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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal parenchymal transit time of the recently introduced radiopharmaceutical 99mTc-MAG3 (mercaptoacetylglycylglycinel) was measured in 37 kidneys, using factor analysis to separate parenchymal activity from that in the collecting system. A new factor algorithm was employed, based on prior interpolative background subtraction and use of the fact that the initial slope of the collecting system factor time-activity curve must be zero. The only operator intervention required was selection of a rectangular region enclosing the kidney (by identifying two points at opposite corners). Transit time was calculated from the factor time-activity curves both by deconvolution of the parenchymal factor curve and also by measuring the appearance time for collecting system activity from the collecting system factor curve. There was substantial agreement between the two methods. Factor analysis led to a narrower range of normal values than a conventional cortical region-of-interest method, presumably by decreasing crosstalk from the collecting system. In preliminary trials, the parenchymal transit time did not well separate four obstructed from seventeen unobstructed kidneys, but it successfully (p less than 0.05) separated six transplanted kidneys with acute rejection or acute tubular necrosis from 10 normal transplants.
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PMID:Measurement of renal parenchymal transit time of 99mTc-MAG3 using factor analysis. 214 52

The retrospective review of 115 case-histories of patients with acute renal failure (ARF) seen over the last two years showed that etiologies were distributed as follows: acute tubular necrosis in 65% of cases, urinary tract obstruction in 16%, acute glomerulonephritis in 3,5%, acute interstitial nephritis (AIN) in 8% and acute microvascular nephropathy in 3,5%. The diagnostic value of renal biopsy in ARF is discussed. In spite of recent advances in the treatment of ARF, the mortality rate remains as high as 48%. This is mainly due to current etiologic circumstances, to the age of the patients and to the complications of ARF, with infectious complications being the most serious. Urea nitrogen accumulation is not a poor prognosis factor. Furosemide in high doses does not alter the prognosis but reduces the total number of dialysis indications (81% in 1970, 60% in 1980), the number of dialysis sessions per patient (1 only in 62% of patients), and the duration of the ARF episode (mean duration: 10,7 days).
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PMID:[Current aspects of acute renal failure]. 629 41

Eight hypertensive children with acute post-streptococcal glomerulonephritis were given intravenous frusemide, 2 mg/kg, and the results compared with 8 similar cases not given the diuretic. Mean urine flow increased from 0.24 ml/min/m2 before frusemide to 3.63 ml/min/m2 in the 6 hours afterwards and was still 0.72 ml/min/m2 48 hours later. In contrast mean urine flow remained unchanged over 48 hours in those not given frusemide. Despite similar initial blood pressures the duration of hypertension was much shorter (mean 4.7 days) after frusemide than in the controls (mean 11.0 days) and the edema-free weight was achieved more rapidly (6.8 days compared with 13.9 days). Plasma renin activity (PRA) did not rise after frusemide in the children with acute nephritis. This was in contrast to the rapid rise seen in normal humans thus indicating a dissociation between the diuretic and renin-releasing activities of frusemide in acute nephritis. Seven children with the hemolytic-uremic syndrome or acute tubular necrosis showed no significant change in either urine flow or PRA after frusemide. Frusemide is therefore effective treatment for both hypertension and oliguria in acute nephritis. Failure of PRA to rise indicates that renin release mechanisms are abnormal in renal failure and that PRA levels need to be interpreted with caution in this condition.
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PMID:Response to frusemide in acute renal failure: dissociation of renin and diuretic responses. 699 79

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.
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PMID:Acute renal failure. 2. Pathophysiology, prevention, management, and prognosis. 714 81