hydroureter and hydronephrosis. Chitosan, instilled in place of acetic acid, partially inhibited the induction of renal papillary necrosis. It appears that the presence of vesico-ureteral reflux with or without associated hydroureter and hydronephrosis is a prerequisite for cyclophosphamide-induced renal damage.
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PMID:The effect of cyclophosphamide administration on the kidney of the rat. 148 76

Groups of 3-week-old male and female Fischer 344 rats were administered 0.5% ethoxyquin-containing diet for varying periods of time, ranging from 4 weeks up to 18 months, to assess renal histopathology. The primary lesion observed was renal papillary necrosis in the male rat, commencing as interstitial degeneration of the papillary tip by 4 weeks exposure, and reaching a complete form of papillary necrosis by 24 weeks. The papillary necrosis in male rats was consistently accompanied by active pyelonephritis affecting the cortex, and urothelial hyperplasia in the renal pelvis. A marked sex difference was evident in that female rats developed papillary change at a later stage than males and the lesion never progressed beyond interstitial degeneration. A further sex difference associated with ethoxyquin treatment was the increasing cellular accumulation of lipofuscin-related pigment involving proximal tubules in female rats. Spontaneous chronic progressive nephropathy (CPN) was exacerbated by ethoxyquin in both males and females, but more so in the former. Proximal tubule hyperplasia was most frequently observed in ethoxyquin-treated males at the later sampling times. In all cases, such proliferative lesions were associated either with pyelonephritis or with the most advanced stages of CPN. Contrary to a previous report, there was no evidence that ethoxyquin directly induced preneoplastic renal tubule hyperplasia.
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PMID:Sequential study of the chronic nephrotoxicity induced by dietary administration of ethoxyquin in Fischer 344 rats. 160 Dec 28

We report a case of biopsy-proved acute pyelonephritis which caused acute renal failure. Despite appropriate antibiotic therapy, recovery of renal function was slow and incomplete. Renal papillary necrosis was an apparent complication, which the patient may have been predisposed to by alcoholism. Although rare, acute pyelonephritis is an important consideration in the differential diagnosis of acute renal failure because of the need for specific therapy.
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PMID:Acute renal failure due to acute pyelonephritis. 196 73

An enhanced frequency and morbidity of urinary tract infections (UTI) have been observed in association with alcoholism and liver disease. The causes of these phenomena may relate, in part, to the defects in humoral and cellular immune mechanisms that occur in alcoholism. Urinary catheterization is the most common cause of UTI in hospitalized alcoholics. The severity of the sequelae of UTI in alcoholism is demonstrated by the unusually frequent occurrence of renal papillary necrosis (RPN) in conjunction with pyelonephritis in these patients. Indeed, in over 90% of the reported cases of RPN occurring with alcoholism or liver disease, pyelonephritis has been a contributing factor. The proclivity to medullary ischemia and RPN in this patient group may be, at least in part, a result of interstitial renal edema secondary both to infection and the effect of ethanol per se and to renal arterial vasoconstriction that occurs in cirrhosis. The frequency with which death due to sepsis or renal failure occurs in association with UTI in alcoholics obliges the physician to exercise caution in the prevention and treatment of UTI in these patients.
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PMID:Urinary tract infections and renal papillary necrosis in alcoholism. 370 22

There are many causes of interstitial nephritis other than pyelonephritis. The term interstitial nephritis does not connote a single etiologic or pathogenetic mechanism; it rather arbitrarily places together a wider variety of renal diseases that have a predilection for early and major involvement of the renal interstitium. The prototype of acute interstitial nephritis is acute pyelonephritis. In addition, there is a drug-related acute interstitial disease that is probably of immunological nature and usually reverses with discontinuance of the offending drug. Chronic interstitial nephritis includes many diverse illnesses. Nonobstructive pyelonephritis occurs but its prevalence is debated. Analgesic abuse nephropathy is not rare and is potentially reversible. Papillary necrosis has many causes and a wide spectrum of clinical presentations. Heavy metals, such as lead, cause interstitial nephritis. Balkan nephropathy occurs in an endemic area and although not bacterial in origin is of unknown cause.
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PMID:Interstitial nephritis. 700 50

At Asama General Hospital, we experienced six cases of urosepsis with septic shock during a period of five years between 1989 and 1993. All six patients, whose average age was 74 years old, recovered. In four patients, the condition was caused by obstructive uropathy. The remaining two cases were caused by renal inflammatory disease, which was complicated by diabetes mellitus. One of them was renal abscess with renal papillary necrosis, and the other was emphysematous pyelonephritis. The patients, who exhibited symptoms such as gram-negative bacteremia, severe hypotension, tachycardia, decrease of urine volume and mental disturbance, were diagnosed with urosepsis with septic shock. In all cases, symptoms such as a high fever of over 39 degrees C, hypoxemia and thrombocytopenia were observed. Renal dysfunction was found in 67%, and both liver dysfunction and disseminated intravascular coagulation (DIC) were found in 50% of the cases. Since no patients suffered from adult respiratory distress syndrome, a high survival rate was apparent. Anti-shock therapy and anti-coagulation therapy were ineffective for the patients who had septic shock due to urinary tract obstruction. Urinary tract drainage was required to treat the latter patients. Nephrectomy could not be avoided in renal parenchymatous inflammatory disease. In the future, what might be essential in therapeutics against urosepsis with septic shock, particularly to avoid nephrectomy, are the treatments such as immunotherapy against endotoxins and their mediators, and hemoperfusion for the removal of endotoxins.
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PMID:[Clinical study on 6 cases of urosepsis associated with septic shock]. 989 24

The authors present a case of a young diabetic patient with acute symptoms of pyelonephritis. The specific and permanent antibiotic treatment was ineffective and septic condition developed complicated by renal papillary necrosis. Because of the strong flank pain extensive examinations were done with negative result. The patient's condition was improving only slowly and there was need for treatment after her discharge as well. Long-term antibiotic treatment is an effective therapy to cure this previously deadly complication. Special attention should be given to diabetic patients because of frequent urinary tract infection and increased risk of renal damage among them.
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PMID:[Renal papillary necrosis in a diabetic patient]. 1132 20

Phenylbutazone is a nonsteroidal anti-inflammatory drug. NTP Toxicology and Carcinogenesis studies were conducted by administering phenylbutazone (greater than 99% pure) in corn oil by gavage to groups of F344/N rats and B6C3F1 mice of each sex for 19 days, 13 weeks, or 2 years. Genetic toxicology studies were performed with Salmonella typhimurium, mouse L5178Y lymphoma cells, and Chinese hamster ovary (CHO) cells. Nineteen-Day Studies: The deaths of 3/5 male and 4/5 female rats that received 600 mg/kg and of 2/5 females that received 300 mg/kg were considered to be chemically related. The final mean body weight of rats that received 300 or 600 mg/kg was 14%-15% or 46% lower than that of vehicle controls. No compound-related deaths occurred in mice (doses up to 600 mg/kg). The final mean body weights of dosed and vehicle control mice were similar. Thirteen-Week Studies: Most rats that received 300 mg/kg and 1/10 male and 2/10 female rats that received 200 mg/kg died early. The final mean body weight of male rats at 300 mg/kg was 31% lower than that of the vehicle controls. The liver weight to body weight ratios were increased in the 200 and 300 mg/kg group of rats. Compound-related lesions occurred mainly in the kidney and included papillary necrosis, papillary edema, and multifocal mineralization. Five of 10 male mice and 4/10 female mice that received 600 mg/kg died early. No other compound-related deaths occurred in mice. Final mean body weights of dosed and vehicle control mice were comparable. The liver weight to body weight ratios were increased for mice at 300 and 600 mg/kg. No compound-related histopathologic effects were observed in mice. Body Weight and Survival in the Two-Year Studies: Two-year studies were conducted by administering 0, 50, or 100 mg/kg phenylbutazone in corn oil by gavage to groups of 50 rats of each sex, 5 days per week for 103 weeks. The doses given groups of 50 mice of each sex on the same schedule were 0, 150, or 300 mg/kg. Mean body weights of high dose rats were generally 6%-11% lower than those of vehicle controls. Mean body weights of mice were similar among all groups except for high dose female mice, which weighed 4%-11% less than vehicle controls. The survival of all groups was similar except for that of the low dose group of male rats, which was significantly lower than that of the vehicle controls at the end of the studies; the survival of the top dose group of female rats and the vehicle control group of female mice was low but not statistically reduced(final survival--male rats: vehicle control, 33/50; low dose, 20/50; high dose, 27/50; female rats: 31/50; 35/50; 22/50; male mice: 36/50; 40/50; female mice: 22/50; 29/50; 32/50). Nonneoplastic and Neoplastic Effects in the Two-Year Studies: Mild pyelonephritis, renal papillary necrosis, and mineralization of the renal papillae in dosed male and female rats and hyperplasia of the renal pelvis epithelium, dilatation of the renal pelvis, and renal cysts in dosed female rats were observed at increased incidences compared with those in vehicle controls. A renal tubular cell carcinoma was observed in one low dose male rat, and renal tubular adenomas were observed in three high dose male rats. A carcinoma of uncertain histogenesis was observed in one low dose female rat. Carcinomas of the renal transitional epithelium were seen in two high dose female rats. When the kidneys were step-sectioned, additional tubular cell adenomas were diagnosed in four low dose and one high dose male rats and in three low dose and one high dose female rats; none was observed in vehicle controls. Papillomas of the transitional epithelium of the urinary bladder were seen in 2/43 low dose male and 1/49 low dose female F344/N rats. The historical incidence of urinary bladder transitional cell neoplasms in male corn oil vehicle control F344/N rats is 5/2,034 (0.2%; highest observed incidence, 2/50) and 4/2,026 (0.2%; highest observed incidence, 1/45) in females. Adrenal medullary hyperplasia was observed at an increased incidence in high dose female rats (veherplasia was observed at an increased incidence in high dose female rats (vehicle control, 3/50; low dose, 6/50; high dose, 19/50). Ulcers of the forestomach were observed at increased incidences in high dose rats (male: 0/50; 5/50; 6/50; female: 2/49; 1/49; 12/49). In high dose female rats, acanthosis (4/49; 0/49; 12/49), hyperkeratosis (3/49; 0/49; 12/49), and basal cell hyperplasia (4/49; 1/49; 12/49) of the forestomach were observed at increased incidences. No neoplasms were associated with these stomach lesions. Peliosis hepatis, centrilobular cytomegaly and karyomegaly, fatty change, hepatocellular degeneration, and coagulative necrosis of the liver were observed in dosed male mice; clear cell foci were observed in five high dose male mice. The incidences of hepatocellular adenomas and adenomas or carcinomas (combined) in male mice were increased in the high dose group (adenomas or carcinomas, combined: 16/50; 14/50; 31/50). Genetic Toxicology: Phenylbutazone was not mutagenic in S. typhimurium strains TA98, TA100, TA1535, or TA1537 when tested with or without exogenous metabolic activation. Phenylbutazone produced a positive response in the mouse lymphoma assay in both the presence and absence of activation. Phenylbutazone induced chromosomal aberrations in CHO cells in the presence, but not the absence, of exogenous metabolic activation; no induction of sister chromatid exchanges was observed in CHO cells in the presence or absence of activation. Conclusions: Under the conditions of these 2-year gavage studies, there was equivocal evidence of carcinogenic activity of phenylbutazone for male F344/N rats, as shown by the occurrence of small numbers of renal tubular cell adenomas or carcinomas. There was some evidence of carcinogenic activity for female F344/N rats, as shown primarily by the occurrence of two rare transitional cell carcinomas in the top dose group; none has ever been seen in vehicle control or untreated control female rats. Tubular cell adenomas may have been associated with the administration of phenylbutazone to female rats. There was some evidence of carcinogenic activity for male B6C3F1 mice, as shown by the increased incidence of hepatocellular adenomas or carcinomas (combined). There was no evidence of carcinogenicity for female B6C3F1 mice administered phenylbutazone in corn oil by gavage at doses of 150 or 300 mg/kg. Phenylbutazone was also nephrotoxic to rats, as shown by the dose-related increase in the severity of age-related nephropathy, necrosis of the renal papilla, and mineralization of the collecting ducts in the papilla. Synonyms: 4-butyl-1,2-diphenyl-3,5-pyrazolidinedione; 3,5-dioxo-1,2-diphenyl-4-n-butylpyrazolidine Trade Names: There have been over 100 registered trade names including: Anerval; Azobutil; Bizolin 200; Butacote; Butadion; Butagesic; Butazolidin; Chembutazone; Equi Bute; Flexazone; Fenibutol; G 13,871; Pyrazolidin; Reumazol; Robizon-V; Uzone
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PMID:NTP Toxicology and Carcinogenesis Studies of Phenylbutazone (CAS No. 50-33-9) in F344/N Rats and B6C3F1 Mice (Gavage Studies). 1269 37


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