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)

Nineteen patients were examined to determine the clinical potential of magnetic resonance imaging (MRI) for evaluation of renal transplants. A 0.6-T cryogenic magnet and spin-echo technique with varying pulsing factors were used. T1-weighted images were best for differentiating the cortical and medullary parts of the transplanted kidney. Of the six living-related transplants with good renal function that were imaged, five demonstrated good corticomedullary differentiation (CMD) and one faint CMD. Three transplants with acute rejection were imaged, and all demonstrated a decrease in CMD and decrease in overall signal intensity compared with baseline. No CMD was seen in the three chronically rejecting transplants imaged. The appearance of cadaveric transplants and acute tubular necrosis was quite variable. All perinephric fluid collections were well depicted by MRI. Lymphoceles could be distinguished from hematomas. MRI may prove to be a useful adjunct in the evaluation of renal transplants and perinephric fluid collections.
AJR Am J Roentgenol 1984 Dec
PMID:Magnetic resonance imaging of renal transplants. 638 81

The assumption that renal allograft histology should be perfectly normal during quiescence in the absence of rejection or nephrotoxic insults has not been adequately investigated. To study this, routine renal allograft biopsies were performed at approximately 1 and 4 weeks, when patients often had normal function or stable acute tubular necrosis (ATN). These were compared with biopsies from other patients during autologous ATN or clinically evident allograft rejection. There were two new findings: (1) Almost all biopsies contained an interstitial infiltrate, so that only the presence of vasculitis provided a clear distinction between rejection and quiescence. Most of the biopsies with infiltrates were from patients who had never received cyclosporine, so that an infiltrate does not necessarily signify toxicity due to this drug. (2) A major proportion of the cells in some biopsies appeared to express both the helper/inducer and the cytotoxic/suppressor phenotype, and a similar finding after in vitro stimulation suggests that this represents a cell population that is activated in some way.
Transplantation 1984 Dec
PMID:Characteristics of early routine renal allograft biopsies. 639 Aug 32

The survival of patients in end-stage renal failure from lupus nephritis offered renal substitution therapy has been the subject of conflicting reports. Trying to clarify the reasons for this discrepancy, we analysed our experience with dialysis and transplantation in systemic lupus erythematosus (SLE). Of our 138 patients with lupus nephritis, 26 reached end-stage renal failure, of whom 24 received replacement therapy. Fourteen patients had a marked acute deterioration in renal function immediately before reaching terminal uremia, associated with active SLE in 12 and acute tubular necrosis after hypotension in one. Nine patients in this group died, 8 within 1 month of beginning dialysis. Nine patients progressed slowly to endstage renal failure over 2 to 7 years, without evidence of active SLE: only 1 required aggressive treatment and only 3 patients died, 1 five years after transplantation. Eight patients received altogether 10 allografted kidneys; 4 still functioning 10-24 months later; 2 patients are back on dialysis and 2 died, 1 of a myocardial infarct. There was no evidence of active SLE after transplantation. Ten patients were dialysed for more than 3 months; most were maintained on prednisolone and azathioprine whilst on dialysis and lupus activity tended to abate. The exclusion of the group of patients with rapid pre-terminal decrease in renal function from some series may explain some of the differences in reported survival. Stable patients with SLE present few problems in end-stage renal failure or after transplantation.
Clin Nephrol 1984 Dec
PMID:End-stage renal failure in systemic lupus erythematosus with nephritis. 639 7

Autopsy findings in post-surgical acute renal failure cases were studied in 131 cases on diaysis collected from annuals of pathological Autopsy Cases in Japan (1958-1981). Fifty (38.2%) abdominal and 48 (36.6%) cardiovascular operative procedures were the origins of the 131 post-operative acute renal failure patients treated by dialysis. The incidence of acute tubular necrosis was 68.7 per cent. There were 13 non-obstetric cases (19.9%) of acute bilateral cortical necrosis. Direct causes of death in postsurgical acute renal failure patients were mainly infection (61.7%) and bleeding (21.0%) The incidence of patients with infectious disease complicating postsurgical acute renal failure was 60.3 per cent and the rate of those between 20 and 70 years of age was constant. The incidence of patients with bleeding was 45.0 per cent and no significant differences were seen in the 20-70 year age range.
Tokai J Exp Clin Med 1984 Dec
PMID:Autopsy findings in postoperative acute renal failure patients, collected from the annuals of pathological autopsy cases in Japan. 654 80

A study was conducted in oliguric and acutely azotemic patients, measuring: (i) the fractional excretion of sodium (FENa) using creatinine clearance as a measure of glomerular filtration rate, and (ii) sodium clearance relative to urea clearance, designated as the sodium/urea clearance ratio (Na:urea CR). It was found that FENa discriminated between "tubular" and "non-tubular" disorders in 96% of patients. Further, Na:urea CR was as discriminating as FENa. Patients with Na:urea CR above 2.5% can be reliably diagnosed as having acute tubular necrosis or acute urinary tract obstruction; those with a value less than 2.5% will have acute glomerulonephritis or pre-renal azotemia. As urea and sodium measurements are so readily available, this test can now be applied in the assessment of the oliguric or acutely azotemic patient in any hospital practice.
Aust N Z J Med 1983 Dec
PMID:A simple aid to the differential diagnosis of oliguria. 658 51

Nephrotoxicity of sodium arsenate was evaluated in dogs to determine the pathophysiologic basis for renal lesions caused by this heavy metal. Examination of biopsy specimens indicated that the low dose of the As salt (0.73 mg/kg of body weight) produced histologic changes consisting of mild degeneration and vacuolation of renal tubular epithelium. Vacuolation involved mainly the ascending thick portion of the nephron. Clinical pathologic changes were not demonstrable at this dosage level according to glomerular filtration rate (creatinine clearance), fractional reabsorption of sodium, potassium, and chloride; plasma osmolar and free water clearance; and urinalysis. The medium dose (7.33 mg/kg) resulted in alterations determined by urinalysis, but did not markedly affect other clinical pathologic measurements. Histopathologic changes were equal to or greater than those seen with the low dose. Tubular necrosis was observed in the cortical portion of the nephron and the ascending thick limb. The high dose (14.66 mg/kg) consistently produced marked changes in all parameters evaluated. Clinical pathologic alterations were compatible with acute tubular necrosis involving all segments of the nephron. Histologically, moderate glomerular sclerosis and severe tubular necrosis were observed. During recovery from the high dose of As, a gradual compensatory healing process was observed that was evident in all clinical pathologic parameters and was confirmed from sequential renal biopsy specimens.
Am J Vet Res 1983 Dec
PMID:Nephrotoxicity of sodium arsenate in dogs. 668 17

In 60 patients with a kidney transplant 86 perfusion studies with 99mTc-DTPA were performed during the early postoperative period. Correlative data and clinical differentiation were obtained by isotope nephrograms, laboratory values and clinical presentation. In addition to evaluation of scintiphotos, time-activity curves were derived from the transplant and evaluated quantitatively, obtaining a perfusion ratio by a computer program. A ratio of greater than 0.80 was found to be normal. In 20 patients with acute rejection, the ratio was decreased. In 13 patients with acute tubular necrosis, the perfusion ratio was between 0.39 and 0.65, decreasing further during an added rejection crisis. Follow-up examinations confirmed rejection through a decrease of the perfusion ratio (mean difference 0.44; p less than 0.025). In 9 cases, successful rejection therapy was documented by an increase (mean difference 0.29; p less than 0.005). In addition to quantitative evaluation, visual analysis revealed acute occlusion of the renal artery, renal infarction, urinoma, ureteral stenosis or necrosis. Quantitative scintigraphy with 99mTc-DTPA broadened the methods of describing kidney transplant function. Its quantitative evaluation enables the definition of acute rejection and its differentiation from acute tubular necrosis combined with acute rejection in the early postoperative period. Since the method recognizes morphological alterations as well, it usefully complements isotope nephrography.
Nuklearmedizin 1980 Dec
PMID:[Evaluation of renal transplant function by 99mTc-DTPA dynamic imaging (author's transl)]. 702 21

We measured prospectively changes in fractional protein clearance ratio (CPr/CCr) in 21 live-related (LR) and 41 cadaver donor (CD) renal transplants before and during onset of first rejections. Fifty-three recipients manifested a rejection within the first post-transplant month. Fractional protein clearance increased in all patients during rejection. An increase in CPr/CCr prior to other evidence of impending rejection, and therefore clinically useful, required at least a 10-day rejection-free interval dated from onset of diuresis (whether diuresis was immediate or delayed by acute tubular necrosis (ATN)). Twenty-three of 25 nonantilymphocyte globulin (ALG)-treated CD transplants manifested clinical and laboratory signs of the first rejection episode prior to the 10th day of diuresis compared with 5 of 21 LR and none of 16 ALG-treated CD transplants. Persistence of elevated CPr/CCr despite treatment forecast graft loss (11 of 13), whereas a decrease in this ratio was associated with ultimate reversal of the rejection process.
Transplantation 1981 Dec
PMID:Diagnostic and prognostic significance of an increase in fractional protein clearance ratio before and during rejection of renal transplant. 704 53

Urinalysis and urine chemistries are most helpful in determining whether acute renal failure is due to a prerenal, renal, or postrenal cause. A plain film of the abdomen should be obtained, with ultrasound or computed tomography also being done if obstruction is suspected. When prerenal and postrenal causes have been excluded, the cause should be considered to be acute tubular necrosis, which progresses through initiating, oliguric (or sometimes nonoliguric), diuretic, and recovery phases. Acute tubular necrosis can produce a variety of clinical consequences affecting the entire body, including hyperkalemia, acidosis, hypocalcemia, anemia, and infection, as well as various cardiovascular, neurologic, and gastrointestinal problems.
Postgrad Med 1982 Dec
PMID:Acute renal failure. 1. Classification, evaluation, and clinical consequences. 714 80

During the past five years, much has been learned about the complex pathophysiology of acute renal failure. A number of mechanisms appear to be involved, including cell swelling, inhibition of prostaglandin synthesis, tubular obstruction, and disruption of the basement membrane of the proximal tubule. For patients at high risk of acute tubular necrosis, prophylaxis with mannitol or furosemide (Lasix) should be considered under certain circumstances. If this syndrome does occur, management should focus on maintenance of proper fluid and electrolyte levels and nutrition, which is facilitated by dialysis. The prognosis of acute tubular necrosis has changed little in the past ten years, and mortality remains high.
Postgrad Med 1982 Dec
PMID:Acute renal failure. 2. Pathophysiology, prevention, management, and prognosis. 714 81


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