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)

Plasma oxalate was measured with use of the enzyme oxalate oxidase (EC 1.2.3.4; normal values 3.3 +/- 1.5 mumol/L, n = 24) in 50 patients with different degrees of renal failure. The following mean concentrations +/- SD (in mumol/L) were found: for glomerular diseases, 12.7 +/- 7.8 (n = 21); tubular diseases, 20.4 +/- 14.0 (n = 16); chronic renal failure before dialysis, 32.5 +/- 13.5, and after dialysis, 17.8 +/- 3.8 (n = 10); and primary hyperoxalemia, 72.2 +/- 14.5 14.5 (n = 2). The course of plasma oxalate was followed in one of these two patients after renal transplantation and in a patient recovering from acute tubular necrosis. No significant differences were found between patients with glomerular and tubular disorders. Overall, plasma oxalate was correlated with plasma creatinine in patients with glomerular and tubular diseases and dialysis patients (r = .84, P less than .001). Patients with primary hyperoxalemia had values outside the 95% confidence area of the regression line. It is concluded that the values obtained with this method, although probably still tending to overestimate the true oxalate concentration to some extent, provide reliable information about relative differences in plasma oxalate levels. In patients with terminal renal failure, plasma oxalate sometimes rises to levels at which deposition of calcium oxalate in tissues can occur.
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PMID:Plasma oxalate concentration in chronic renal disease. 638 28

A study of the magnetic resonance imaging (MRI) appearances of the kidneys in six normal volunteers and 52 patients is reported. Corticomedullary differentiation was seen with the inversion-recovery (IR 1400/400) sequence in the normal volunteers and in patients with functioning transplanted kidneys and acute tubular necrosis. Partial or total loss of corticomedullary differentiation was seen in glomerulonephritis, acute and chronic renal failure, renal artery stenosis, and transplant rejection. The T1 of the kidneys was increased in glomerulonephritis with nephrotic syndrome, but the T1 was within the normal range for renal medulla in glomerulonephritis without nephrotic syndrome, renal artery stenosis, and chronic renal failure. A large staghorn calculus was demonstrated with MRI, but small calculi were not seen. Fluid within the hydronephrosis, simple renal cysts, and polycystic kidneys displayed very low signal intensity and long T1 values. Evidence of recent hemorrhage into cysts was seen in polycystic kidneys. Tumors displayed varied appearances. Hypernephromas were shown to be hypo- or hyperintense with the renal medulla on the IR 1400/400 sequence. After intravenous injection of gadolinium-DTPA, there was marked decrease in the tumor T1.
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PMID:Magnetic resonance imaging of the kidneys. 638 80

The present prospective study was undertaken to evaluate the usefulness of urinary chloride concentration in determining the cause of an abrupt decline in renal function. 99 patients from diverse clinical settings with multiple causes of acute renal failure were evaluated. Urinary chloride concentrations of less than 20 mEq/l were observed in most cases of reversible prerenal azotemia (20 of 21 cases) and were observed in more frequently than urinary sodium concentration of less than 20 mEq/l (13 of 21 cases, p less than 0.01). Only prerenal azotemia accompanying diuretic use was associated with high urinary chloride concentrations (57 +/- 7 mEq/l). When prerenal azotemia occurred in the setting of metabolic alkalosis with bicarbonaturia, urinary chloride was low (4.0 +/- 1.0 mEq/l) while urinary sodium was high (65.0 +/- 19.0 mEq/l). In patients with oliguric and nonoliguric acute tubular necrosis, and in patients with acute exacerbations of chronic renal failure, mean urinary chloride concentration ranged from 40 to 67 mEq/l and mean fractional excretions of chloride ranged from 7.2 to 8.4%. Only 11% of patients with oliguric and nonoliguric acute tubular necrosis had urinary chloride concentrations of less than 20 mEq/l. Urinary chloride concentrations exhibited greater sensitivity and equivalent specificity as urinary sodium concentrations in differentiating patients with reversible prerenal azotemia from those with oliguric and nonoliguric acute tubular necrosis.
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PMID:Urinary chloride concentration in acute renal failure. 670 May 67

Two elderly women suffered an acute deterioration of renal function after treatment with cefoxitin sodium. One with stable chronic renal failure due to reflux nephropathy underwent a rapid deterioration of renal function which proved fatal. The other woman had rheumatoid arthritis and developed acute tubular necrosis after treatment with gentamicin and cefoxitin. All the data suggested that the antibiotic was responsible for the deterioration in renal function. The dose of cefoxitin should be reduced in patients with renal functional impairment. Cefoxitin should either be used with great caution or not prescribed in combination with aminoglycoside antibiotics.
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PMID:Cefoxitin-associated renal failure. 701 86

Acute tubular necrosis is the most common cause of acute renal failure making up two-thirds of such cases. Mortality is best correlated to basic disease. Surgery, particularly in the abdomen, carries an unusually sinister prognosis. The influence of age on outcome is controversial. Intensified dialysis, early reoperations, hyperalimentation, and possibly continuous dialysis and antibiotic barrage deserves close investigation as tools of improving survival. Almost all surviving patients recover renal function within 30 days and beyond two months recovery almost never occurs. Approximately 3% of the patients initially suspected of having acute tubular necrosis will need chronic hemodialysis indefinitely or have a transplant to regain renal function. The older patient seems to be more susceptible to this problem. Delayed recovery and chronic renal failure is unusual. High dose loop diuretic therapy and hyperalimentation with intravenous amino acids may shorten the time for recovery, although considerable controversy exists.
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PMID:Recovery from acute renal failure. 733 33

E-Selectin is a 115-kDa cell surface glycoprotein transiently expressed on vascular endothelium in response to interleukin-1 and tumour necrosis factor-alpha with a peak in expression at four hours. Its distribution in transplant biopsies has been associated with inflammatory events such as allograft rejection. Recently, a soluble isoform of E-selectin has been detected in the culture medium of cytokine activated endothelial cells by an ELISA method. In this study soluble E-selectin levels in renal allograft recipients were compared with the incidence of rejection, acute tubular necrosis (ATN), cyclosporin A (CyA) toxicity, and use of orthoclone OKT3 (muromonab-CD3) to establish whether early endothelial activation and inflammatory damage could be detected. The mean soluble E-selectin level in normal volunteers was 89 ng/ml serum compared to 120 ng/ml for a group of chronic renal failure patients. Soluble E-selectin levels declined upon transplantation but this was not significant, nor was the difference in samples from patients experiencing rejection, ATN or CyA toxicity. A dramatic and sustained rise in soluble E-selectin levels was found within 24 hours of the first dose of OKT3 treatment. This study shows that soluble E-selectin does not provide early unequivocal indication of pathological sequelae in renal transplantation, although extensive endothelial activation can be demonstrated with OKT3 treatment.
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PMID:Lack of correlation of soluble E-selectin level with renal transplant rejection. 755 79

The kidney is one of the organs susceptible to heavy metal intoxication. The total body burden and "saturation" level in renal tissue are important limiting factors to the onset of renal injuries. Acute or chronic exposure to many of heavy metals can induce renal tubulointerstitial injuries, including acute tubular necrosis, chronic tubulointerstitial nephritis, Fanconi syndrome, renal tubular acidosis, and renal tubular dysfunction without morphological changes. Chronic cadmium intoxication can cause irreversible Fanconi syndrome with chronic tubulointerstitial nephritis. Both urinary low-molecular weight protein excretion and urinary cadmium excretion (greater than 200-400 ppm) are the most reliable earlier markers of tubulointerstitial injury in chronic cadmium intoxication. The role of metallothionein is central to an understanding of cadmium-induced nephropathy. Acute lead intoxication in children can cause reversible Fanconi syndrome. Hypertension, hyperuricemia, and elevated serum creatinine, without Fanconi syndrome, are clinical manifestations of chronic lead exposure in adults. Nuclear inclusion body in proximal tubular cell is characteristic. Chronic exposure to inorganic germanium can cause chronic renal failure without urinary abnormalities, due to tubular degeneration and interstitial fibrosis, mainly in the thick ascending limb of Henle and distal tubulus.
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PMID:[Tubulointerstitial injuries in heavy metal intoxications]. 756 49

The mortality rate of acute renal failure is still high, about 50%. About 10% of the survivors have chronic renal failure, sometimes requiring dialysis. The course of some of these cases can be improved by appropriate therapeutic measures, if they are undertaken early. Early identification of these lesions is therefore mandatory. The clinical diagnosis is often difficult: 1. rare atypical forms of acute tubular necrosis, with renal or extrarenal signs, may lead to renal biopsy; 2. vascular and glomerular disease are most often recognized clinically (sometimes misdiagnosed), but the histological type (and therefore the appropriate treatment) cannot be determined; 3. acute interstitial nephritis is rarely diagnosed clinically and the nature of the infiltrate remains unknown. In certain cases of acute renal failure, the contribution of early renal biopsy to the etiological diagnosis and to prognosis and therapy is obvious. In acute renal failure, renal biopsy should be considered early in a rather limited number of patients (about 20%), everytime the diagnosis of tubular necrosis is doubtful, especially in acute renal failure associated with persistent infection, in order to guide the therapy.
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PMID:[Contribution of renal biopsy to the diagnosis and treatment of acute kidney failure]. 756 93

Scant information exists on the prognosis of infants with renal failure who receive peritoneal dialysis in the first month of life. We reviewed the outcome of 23 such patients 1 year after the onset of renal failure. Diagnoses included acute tubular necrosis (11 infants), renal dysplasia (5), obstructive uropathy (4), polycystic kidney disease (1), renal vein thrombosis (1), and renal artery thrombosis (1). Seven of the eleven patients with acute tubular necrosis had had cardiac surgery. At 1 year, eight (35%) of the patients had died, six (26%) had a full recovery, seven (30%) were receiving long-term dialysis awaiting a transplant, and two (9%) had chronic renal failure. Effective dialysis, characterized by the reversal of metabolic disturbances or attainment of fluid balance, was accomplished in all patients. The mean duration of dialysis was 4.5 months (range, 0.1 to 12 months). The most common complications of dialysis were peritonitis and catheter exit site infection. Despite the provision of supplemental calories via nasogastric tube, the majority of patients receiving long-term dialysis showed impaired growth and mild developmental abnormalities. Peritoneal dialysis is an effective means of renal replacement therapy in the neonatal period; however, the morbidity and mortality rate for this population remains high.
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PMID:Peritoneal dialysis in the neonatal period: outcome data. 844 49

There are conflicting reports on the ability of aspirin as a single agent to cause acute or chronic renal failure in experimental animals. Chronic administration of aspirin alone over 18 to 68 weeks in doses of 120 to 500 mg/kg/d has been reported to cause renal papillary necrosis in rats. However, some investigators have been unable to produce renal papillary necrosis in other species or in rats given lower divided doses comparable to therapeutic doses used in humans. In a variety of rat strains, aspirin administered as a single high dose intravenously or by oral gavage produces acute tubular necrosis of proximal tubules, rarely accompanied by renal papillary necrosis in susceptible strains. Several human studies have addressed the chronic nephrotoxicity of aspirin alone or relative risk of end-stage renal disease in association with aspirin use after correction for other analgesics. With the exception of one case control study demonstrating a low, but statistically significant risk of end-stage renal disease in association with aspirin use, all other case control studies and several prospective studies have been unable to identify a significant risk of chronic renal failure in patients using aspirin alone in therapeutic doses. In healthy adults, short-term aspirin administration in therapeutic doses has no effect on creatinine clearance, urine volume, osmolar clearance, or sodium and potassium excretion. However, in predisposed individuals with glomerulonephritis, cirrhosis, and chronic renal insufficiency, and in children with congestive heart failure, short-term aspirin use in therapeutic doses may precipitate reversible acute renal failure. Acute aspirin intoxication (>300 mg/kg) frequently causes acute renal failure and doses of 500 mg/kg may be lethal. Chronic salicylate intoxication has been reported to cause reversible or irreversible acute renal failure in association with a pseudosepsis syndrome.
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PMID:Does aspirin cause acute or chronic renal failure in experimental animals and in humans? 866 25


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