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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a consecutive series of 88 cases of carcinoma of the kidney and upper urinary tract seen at one hospital, 31 had malignant urothelial tumours of the renal pelvis or ureter. Forty-two per cent of these transitional-cell carcinomas occurred in patients with renal papillary necrosis following upon prolonged and heavy analgesic ingestion. Other possible aetiological factors were heavy cigarette smoking (61% of cases), long standing urinary obstruction or infection (23%) and possible occupational exposure (6%); in only four cases (13%) was there no identifiable aetiological factor. Those cases with analgesic nephropathy were characterised by renal functional impairment, hypertension and interstitial nephritis, but there was no difference in the clinical behaviour or pathological appearances of the tumours in the two groups. The clinical and experimental evidence that certain metabolites of phenacetin are carcinogenic is reviewed.
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PMID:Analgesic abuse, renal parenchymal disease and carcinoma of the kidney or ureter. 27 65

The radiological changes of renal papillary necrosis are independent of its etiology. If total papillary necrosis (TPN) or partial papillary necrosis (PPN) is present, radiological findings are diagnostic. Whereas, if the necrotic papillae remain in situ (NIS) none of the typical radiologic features of papillary necrosis are seen. Serial radiologic studies are useful in renal papillary necrosis. Extension of papillary or medullary cavities, shrinkage of the kidney, and calcification thereby may be noted. Radiologic changes involving the ureter and bladder are those of complications such as ureteritis or development of a transitional cell carcinoma. The latter most often appears in the renal pelvis.
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PMID:Radiological changes of renal papillary necrosis. 71 72

Enzyme histochemistry was assessed in semi-thin glycolmethacrylate sections after 100 mg/kg 2-bromoethanamine (BEA) hydrobromide had been given ip to male Wistar rats to induce renal papillary necrosis. Changes in the proximal tubular marker enzymes alkaline phosphatase (Alk Phos), gamma-glutamytranspeptidase (GGT) and adenosine triphosphatase (ATPase) were not apparent before 8 hr, but there was a progressive loss up to 144 hr. The proteinaceous PAS-positive casts in the loops of Henle and the collecting ducts stained for Alk Phos and GGT (from 12 hr) and for ATPase (from 18 hr). Acid phosphatase (Acid Phos) staining was increased in the proximal tubule lysosomes from 18 hr. There was a marked increase in Alk Phos in all hyperplastic upper urothelial cells from 8 to 24 hr, and a mosaic of staining remained in the pelvis adjacent to the necrosed papilla at 144 hr. At 12 hr, there was an increase in the staining of the pelvic, ureter and bladder vascular endothelial ATPase, the intensity and area of which increased progressively from 18 hr and almost occluded the capillary lumens in the worst affected areas by 144 hr. These data show several distinct series of pathological changes after the administration of BEA. The subtle degenerative changes in the proximal tubule followed the papillary lesion, but exfoliated brush border and proximal tubular cells were important components of the protein casts in the distal nephron. Similarly, the intense Alk Phos staining in the hyperplastic regions of the upper urothelium and the increased pelvic, ureteric and bladder endothelial ATPase staining suggested they develop as a consequence of the papillary lesion.
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PMID:Enzyme histochemical changes in an acutely induced renal papillary necrosis. 197

Morphological changes were followed in semi-thin glycolmethacrylate sections, after treating male Wistar rats with a single ip dose of 2-bromoethanamine (BEA) hydrobromide (100 mg/kg) to induce renal papillary necrosis. Medullary interstitial cells had irregular nuclei at 4 hr and focal necrosis by 8 hr which spread from the papilla tip to the cortico-medullary junction from 12 hr. Increased mucopolysaccharide staining was observed in the papilla tip at 4 hr, and was lost from those regions where necrosis had developed by 48 hr. Endothelial platelet adhesion, first seen at 8 hr, was very marked at 18 hr, but affected capillaries in necrotic regions only, up to 144 hr. The absence of extravasated Monastral Blue B demonstrated the integrity of the medullary microvascular endothelia. The distal nephron showed degenerative changes at 12 hr and cell exfoliation at 18 hr. Cortical changes were confined to PAS-positive casts in the collecting duct and loop of Henle from 8 hr and dilatation of distal and proximal tubules at 8 and 72 hr, respectively. There was active repair at the junction between viable and necrotic tissue in the papilla from 24 hr with mitoses in the collecting ducts and loops of Henle. Normally the urothelium is less than 3-4 cells thick, but upper urothelial proliferation followed BEA administration. Hyperplasia was especially marked at the mouth of the ureter and in the pelvis opposite the region of necrosis (7-8 cells thick at 18 hr) and had only partially resolved by 144 hr.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:High resolution light microscopic morphological and microvascular changes in an acutely induced renal papillary necrosis. 219 75

The risk of developing renal papillary necrosis or cancer of the renal pelvis, ureter or bladder associated with consumption of either phenacetin or paracetamol was calculated from data acquired by questionnaire from 381 cases and 808 controls. The risk of renal papillary necrosis was increased nearly 20-fold by consumption of phenacetin, which also increased the risk for cancer of the renal pelvis and bladder but not for ureteric cancer. By contrast, we were unable to substantiate an increased risk from paracetamol consumption for renal papillary necrosis or any of these cancers although there was a suggestion of an association with cancer of the ureter.
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PMID:Does paracetamol cause urothelial cancer or renal papillary necrosis? 341 44

We report a case where renal papillary necrosis caused ureteral obstruction. Sloughed papillary bodies could be successfully removed from the ureter using a rigid ureteroscope.
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PMID:Ureteroscopy in the treatment of ureteral obstruction caused by papillary necrosis. 358 47

We recently experienced a case of renal papillary necrosis which we removed by endourological treatment. A 58-year-old female diabetic patient complaining of left flank pain, fever and chills was admitted to our clinic. She had no past history of analgesic abuse or atypical vasculitis. Physical examination revealed a body temperature of 38 degrees C and tenderness in the left costovertebral angle. Pyuria was noted, and urine cultures grew more than 100,000 colonies of Escherichia coli per cubic millimeter. DIP revealed a diminished renal function, hydronephrosis, distorted middle and lower calyces and filling defect in the dilated ureter. However, there was no evidence of obstruction or ureteral reflux. Retrograde pyelography confirmed distortion and irregularity of the calyces and hydronephrosis due to a shadow defect which was movable during radiographic examinations. Laboratory studies revealed anemia, leucocytosis and hyperglycemia, but no elevation of BUN. Therefore, the patient was diagnosed as renal papillary necrosis. We succeeded in its endourological removal through nephrostomy with a choledochoscope (Olympus Co.) under epidural anesthesia. After surgery, the patient made a satisfactory recovery.
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PMID:[Renal papillary necrosis cured with endourological treatment]. 372 27

To produce renal papillary necrosis experimentally by means of the Shwartzman mechanism in rabbits, E. coli endotoxin was injected into the renal pelvis unilaterally through the ureter as a preparative procedure after pretreatment by local administration of alcohol, and the same endotoxin was given again 24 hours later, but intravenously this time via the ear vein, as a provocation. Marked necrosis was produced in the renal papillae, where many intravascular fibrin thrombi were found histologically. Such papillary necrosis was largely prevented by heparin administration, and this lesion was considered to be the univisceral Shwartzman reaction occurring in the renal papillae. The lesion produced in the new experimental system of renal papillary necrosis described here has a good similarity to that of human cases in etiology, pathogenesis and morphology. The present system may therefore be a good model of human renal papillary necrosis, and should be useful for future studies.
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PMID:A study on renal papillary necrosis experimentally produced by the Shwartzman mechanism in rabbits. 637 24

The patient was a 66-year-old female who had been commonly using an analgesic for rheumatism from age 40. She visited our hospital with the complaints of fever up and right flank pain. Right hydronephrosis and renal failure were pointed out, and she was referred to the urologic clinic. Retrograde pyelography showed a clubbed upper calyx and filling defect in the lower ureter. A ureter stent was positioned for drainage in the right ureter. Then her general state improved. Three weeks later, retrograde pyelography was performed again. Two filling defects were detected in the upper ureter. Since the obstruction persisted we observed the ureter by ureteroscopy. Two specimens black-brown in color and 8 mm in diameter were observed through the ureteroscope and were removed with a basket catheter. Histological examination of the specimens revealed necrotic transepithelial tissues. It was assumed that the tissues were derived from necrotic renal papilla. Four months later, a similar episode was observed in the left upper urinary tract. The same procedures were performed to manage the patient. In this case, drainage using a ureter stent was effective and conservative therapy was possible. This is the first reported case of renal papillary necrosis managed by transurethral procedures in Japan.
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PMID:[Renal papillary necrosis managed by transurethral procedures: a case report]. 1289 30

Renal papillary necrosis is not a pathologic entity but rather a descriptive term for a condition--necrosis of the renal papillae--that has various possible causes. The renal medulla and papillae are vulnerable to ischemic necrosis because of the peculiar arrangement of their blood supply and the hypertonic environment. The etiology of renal papillary necrosis includes diabetes, analgesic abuse or overuse, sickle cell disease, pyelonephritis, renal vein thrombosis, tuberculosis, and obstructive uropathy. Renal papillary necrosis has been diagnosed with the use of intravenous urography and ultrasonography, but contrast material-enhanced computed tomography (CT) may better depict a full range of typical features, including contrast material-filled clefts in the renal medulla, nonenhanced lesions surrounded by rings of excreted contrast material, and hyperattenuated medullary calcifications. In the presence of papillary sloughing, CT may depict hydronephrosis and filling defects in the renal pelvis or ureter, which also may contain calcifications. During healing, the epithelialized papillary tip appears blunted. Shrinkage of the kidney, a common sequela, also may be detected at CT. Multi-detector row CT depicts these and other features more clearly and directly than single-detector row CT, given the advantages of thinner sections and multiplanar reformation, and it may help identify the condition at an earlier stage, when effective treatment can reverse the ischemic process. Familiarity with the CT features of the condition therefore is useful for its successful diagnosis and management.
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PMID:Renal papillary necrosis: review and comparison of findings at multi-detector row CT and intravenous urography. 1710 53


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