kidney papillary necrosis/وذمة

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Nonsteroidal anti-inflammatory drug-associated renal papillary necrosis in a white-tailed deer (Odocoileus virginianus).

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Renal papillary necrosis was diagnosed during postmortem examination of a juvenile white-tailed deer (Odocoileus virginianus) from Oklahoma. The deer was surgically treated for a Salter Harris type II fracture of the proximal tibia of the left hind limb. The animal was administered multiple

Nephrosis and papillary necrosis after pyelonephritis.

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We present a case of nephrotic syndrome complicating acute pyelonephritis in a 45-year-old man. His first attack of acute bacterial pyelonephritis had two unusual features: transient nephrotic syndrome and chronic recurrent episodes of papillary necrosis. The former, which lasted for two weeks, was

Experimental renal papillary necrosis in the Mongolian gerbil (Meriones unguiculatus).

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Sequential light microscopic and ultrastructural examination of kidneys from male and light microscopic examination of female Mongolian gerbils given 250 mg 2-bromoethylamine hydrobromide (BEA)/kg body weight ip were performed. In addition, male Mongolian gerbils were treated with both BEA and ip

[Acute papillary necrosis in transplanted kidney].

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After a short literature survey, indicating the rarity of acute papillary necrosis in transplanted kidneys, the authors reported one of their patients, aged 32, with transplanted dead body kidney from a male, aged 30, with blood group compatibility and compatibility of two antigens in locus A. Two

[Acute papillary necrosis in the transplanted kidney].

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After a brief literature survey revealing the rarity of the papillary necrosis in transplanted kidneys, the authors report the case of one of their patients, aged 32, transplanted a corpse kidney of a 30-year old male with blood-group compatibility and with coincidence of the two antigens in locus

Celecoxib-related renal papillary necrosis.

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Selective cyclooxygenase 2 (COX-2) inhibitors are known to affect renal prostaglandins (epoprostenol and dinoprostone), which are at least in part COX-2 dependent. Consequently, adverse events including hypertension, peripheral edema, hypercalemia, hyponatremia, and acute renal failure have been

Phenylbutazone toxicosis in the horse: a clinical study.

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In a retrospective study of 269 horses that had been treated with phenylbutazone, horses receiving less than or equal to 8.8 mg/kg of body weight/day for less than or equal to 4 days or 2 to 4 mg/kg of body weight/day for up to 50 days remained clinically normal. Anorexia, depression, colic,

[Nonsteroidal antiinflammatory drugs and the kidney].

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Nonsteroidal antiinflammatory drugs (NSAIDs) have potentially important renal adverse effects. With regard to renal adverse effects there is no indication of significant differences between conventional NSAIDs and selective COX-2 inhibitors. Their nephrotoxicity has been well documented. Many of the

Renal effects of nonsteroidal anti-inflammatory drugs.

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All nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase, and consequently renal functions dependent upon prostaglandin synthesis can be affected. Fortunately, renal function in normal individuals is relatively independent of the PG system, and thus the NSAIDs don't usually produce

Examination of lesions in the urinary bladder and kidney of dogs induced by nefiracetam, a new nootropic agent.

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Toxic lesions induced by nefiracetam, a nootropic drug, in the urinary bladder and kidney were examined by repeated oral administration of 300 mg/kg/day for 1, 2, 3, 4, or 11 wk to male and female beagle dogs. Each dog was sacrificed after each treatment period, and urinalysis and serum biochemistry

[Renal tolerance of selective inhibitors of cyclooxygenase type 2].

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ANTIINFLAMMATORY DRUGS: Non-steroidal antiinflammatory drugs (NSAID) constitute one of the most widely prescribed drug classes. Selective inhibitors of cyclooxygenase type 2 (Cox-2) can have antiinflammatory and antialgesic activities without affecting prostaglandin synthesis at sites where

Renal medullary crest necrosis associated with phenylbutazone therapy in horses.

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Thirty-five cases of renal medullary crest necrosis morphologically similar to the renal papillary necrosis of analgesic nephropathy as described in man and rats are reported in horses receiving maintenance dosages of phenylbutazone. The primary lesion is a well-demarcated focal medullary necrosis

NTP Toxicology and Carcinogenesis Studies of Phenylbutazone (CAS No. 50-33-9) in F344/N Rats and B6C3F1 Mice (Gavage Studies).

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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

Cyclooxygenase-2 selective inhibitors and the kidney.

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Cyclooxygenases (COX) are the target of non-steroidal anti-inflammatory drugs (NSAIDs) which exert their therapeutic effect by blocking COX's capacity to metabolize arachidonate to a series of biologically active fatty acids, designated prostaglandins. NSAID use is associated with two major

Nonsteroidal anti-inflammatory drugs: effects on kidney function.

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Nonsteroidal anti-inflammatory drugs (NSAIDs) are capable of inducing a variety of renal function abnormalities, particularly in high-risk patients with decreased renal blood perfusion who depend on prostaglandin synthesis to maintain normal renal function. Fluid retention is the most common

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