Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate the rate and associated factors for recovery of renal function in patients labeled by their nephrologists as having end-stage renal disease (ESRD), the data base of the Michigan Kidney Registry was used. All patients reported as starting treatment for ESRD between 1976 and 1985 (N = 7,404) were evaluated, excluding patients with acute tubular necrosis (ATN) or transplantation cases. While patients with ESRD due to diabetes and cystic diseases had lower recovery rates than average, patients with glomerulonephritis associated with a systemic illness, vasculopathies, and crescents had threefold to fourfold higher recovery rates. White race, older age, and later year of ESRD were associated with significantly higher recovery rates. Recovery rates did not differ substantially for patients receiving peritoneal dialysis or hemodialysis. Recovery occurred within 6 months of ESRD in approximately 48% of those recovering, 74% within 1 year, and lasted at least 1 year in 75% of the cases. The authors conclude that caution should be applied when the diagnosis of ESRD is made; the possibility of recovery should be sought and assessed, especially when early renal transplantation is considered.
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PMID:Recovery from end-stage renal disease. 229 34

A previously healthy 29-year-old homosexual man presented with a 4-day history of fever, malaise, sore throat, and bleeding gums. Rhabdomyolysis, acute renal failure, and nephrotic range proteinuria were also present. The patient was found to have acute human immunodeficiency virus (HIV) infection confirmed by the presence of HIV antigen in his serum and subsequent evolution of an HIV antibody profile typical of acute seroconversion. A kidney biopsy revealed acute tubular necrosis and mesangioproliferative glomerulonephritis, with tubuloreticular inclusions. In the presence of otherwise unexplained acute renal failure, rhabdomyolysis, or new onset nephrotic syndrome, acute HIV infection should be considered in the differential diagnosis.
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PMID:Acute human immunodeficiency virus infection temporally associated with rhabdomyolysis, acute renal failure, and nephrosis. 233 Apr 81

Acute renal failure is a frequent and dramatic clinical syndrome, producing a wide variety of serious and potentially lethal disorders in infancy. Review of 30 cases of severe acute renal failure occurred from 1985 in our unit reveals that the major causes are: acute tubular necrosis (33%), hemolytic uremic syndrome (16%), post-streptococcal glomerulonephritis (16%). 16 patients aged from 7 days to 15 years weighing 2 to 59 kilos, underwent dialysis: 8 HD, 7 PD, 1 both. Functional recovery occurred in 13 patients (82%); 3 patients died for the condition that precipitated renal insufficiency.
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PMID:[Acute renal failure. 3 years' activity of a pediatric dialysis unit]. 238 22

Eosinophiluria is considered a useful marker of drug-induced acute interstitial nephritis. However, recognition of eosinophiluria by Wright's staining is technically difficult, and the spectrum of disorders causing eosinophiluria is not completely defined. We have adapted Hansel's stain for the examination of urinary sediment. Whereas there was a variable uptake of Wright's stain by eosinophils in the urine, such eosinophils were readily recognized with Hansel's stain by the presence of bright red granules. The prevalence of eosinophiluria in acute interstitial nephritis was 10 of 11 patients, in acute tubular necrosis none of 30, in acute pyelonephritis none of 10, in acute cystitis 1 of 15, in postinfectious glomerulonephritis 1 of 6, in rapidly progressive glomerulonephritis 4 of 10, and in acute prostatitis 6 of 10. Eosinophiluria in acute interstitial nephritis was demonstrated by Hansel's stain in 10 of 11 patients but by Wright's stain in only 2 of 11 patients. We conclude that Hansel's stain substantially improves the recognition of eosinophiluria as compared with Wright's stain. Eosinophiluria is useful in distinguishing acute interstitial nephritis from acute tubular necrosis. The clinical spectrum of eosinophiluria also includes rapidly progressive glomerulonephritis, acute prostatitis, and occasionally, acute cystitis or postinfectious glomerulonephritis.
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PMID:Eosinophiluria--a new method of detection and definition of the clinical spectrum. 1842 May 15

Hansel's stain is a simple technique that can easily be performed in a clinical or office setting. It allows for improved detection of the eosinophiluria when compared with conventional Wright's stain. The mechanism underlying the superiority of the Hansel's stain remains to be elucidated. Eosinophiluria demonstrated by Hansel's stain appears to be a sensitive marker for drug-induced acute interstitial nephritis and probably allows differentiation from acute tubular necrosis. However, the spectrum of eosinophiluria also includes acute glomerulonephritis, rapidly progressive glomerulonephritis, prostatitis, and urinary tract obstruction. Therefore, the finding of eosinophiluria on Hansel's stain clearly cannot be considered diagnostic of acute interstitial nephritis. In the absence of renal biopsy or other clinical clues to suggest the diagnosis, eosinophiluria should not be used as the sole criterion for the diagnosis of acute interstitial nephritis or a a justification for empiric steroid therapy.
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PMID:Eosinophiluria. 245 85

This review gives a survey of the most important tubulo-interstitial and glomerular lesions in kidney transplants. Among the tubulo-interstitial lesions subcapsular interstitial fibrosis, acute tubular necrosis, cellular tubulo-interstitial rejection and Ciclosporin associated lesions are briefly described. The review of the glomerular lesions is focused upon intraglomerular coagulation, transplant glomerulitis and transplant glomerulopathy. Among the immunocomplex diseases the preexisting glomerular lesions are stressed. Furthermore the differential diagnosis between rejection associated glomerular lesions and glomerulonephritis is discussed. Finally the prognostic significance of the different morphologic lesions is outlined based on an analysis of 500 biopsies from Basel.
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PMID:[Interstitial and glomerular changes in kidney transplants]. 248 6

Renal involvement in Hansen's disease was evaluated in 94 Portuguese patients, average age and duration of disease of 47.6 and 6.8 years respectively. Sixty-seven were studied retrospectively and 27 prospectively; renal biopsy was obtained in 4, fat-tissue needle aspiration for amyloidosis in 20, and tubular function was tested in ten. Mild proteinuria and/or haematuria was found in 33 patients, the severity increasing during erythema nodosum leprosum reactions, but without overt nephritic or nephrotic syndrome. Two patients had renal amyloidosis on biopsy and two more were confirmed by fat biopsy, a 10.5% incidence in those studied prospectively; all but one were of the lepromatous type, with frequent bouts of erythema nodosum leprosum. The two other renal biopsies showed mesangial glomerulonephritis, and one unexplained acute tubular necrosis; none had immune deposits by immunofluorescence. Proximal acidification was always normal, distal acidification tested by bicarbonate infusion was abnormal in one of nine patients, and six of nine patients had concentration defects. Leprosy causes frequent urinary sediment changes and concentration defects, usually without clinical expression; proteinuria and/or glomerular involvement is mainly due to amyloidosis.
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PMID:Renal involvement in leprosy. 249 59

Nucleated nonsquamous cells in urine of patients with crescentic glomerulonephritis (CN), noncrescentic glomerulonephritis (NCN), acute tubular necrosis (ATN) and drug related acute interstitial nephritis (AIN) were identified using monoclonal antibodies and immunoperoxidase stain. Cell viability was determined by trypan blue permeability. CN was distinguishable from NCN by total cell numbers exceeding 30,000/ml (p less than 0.001) and counts of granulocytes exceeding 10,000/ml (p less than 0.05), monocytes exceeding 3,000/ml (p less than 0.001), T4 lymphocytes exceeding 1,500/ml (p less than 0.001), T8 lymphocytes exceeding 1,500/ml (p less than 0.001), glomerular epithelial cells exceeding 4,000/ml (p less than 0.001), proximal tubular cells exceeding 8,000/ml (p less than 0.001), loop of Henle cells exceeding 1,500/ml (p less than 0.01) and urothelial cells exceeding 1,500/ml (p less than 0.05). AIN was distinguishable from ATN by total cell numbers exceeding 75,000/ml (p less than 0.001) and counts of granulocytes exceeding 150,000/ml (p less than 0.001), monocytes exceeding 5000/ml (p less than 0.001), T4 lymphocytes exceeding 3,000/ml (p less than 0.01), T8 lymphocytes exceeding 2,500/ml (p less than 0.01) and cell viability exceeding 60% (p less than 0.05). Proximal tubular, loop of Henle, distal tubular/collecting duct and urothelial cells were present in high numbers in CN, ATN and AIN. CN can be distinguished from NCN, and ATN can be distinguished from AIN by identifying and quantifying the nucleated cells present in the urine.
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PMID:Immunoperoxidase identification of nucleated cells in urine in glomerular and acute tubular disorders. 266 90

A method to identify nucleated nonsquamous cells in urine using monoclonal antibodies and immunoperoxidase stain is described. Cells from washed deposits of midstream urine samples were transferred to gelatinized slides in a cytocentrifuge, air-dried, acetone fixed, and subjected to microwave irradiation. Slide preparations were then treated with monoclonal antibodies with the use of a four-layer peroxidase-antiperoxidase technique. It was possible to identify granulocytes, monocytes, lymphocytes, and renal epithelial and urothelial cells. This method was found to be helpful in determining the profiles of cells in urine in acute tubular necrosis, drug-related acute interstitial nephritis, and crescentic glomerulonephritis.
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PMID:Immunocytologic dissection of the urine sediment using monoclonal antibodies. 305 61

Eight nephrectomies and 13 biopsies of renal allografts (living 15, cadaveric 6) were investigated on the origin of inflammatory cells in the graft tissues by the use of an immunohistologic method (ABC method). Various monoclonal antibodies and heterosera were used to identify different leukocyte subsets. In all specimens the most predominant inflammatory cells were T cells. Other cells decreased in the following order; B cells, neutrophils and monocytes, and natural killer cells. In T cell subsets Leu 2a-positive cells (suppressor/cytotoxic T cells) predominated over Leu 3a-positive cells (helper/inducer T cells) in 4 nephrectomies (living 1, cadaveric 3) and 12 biopsies (living 11, cadaveric 1). Among these 16 cases, 7 were undergoing acute rejection in various degrees, and 9 were without clinical rejection. In the former 7 cases only one was suffering from another disease. In contrast, Leu 3a-positive cells predominated over Leu 2a-positive cells in 1 biopsy (living) and 4 nephrectomies (living 2, cadaveric 2). Four of these 5 cases concurrently had other diseases in addition to acute rejection. Two cases underwent acute tubular necrosis (cadaveric graft nephrectomies) and 2 underwent chronic rejection and crescentic glomerulonephritis (living graft nephrectomies). The one remaining case was without clinical rejection.
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PMID:Identification of inflammatory cells infiltrating renal allografts. 309 67


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