Gene/Protein Disease Symptom Drug Enzyme Compound
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 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

"Acute tubular necrosis" (ATN) in the transplanted kidney, when properly differentiated from other causes of acute renal failure, appears to be a relatively benign condition. It has been widely assumed to be pathologically identical to ATN in the native kidney, but its histopathologic features have not been studied in detail. Because immunosuppressive therapy with cyclosporine adds an additional layer of complexity to the morphologic changes observed, in the present study we have confined our observations to patients immunosuppressed with steroids and azathioprine. Thirteen renal allograft biopsies from patients with ATN and 5 biopsies from patients with normal allograft function were compared with the previously obtained series of 57 native kidney ATN biopsies and 20 control biopsies. Both qualitative and quantitative differences between transplant and native kidney ATN were found. Compared with native kidney ATN, transplant ATN showed significantly less thinning and absence of proximal tubular brush border and less variation in size and shape of cells in individual tubular cross-sections. There were also significantly fewer casts and less dilatation of Bowman's space and a significantly greater number of polarizable crystals presumed to be oxalate in transplant ATN. In native kidney ATN the tubular injury sites were mostly characterized by desquamation of individual epithelial cells leaving areas of bare basement membrane (the "non-replacement" phenomenon). In transplant ATN, sites of tubular injury, although rare and affecting only short tubular segments, were characterized by the actual presence of identifiable necrotic tubular cells, a finding seldom seen in native kidney ATN. There also was a greater interstitial infiltrate of mononuclear inflammatory cells in transplant ATN compared to native kidney ATN. Electron microscopic studies of 9 transplant ATN biopsies showed a mild reduction in proximal tubular brush border compared with controls but this alteration was significantly less than that observed in native kidney ATN. There was no significant alteration in proximal or distal basolateral infoldings and this contrasted sharply with the marked reduction in basolateral infoldings of the plasma membrane observed in native kidney ATN. Disintegrated necrotic cells were found by electron microscopy in transplant ATN whereas these were not observed in native kidney ATN. There were significantly more cells with apoptosis (shrinkage necrosis) in transplant ATN than in native kidney ATN. There were significantly more cells with apoptosis (shrinkage necrosis) in transplant ATN than in native kidney ATN. On the other hand, there were significantly greater numbers of "non-replacement" sites in the distal tubules in native kidney ATN compared to transplant ATN.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Primary acute renal failure ("acute tubular necrosis") in the transplanted kidney: morphology and pathogenesis. 265 37

Clinical histories and renal biopsies were reviewed in 12 children with acute tubulointerstitial nephritis, which was drug related in eight, idiopathic in one, and multifactorial in three. Presentation with rashes and hypertension was most common in patients with drug-associated nephritis. Eosinophils, which were present in the majority of the renal biopsies, did not distinguish between drug-related and non-drug-related disease. The majority of the children had a good outcome irrespective of the insulting agent. Frequent tubular basement membrane breaks were identified in seven of the biopsies but were not associated with a poor outcome. Proximal tubule brush border thinning, demonstrated by periodic acid-Schiff and Tetragonolobus lotus staining, paralleled the severity of acute renal failure. Lectin and immunohistochemical techniques to identify proximal tubules (Tetragonolobus lotus), thick ascending limb of Henle (anti-Tamm-Horsfall protein antibodies), and collecting ducts (Arachis hypogaea) allowed better delineation of sites of inflammation and injury, showed collecting tubules to be involved in all cases, and demonstrated that small atrophic tubules were able to maintain the ability to stain with the appropriate lectin/antibody. It is proposed that studies using these techniques may better identify the nephron sites involved in a variety of renal diseases involving tubular segments.
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PMID:Acute tubulointerstitial nephritis in children: clinical, morphologic, and lectin studies. A report of the Southwest Pediatric Nephrology Study Group. 268 4

Fifteen percutaneous renal biopsies from patients with acute renal failure due to acute interstitial nephritis (AIN), in almost all cases due to drugs, were studied by electron microscopy. Differential counting of interstitial cells showed an average of 69% lymphocytes (small and large) and 11% macrophages. Plasma cells and eosinophils were comparatively rare. The infiltrate resembled that of acute rejection, suggesting a cellular hypersensitivity reaction. Proximal and distal tubules were severely affected focally. Migration of lymphocytes through the tubular basement membrane of otherwise well-preserved tubules was considered to be the first phase. Other tubules showed extreme thinning of the tubular basement membrane, with still intact cellular walls. Rupture of the tubular basement membrane and necrotic disintegration of tubular epithelial cells are probably late phenomena. The non-necrotic tubules displayed severe reduction of proximal brush border and proximal as well as distal tubular basolateral infoldings. Focal tubular disintegration leading to tubular block and/or backleak as well as decrease of proximal tubular sodium resorption leading to a decreased glomerular filtration (a mechanism probably also acting in ischemic acute renal failure) may all be factors responsible for the acute renal failure in AIN.
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PMID:Ultrastructure of the kidney in acute interstitial nephritis. 396 19

Light microscopy, transmission electron microscopy and scanning electron microscopy were used to characterize the morphologic alterations and to localize the site of injury within the kidney 1, 2, 3, 5 and 7 days after the intraperitoneal injection of cis-diamminedichloroplatinum. Pathologic alterations were evident 3 days after the injection of the drug and were localized to the S3 segment of the proximal tubule situated in the outer stripe of the outer medulla. A spectrum of changes was seen in this S3 segment which included a thinning or focal loss of brush border, cellular swelling, condensation of the nuclear chromatin and focal areas of necrosis. After 5 days, widespread tubular necrosis of the S3 segment in the outer stripe was the predominant finding. Necrotic tubular epithelial cells could be seen detaching from the basal lamina and being sloughed into the tubular lumen. Only a bare basal lamina remained in many areas. Regeneration of the S3 segment was seen after 7 days and was characterized by tubules with widely dilated lumens which were lined by many low-lying epithelial cells. The observation that cis-diamminedichloroplatinum exerts its nephrotoxic effect on the S3 segment of the proximal tubule located in the outer stripe of the outer medulla demonstrates that the pattern of injury produced by this antitumor drug is similar to that associated with other nephrotoxic and ischemic models of acute renal failure.
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PMID:Mechanism of cis-platinum nephrotoxicity: II. Morphologic observations. 719 26

Benign recurrent hematuria usually indicates a good prognosis. This condition is associated with abnormally thin glomerular basement membranes. Of 680 renal biopsy cases in which lower urinary tract disease had been excluded by careful study, 25 cases from seven children and eighteen adults met the criteria for thin glomerular basement membrane disease, placing the incidence of the disease at 3.7%. The mean patient age was 32.4 years and the male to female ratio was 1 to 5.3. The primary finding was microscopic hematuria in eighteen patients and gross hematuria in five patients. Among eighteen patients who had microscopic hematuria, one patient also exhibited proteinuria and one patient suffered from acute renal failure due to acute drug-induced interstitial nephritis. Proteinuria was only found in one patient. All of the patients had normal renal function, with the exception of one who suffered from acute renal failure. The duration of hematuria from the time of detection to the date of biopsy ranged from 3 months to 30 years with a mean interval of 56.6 months. No apparent evidence of familial hematuria in any patient was noted. Under light microscopy most glomeruli were normal. However, five cases showed focal global sclerosis. Under immunofluorescence microscopy seventeen cases were negative for all immunoglobulins, for complement, and for fibrinogen. Eight cases showed nonspecific mesangial deposition of fibrinogen and/or IgM. Ultrastructurally, extensive diffuse thinning of the GBM was a constant finding. The mean thickness of the GBM was 203.2 +/- 28.3 nm (n = 25); the thickness in adult (201.4 +/- 27.5 nm; n = 18) did not differ from that in children (208.1 +/- 32.0 nm; n = 7).
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PMID:Thin glomerular basement membrane disease: light microscopic and electron microscopic studies. 925 Sep 20