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)

An episode of acute pustular psoriasis in a middle-aged man was associated with cholestatic jaundice and followed by acute tubular necrosis. It is suggested that renal failure was due to oligaemia after the loss of albumin into and from the skin. Fluid balance, central venous pressure, and arterial blood pressure should be monitored in patients with acute pustular psoriasis.
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PMID:Oligaemia, renal failure, and jaundice associated with acute pustular psoriasis. 483 97

The biochemistry laboratory records of a 400-bed general hospital serving a population of about 120,000 showed that during the three-year period 1966-8 inclusive 487 patients had at some stage during their admission a blood urea of 100 mg/100 ml or more. Ninety per cent. were aged 50 or over, 79% were 60 or over, and 52% were 70 or over.The case notes of all patients with renal failure admitted during 1966 and 1967 were examined together with those of patients under 60 admitted during 1968. Three observers agreed about the most likely cause of the renal failure in 90% of patients whose case notes were available, or 74% of the total. The raised blood urea was thought to be due to "prerenal" factors in 60% of the patients, to acute tubular necrosis in 80%, to obstructive uropathy in 12%, and to "intrinsic" renal disease in 20%. Renal failure precipitated by such factors as cardiac failure, chest infections, cerebrovascular accidents, and shock was particularly common in old people.The hospital survey and replies to a questionnaire sent to all general practitioners in the area suggest that in the three-year period 14 patients may have been suitable for treatment by maintenance haemodialysis or renal transplantation. This represents a rate of about 39 per million per year under the age of 60 and 28 per million per year under 50.
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PMID:Incidence of uraemia and requirements for maintenance haemodialysis. 521 79

Of 41 cases of acute paracetamol poisoning one died of gastrointestinal haemorrhage and acute massive necrosis of the liver, three became jaundiced, and 13 others had biochemical evidence of hepatocellular damage. Liver damage is a toxic effect which is present in most patients who ingest more than 15 g. of paracetamol. One patient with liver damage survived renal failure due to acute tubular necrosis. It is suggested that the renal lesion was also the result of paracetamol overdosage.Profound hypoglycaemia and metabolic acidosis may also complicate severe poisoning. Plasma levels of para-aminophenol fall rapidly, and procedures currently used to enhance the elimination of the drug cannot be expected to prevent development of hepatic damage.
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PMID:Acute paracetamol poisoning. 531 16

Six cases of edema, three due to the nephrotic syndrome, one to congestive heart failure and two to chronic renal failure, are reported in which furosemide was administered in oral doses higher than those usually prescribed (up to 720 mg. a day), in order to obtain a satisfactory diuresis. In one case of severe prerenal failure secondary to cardiogenic shock and in one case of acute tubular necrosis secondary to hypotension at the time of operation, intravenous doses up to 990 and 1400 mg. per day respectively were able to reverse the oliguria. In eight additional patients who were on chronic hemodialysis, furosemide was administered to the amount of 1000 mg. per day orally in divided doses for two weeks, and produced a moderate diuretic response.The use of high doses of furosemide in edema and renal failure resistant to the usual therapeutic measures appears to be safe and effective.
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PMID:Experiences with high doses of furosemide in renal disease and resistant edematous states. 543 50

High doses of colistin were used in the treatment of severely ill patients with refractory klebsiella chest and urinary tract infections. At the same time renal function was monitored to determine possible nephrotoxicity. In all patients it produced acute renal failure and in some acute tubular necrosis. Though renal failure contributed to the final cause of death in some cases, in the majority death was due to the primary neurological illness.
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PMID:Effects of large doses of colistin sulphomethate sodium on renal function. 548 21

The urine/plasma creatinine ratio (U/P Cr), the urine sodium concentration (UNa), and the diuretic response to mannitol infusion in 23 patients were reviewed in an attempt to differentiate functional renal failure (FRF) from acute tubular necrosis (ATN). FRF was diagnosed if the plasma urea nitrogen (PUN) or serum creatinine stabilized within 72 hours. When renal failure persisted longer, patients had ATN. Subjects dying within 72 hours were excluded. Ten patients had ATN and five survived. The minimum duration of renal failure among survivors was 10 days. None responded to mannitol. Of 13 patients with FRF, 11 survived. Seven of 12 who received mannitol responded with a diuresis. The mean UNa in the patients with ATN was 51.4 mEq./1. +/- 9.48 (SE). The mean U/P Cr was 11.2 +/- 1.12. In patients with FRF, the mean UNa was 14.0 mEq./1. +/- 4.2 and the mean U/P Cr was 42.5 +/- 11.5. A significant overlap was present between the two groups. When UNa was factored by the U/P Cr, the resultant ratio was significantly different for the two groups of patients (P < 0.01), and this proved to be a useful clinical index with which to distinguish FRF from established ATN.
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PMID:Diagnostic indices in acute renal failure. 601 69

Snake venom poisoning accounted for 1.4% of 4360 infants and children admitted to a south Indian hospital during the years 1976-1979 and was the commonest cause of acute renal failure encountered. Most of the 42 children with anuria following snake bite had evidence of intravascular coagulation and acute tubular necrosis. Russell's viper was the only snake recognized in all the cases of anuria in which species identification was possible. Renal failure complicating snake bite was relatively more frequent and more severe in children than in adults.
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PMID:Acute renal failure in children following snake bite. 618 55

A case of acute renal failure associated with captopril administration is reported. A woman, age 57, with a two-year history of hypertension presented with a generalized maculopapular rash preceded by pruritus after three weeks of captopril therapy. Her serum creatinine level on admission was 11.0 mg/dl. Renal biopsy was compatible with acute tubular necrosis without evidence of interstitial nephritis. A skin biopsy did not show any evidence of vasculitis. Captopril was discontinued, and her renal failure reversed over the course of nine days. A year later, the patient has good blood pressure control with stable renal function. Captopril has been associated with renal failure in patients with preexisting renovascular hypertension, and with acute interstitial nephritis in one case. The presentation of this case was similar to the latter case, but the renal biopsy did not show any evidence of acute interstitial nephritis.
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PMID:Acute renal failure, skin rash, and eosinophilia associated with captopril therapy. 622 49

Most antipyretic analgesics can cause acute nephrotoxic effects, including acute tubular necrosis, acute interstitial nephritis, glomerular toxicity, and functional changes, such as "salicyl edema," following large doses of sodium salicylate. Most functional changes are related to acute suppression of prostaglandin synthesis, "the acute prostaglandin-effect," and have been primarily noted with the use of indomethacin. The association between prolonged and excessive consumption of compound analgesics and the development of renal disease and renal failure, characterized by renal papillary necrosis, is now well established. Studies in several countries have shown that the incidence of analgesic nephropathy as an indication for dialysis and transplantation corresponds to the per capita consumption of phenacetin in compound analgesics. Analgesic nephropathy, which is part of a wider clinical syndrome, the analgesic syndrome, is uncommon following the use of single analgesics. Analgesic nephropathy and the analgesic syndrome are discussed in detail, including the development of uroepithelial tumors.
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PMID:Renal effects of antipyretic analgesics. 635 70

Patients with renal disease are at risk of further deterioration of renal function and acute tubular necrosis when subjected to anaesthesia and surgery. Optimal fluid loading and careful selection of anaesthetic techniques and agents, appropriate monitoring and the use of mannitol and dopamine assist in the maintenance of renal blood flow and help preserve renal function in these patients. In association with renal failure, physiological changes in other systems result in reduced oxygen supply to the tissues, metabolic disturbances, impairment of the coagulation and immune defence mechanisms and an increased risk of cardiac and cerebrovascular catastrophe. Although many anaesthetic techniques including regional analgesia may be used successfully in these patients caution with most drugs, especially pethidine, phenoperidine, suxamethonium and all non-depolarising neuromuscular relaxants is recommended. Of the volatile anaesthetics currently available, halothane is the agent of choice. Oxygen therapy and close monitoring of cardiorespiratory function are necessary postoperatively.
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PMID:Anaesthesia for the patient with impaired renal function. 635 49


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