Acute Renal Failure in an Alcoholic Patient Taking Therapeutic Doses of Acetaminophen

Maze, Gregory L.; Lee, Makau

doi:10.3122/15572625-11-5-410

Cited by 9 publications

(8 citation statements)

References 8 publications

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“…23 The renal function can be expected to return to baseline within 4 weeks unless multiple organ failure develops. [7][8][9]17 There is no report in the literature of patient mortality occurring without hepatic failure.…”

Section: Discussionmentioning

confidence: 99%

“…30 Compared to the liver, the cytochrome P450 enzymes in the kidney are less able to detoxify paracetamol. 7 Thus, the renal glutathione stores are depleted more rapidly, and kidney cell injury occurs as acute tubular necrosis.…”

Section: Mechanism Of Renal Injurymentioning

confidence: 99%

“…5 In 45 adolescents aged 12 to 18 years, mild and severe nephrotoxicity was observed in 8.9% and 2.2% of patients respectively. 6 While many reports associate the renal effects of large doses of paracetamol with severe hepatotoxicity or hepatic failure, 7 there are also reports of paracetamol-induced renal failure in patients with mild, or no evidence of hepatotoxicity. [6][7][8][9][10][11][12][13][14][15][16][17][18] The objectives of this case report are to describe the clinical presentation of nephrotoxicity with acute paracetamol overdose in a low-risk patient, and to discuss the literature on paracetamol-induced nephrotoxicity.…”

Section: Introductionmentioning

confidence: 99%

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Nephrotoxicity Associated with Acute Paracetamol Overdose: A Case Report and Review of the Literature

Loh¹,

Ponampalam

2006

Hong Kong j. emerg. med.

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A 29-year-old, 65 kg, Chinese man presented to hospital 10 hours after ingesting 30 g of paracetamol (462 mg/kg body weight). The blood paracetamol level was 145 µg/ml at 10 hours post-ingestion. He had no known risk factors for hepatotoxicity and was treated with intravenous N-acetylcysteine (NAC). Serum creatinine level rose to a maximum of 455 µmol/L on day 8; it gradually declined without the need for dialysis. Little is known of the risk factors for nephrotoxicity, which may occur with or without concurrent liver damage, suggesting possible primary toxic effects on the kidney. The use of NAC in this case may have prevented the progression to liver failure and reduced the severity of the nephrotoxic effects. (Hong Kong j. emerg.med. 2006;13:105-110) 29 65 kg 30 g 462 mg/kg 10 145 µg/ml 10 8 455 µmol/L

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Section: Discussionmentioning

confidence: 99%

Section: Mechanism Of Renal Injurymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Nephrotoxicity Associated with Acute Paracetamol Overdose: A Case Report and Review of the Literature

Loh¹,

Ponampalam

2006

Hong Kong j. emerg. med.

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“…7 Clinically, acetaminophen toxicity has been postulated to manifest in 3 phases. 9 Within the first 24 hours, patients may complain of gastrointestinal symptoms such as nausea, vomiting, anorexia, and abdominal pain. During the next 24 to 48 hours, the gastrointestinal symptoms tend to subside, which can lead to underestimation of the severity of the underlying illness.…”

Section: Discussionmentioning

confidence: 99%

43-Year-Old Man With Ear Pain, Confusion, and Agitation

Anavekar

Mangan²

2006

Mayo Clinic Proceedings

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“…Several case reports have appeared in the literature describing acute hepatotoxicity in alcoholic subjects consuming acetaminophen. 1,2,[4][5][6][7][8][9][10][11][12] Hepatotoxicity occurred in most of the heavy drinkers as a result of a large overdose and delay in receiving treatment with N-acetylcysteine. 37 A case study reported a 58-year-old woman with rheumatoid arthritis who consumed acetaminophen 15-20 g/day for 5 years without sequelae of hepatotoxicity.…”

Section: Acetaminophen-induced Hepatotoxicity In Alcoholic Subjectsmentioning

confidence: 99%

Acetaminophen Usage Patterns and Concentrations of Glutathione and γ‐Glutamyl Transferase in Alcoholic Subjects

Seifert

Anderson

2007

Pharmacotherapy

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Daily drinkers were more than twice as likely as non daily drinkers to be regular daily acetaminophen users and abusers. Alcoholic subjects with elevated GGT concentrations had significantly lower plasma total glutathione concentrations, and plasma total glutathione concentrations inversely correlated with GGT concentrations. Elevated GGT concentrations may be a clinical marker of depleted glutathione in alcoholic subjects. Acetaminophen-induced hepatotoxicity appears to be uncommon in alcoholic subjects, despite the 31.9% (60/188 patients) who took doses that are potentially hepatotoxic.

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Acute Renal Failure in an Alcoholic Patient Taking Therapeutic Doses of Acetaminophen

Cited by 9 publications

References 8 publications

Nephrotoxicity Associated with Acute Paracetamol Overdose: A Case Report and Review of the Literature

Nephrotoxicity Associated with Acute Paracetamol Overdose: A Case Report and Review of the Literature

43-Year-Old Man With Ear Pain, Confusion, and Agitation

Acetaminophen Usage Patterns and Concentrations of Glutathione and γ‐Glutamyl Transferase in Alcoholic Subjects

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