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)

Acute renal failure (ARF) is a serious complication in clients who have undergone bone marrow transplantation (BMT). The majority of cases develop as a result of intrarenal damage. Renal ischemia or nephrotoxic drugs, free hemoglobin, and free myoglobin contribute to acute tubular necrosis (ATN), which is the most likely cause of ARF in BMT clients. Nursing care of hospitalized BMT clients is directed toward the prevention of ARF by identifying clients who are at risk, the early diagnosis of renal impairment, and the administration of comprehensive treatment. Nurses play a vital role in the early diagnosis of renal impairment by assessing the client's fluid status, serum and urine electrolyte levels, and daily weights. The nursing role in managing clients with ARF includes preventing drug nephrotoxicity, maintaining fluid and electrolyte balance, preventing infection, and providing emotional support.
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PMID:Acute renal failure in bone marrow transplantation. 143 67

We observed 3 patients with a severe falciparum malaria infection. Although the patients appeared not to be seriously ill on admission, severe complications occurred. Renal impairment was a prominent feature and haemodialysis was sometimes necessary. Many hypotheses have been proposed regarding the aetiology of renal failure in Plasmodium falciparum but cannot yet be fully substantiated. Whatever the aetiology of renal failure might be, we believe that treatment should not differ essentially from that of acute tubular necrosis after circulatory shock and early diagnosis and treatment is imperative in spite of an initially ostensibly good clinical condition.
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PMID:Acute renal failure in severe chloroquine resistant falciparum malaria. 164 68

Sprague-Dawley rats were treated for 14 days with rapamycin (RAP; 1.5 mg/kg/day i.p.), cyclosporine (15 mg/kg/day by gavage), both drugs in combination, or appropriate drug vehicles. Hematological parameters and biochemical indices of renal and hepatic function were determined throughout the experimental period, at the end of which the rats were killed and tissues examined histologically. There was a significant reduction in weight gain in RAP- but not CsA-treated animals, while rats given both drugs showed a reduction in body weight over the 14-day experimental period. There were no significant alterations in absolute or differential white blood cell counts or in T or B cell numbers, except in the drug combination group, in which an absolute lymphopenia was detected on day 14. Small but significant increases in urinary flow rate (UFR) were found with either drug alone, and there was a marked (4-fold) increase in UFR in response to drug combination. Both RAP and CsA caused a small elevation in serum creatinine concentrations, but only with CsA was there a significant elevation in urinary enzyme activity and reduction in 51Cr. EDTA clearance. The drug combination exacerbated renal impairment, the extent of which was greater than the additive effect of either drug alone. Hyperbilirubinemia of similar magnitude was observed in rats receiving either CsA alone or in combination with RAP. In contrast to its effect on renal function, however, the CsA+RAP combination was without additional effect on liver function compared with the minor changes seen with either drug alone. Plasma and urinary glucose levels were elevated in all drug treatment groups and especially in animals given both drugs. RAP administration did not significantly affect whole-blood CsA concentrations, although the possibility of a pharmacokinetic interaction cannot be totally excluded. Histological studies revealed striking thymic medullary atrophy in all drug-treated animals. In addition, all rats given RAP showed focal myocardial necrosis of overall mild-moderate severity. Kidneys of RAP-treated rats appeared normal, whereas mild, focal, acute tubular necrosis was evident in all CsA-treated animals. Pancreases of all drug-treated animals were normal.
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PMID:Toxicity of rapamycin--a comparative and combination study with cyclosporine at immunotherapeutic dosage in the rat. 187 90

A woman with a history of drug allergy, renal impairment and carcinoma of the breast with pulmonary micrometastases developed haemolytic anaemia and Stevens-Johnson syndrome following the use of mefenamic acid, paracetamol (acetaminophen) and furosemide (frusemide). In addition there was severe cholestatic hepatitis in the absence of clinical evidence of sepsis, biliary obstruction or recurrent metastases. The rash resolved on steroid therapy but the patient eventually died from both renal and liver failure. Acute tubular necrosis with a background of chronic tubulointerstitial nephritis was also found at autopsy. Although in the presence of multiple drug therapy the causative agent cannot be identified with absolute certainty, the association of these severe idiosyncratic hepatic and dermatological reactions with haemolytic anaemia strongly suggests mefenamic acid as the most likely culprit.
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PMID:A case of Stevens-Johnson syndrome, cholestatic hepatitis and haemolytic anaemia associated with use of mefenamic acid. 206 63

The renal handling of cyclosporine was studied in ischemically damaged kidneys in New Zealand White rabbits and nonischemic control animals. CsA, 25 mg/kg/day, was administered intravenously for 10 days starting with the day of operation. Blood CsA (B CsA) was higher in the ischemic group compared with the controls (median: 285 micrograms/L, range 95-785 micrograms/L vs. 170 micrograms/L, range 110-185 micrograms/L, P = 0.05) on day 1 after operation. B CsA dropped rapidly to a level equivalent to the controls by day 4 (median: 105 micrograms/L, range 60-280 micrograms/L vs. 195 micrograms/L, range 70-215 micrograms/L, P = NS). Median CsA clearance (C CsA) as a percentage of creatinine clearance (C Cr) was some ten-fold greater in the ischemic animals (6.32%, range 2.93-18.41% vs. 0.55%, range 0.13-0.78%, P less than 0.001) on day 1. The ratio gradually declined, approaching the value in controls by day 10 (0.86%, range 0.24-7.21% vs. 0.23%, range 0.16-0.73%, P = 0.05). The data suggest that renal impairment has an important effect on CsA blood levels. In the clinical situation this may be of particular importance during both oliguria and the recovery from acute tubular necrosis.
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PMID:The effect of renal ischemia on cyclosporine clearance in rabbits. 231 10

In 3 years seventeen patients presented to one unit with renal failure associated with the use of non-steroidal anti-inflammatory drugs (NSAID). Seven patients presented with acute renal failure, in four due to acute tubular necrosis and in three to acute interstitial nephritis; all recovered when NSAID treatment was stopped. Four patients presented with symptomless renal impairment discovered during routine follow-up in a rheumatology clinic; again all improved on withdrawal of NSAID. The remaining six patients presented with chronic renal failure, a disorder not previously associated with NSAID treatment. The pattern of renal disease associated with NSAID may be more extensive than has previously been recognised. A history of NSAID use should be sought in all patients presenting with unexplained renal failure.
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PMID:Non-steroidal anti-inflammatory drugs and renal failure. 286 13

At 6 months after kidney transplantation 59 adults with impaired renal function were divided into three groups according to their serum creatinine level: group I 150-199 mumol/l; group II 200-299 mumol/l; and group III greater than or equal to 300 mumol/l. These patients were followed up for 5 years or to graft loss when it became apparent that the eventual outcome was related to the degree of renal impairment at 6 months. Age of donor and age of recipient did not have a bearing on the eventual outcome nor did the frequency of acute tubular necrosis or rejection episodes. Patients with severely impaired renal function with serum creatinine levels greater than or equal to 300 mumol/l have a poor outlook but there are no particular prognostic features on which to base a forecast for the individual patient.
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PMID:Outcome of renal transplants with impaired renal function at 6 months. 354 50

Of 48 patients with fulminant hepatic failure who progressed to grade III or IV encephalopathy 38 showed evidence of renal impairment. In 32 of these patients the underlying cause could be placed initially into one of three categories-prerenal uraemia (4 patients), acute tubular necrosis (16), and "functional renal failure" (12). The latter differed in several respects from that seen with liver failure secondary to cirrhosis. The frequency and type of renal impairment was the same in those patients in whom the fulminant hepatic failure had resulted from an overdose of paracetamol as in the other aetiological groups.Abnormalities in plasma electrolytes were common-in particular hypernatraemia occurred in 11 patients from an osmotic diuresis precipitated by hypertonic dextrose or fructose given intravenously, and from the sodium in the fresh frozen plasma used to correct the coagulation disturbance when renal excretion of this ion was inappropriately low.
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PMID:Frequency and type of renal and electrolyte disorders in fulminant hepatic failure. 481 48

An animal model is described in which mild transitory renal impairment is induced with glycerol and the nephrotoxic effects of cephalosporin antibiotics and furosemide studied. Cephaloridine and cephalothin were found to produce extensive acute tubular necrosis in rats when given in subnephrotoxic doses in combination with furosemide; this damage occurred at serum antibiotic levels not much higher than those obtained in clinical practice. No significant renal damage was found with cephalexin or Cephapirin given in equivalent dosage. It is suggested that the cephalosporin antibiotics should be used with caution in the presence of even minor transient renal impairment and particularly if furosemide is being given concurrently.
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PMID:Relative nephrotoxicity of cephalosporin antibiotics in an animal model. 507 52

We have previously shown that the rat with experimental diabetes (DM) of 4-6 months' duration exhibits complete functional and morphologic protection against gentamicin-induced acute renal failure. To assess the role of the duration of the diabetic state per se on the resistance to gentamicin, female Sprague-Dawley rats with diabetes of short (5 days, n = 7), intermediate (5 weeks, n = 5) and long duration (5 months, n = 7) were studied. Diabetes was induced by streptozotocin, 50-65 mg/kg b.w. i.v. Controls were identically treated sex- and age matched nondiabetic rats. The animals were kept in individual metabolic cages for 2 weeks and all received gentamicin 40 mg/kg/day for 9 days. Sham animals (DM and control) received Ringer's solution in place of gentamicin. Prior to gentamicin, plasma glucose levels and creatinine clearances (Ccr) were higher in the DM long duration group (619 +/- 25 (SE) mg/dl; 2.6 +/- 0.2 ml/min, respectively) than in the DM short (514 +/- 24; 2.0 +/- 0.1) and DM intermediate duration (442 +/- 30; 2.1 +/- 0.1) groups, while urine volume and glycosuria were similar. Following gentamicin the three control groups developed acute renal failure (maximal decrease in Ccr of 60 +/- 7, 72 +/- 9 and 71 +/- 7%, respectively; p less than 0.01 to less than 0.001), lysozymuria and acute tubular necrosis. There were no significant differences in the degree of renal impairment observed among the three control groups. In marked contrast, in the three DM groups these changes were absent and the renal cortical gentamicin content was lower than that of the control groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of duration of diabetes on the protection observed in the diabetic rat against gentamicin-induced acute renal failure. 672 8


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