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

It is generally assumed that acute tubular necrosis is the etiology of renal failure that can occur during the course of Rocky Mountain spotted fever (RMSF). However, histologic examination of kidneys has been mainly limited to autopsy cases of fulminant infections. Acute glomerulonephritis due to glomerular immune complex deposition has not been reported in RMSF. We describe a case of acute oliguric renal failure that developed more than 2 weeks following the onset of RMSF. Renal biopsy showed acute glomerulonephritis with inflammatory cell infiltration and subendothelial immune deposits. Thus, acute glomerulonephritis should be in the differential diagnosis of acute renal failure that occurs in RMSF.
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PMID:Acute glomerulonephritis in a patient with Rocky Mountain spotted fever. 199 79

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

The value of magnetic resonance imaging in the differential diagnosis of non-obstructive dysfunction of renal allografts was studied in a series of 58 examinations at 0.5 T. Four parameters were evaluated: the corticomedullary differentiation; the relative thickness of the cortex; the evolution, with echo number, of the relative signal intensities of kidney parenchyma and adjacent fatty tissue on images generated by a long time to repeat multiecho sequence; and the proximal vascularization. The loss of corticomedullary differentiation is the major finding in acute rejection, but it is not specific as it is also observed in chronic rejection and in the much rarer acute glomerulonephritis. Thickening of the cortex is helpful for the detection of rejected transplants with visible corticomedullary delineation (26% of the cases). Uncomplicated acute tubular necrosis appears as a normal transplant.
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PMID:Non-obstructive kidney transplant dysfunction: magnetic resonance evaluation. 328 51

MR appearance of the kidney transplant is evaluated on a series of 80 examinations performed on a supraconductive unit operating at 0.5 T. Normal function kidneys displayed a clearly delineated corticomedullary differentiation (CMD); the ratio between the thickness of cortex and medulla didn't exceed 0.6. The same appearance was observed in non complicated acute tubular necrosis. Complete loss of CMD was the major finding in acute rejection (74% of the cases), but it was not specific as it was also observed in chronic rejection and in acute glomerulonephritis. Cortex thickening was helpful for the detection of rejected transplants with visible CMD. The sensitivity of MR in the detection of acute rejection was 94%. Specificity of MR findings for acute rejection depended on the transplant age: it varied from 100% for examinations performed during the first 3 months after transplantation, to less than 50% for examinations of the second year.
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PMID:[Magnetic resonance imaging, with surface coil, of a transplanted kidney]. 332 87

The pathogenetic factors leading to acute renal failure (ARF) in 223 children between the ages of 20 days and 14 years were studied. Diarrhoeal diseases were responsible for ARF in 49.8%, acute glomerulonephritis in 34.1%, drug induced intravascular hemolysis in glucose -6-phosphate dehydrogenase deficiency in 4.5%, snake bite in 4%, hemolytic uremic syndrome in 2.2%, and miscellaneous causes in 5.4%. Dialysis was instituted in 178 children and the others were treated conservatively. Renal histology in 39 out of 76 children who presented with an acute nephritic illness revealed acute endocapillary proliferative glomerulonephritis in 27 and crescentic glomerulonephritis in 12. The histology in 79 out of 147 remaining patients showed acute tubular necrosis in 64, acute cortical necrosis in 13, and acute interstitial nephritis in 2. Overall mortality was 27.4%. This high incidence of ARF due to infective diarrhoeas and dysentery reflects poor socio-economic and hygienic conditions, inadequate facilities in rural areas, delays in seeking medical advice, and lack of knowledge about fluid and electrolyte therapy amongst the staff.
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PMID:Acute renal failure amongst children in a tropical environment. 358 35

High-dose intravenous urography (IVU) was performed 62 times in 59 patients with acute (ARF) and chronic (CRF) renal failure. The major diagnostic categories were chronic glomerulonephritis, malignant hypertension, acute tubular necrosis (ATN), and acute glomerulonephritis. The cause of the renal failure, whether CRF or ARF, oliguric or nonoliguric, could not be reliably determined by either the evolving pattern or density of nephrogram, or the size of the kidneys. Although a persistent dense nephrogram favored the diagnosis of ATN, the major correlate was a decreasing density of nephrogram as the serum creatinine level increased (P less than 0.005).
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PMID:Diagnostic role of intravenous urography in acute and chronic renal failure. 378 76

Determining the cause of acutely deteriorating renal function is a common problem in clinical nephrology. The fractional excretion of filtered sodium (FENa) has been demonstrated to be a reliably discriminating test between prerenal azotemia and acute tubular necrosis. However, with increasing clinical use of the FENa, numerous reports of low FENa (less than 1%) have appeared. The clinical settings of these reports include oliguric and nonoliguric acute tubular necrosis, urinary tract obstruction, acute glomerulonephritis, hepatorenal syndrome, renal allograft rejection, sepsis, and drug-related alterations in renal hemodynamics. One particular urinary index cannot be expected to reliably discriminate between prerenal azotemia and acute renal failure in all cases. The utility of the FENa test in the differential diagnosis of acute renal failure must be interpreted in conjunction with the patient's clinical course and the use of additional urinary and serum tests.
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PMID:Fractional excretion of sodium. Exceptions to its diagnostic value. 397 Jun 21

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

Nifedipine caused acute, reversible deterioration in renal function in four patients with chronic renal insufficiency. The absence of hypotension, clinical course, benign urinary sediments, and normal results of renal ultrasound examinations excluded acute tubular necrosis, pyelonephritis, interstitial nephritis, obstructive uropathy, and acute glomerulonephritis. It is postulated that this slow calcium channel blocker produced deleterious intrarenal hemodynamic alterations in the setting of moderate to severe renal functional impairment. Nifedipine may alter renal function by blocking calcium entry into renal vascular smooth muscle, thereby reducing the efficacy of vasoconstrictor hormones in regulation of renal blood flow and glomerular filtration rate. An alternative explanation is that nifedipine may inhibit the compensatory synthesis of vasodilatory prostaglandin E2 analogous to the clinical observation of acute deterioration in renal function by nonsteroidal anti-inflammatory drugs in patients with pre-existing renal insufficiency. These observations suggest that clinicians should monitor renal function closely and exercise caution when administering nifedipine to patients with underlying renal insufficiency.
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PMID:Nifedipine-induced renal dysfunction. Alterations in renal hemodynamics. 649 46

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.
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PMID:A simple aid to the differential diagnosis of oliguria. 658 51


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