Acute renal failure is a recognized manifestation of paracetamol toxicity, but comparatively little data is available concerning its onset and duration. The present study sought to characterize the time course of rising serum creatinine concentrations in paracetamol nephrotoxicity. Renal failure was defined by serum creatinine concentration ≥150 μmol/L (1.69 mg/dL) or ≥50% increase from baseline. Serum creatinine concentrations and alanine aminotransferase activity were considered with respect to the interval after paracetamol ingestion. There were 2068 patients with paracetamol overdose between March 2005 and October 2007, and paracetamol nephrotoxicity occurred in 8 (0.4%). All had significant hepatotoxicity, and peak serum alanine aminotransferase activity occurred at 2.5 days (2.2 to 2.9 days) after ingestion. Peak serum creatinine concentrations did not occur until 5.5 days (4.4 to 5.9 days) after ingestion (p = .031 by Wilcoxon test). Serum creatinine concentrations slowly restored to normal, and renal replacement was not required. In this patient series, rising serum creatinine concentrations only became detectable after more than 48 hours after paracetamol ingestion. Therefore, renal failure might easily be missed if patients are discharged home before this. Further work is required to establish the prevalence of paracetamol-induced nephrotoxicity, and its clinical significance.
Antidepressant overdose is associated with impaired heart rate variability in a pattern consistent with excess cardiac sympathetic activity. Further work is required to establish the significance of these findings and to explore whether the impairment of heart rate variability may be used to predict the development of arrhythmia in this patient group.
Background: Acute renal failure is a recognized complication of acute acetaminophen overdose. Its detection depends on rising creatinine concentrations, which is an insensitive method. The present study examined whether proteinuria might correspond with the extent of acute acetaminophen exposure as a possible early marker of renal effects.Methods: A prospective case-control study included patients attending the emergency department within 24 hours of acetaminophen ingestion. A urine specimen was collected within 12 hours of hospital attendance for creatinine, albumin, and protein determination. Equivalent 4-hour acetaminophen concentrations were used to indicate drug exposure:. Data are presented as median (interquartile range) and groups compared using Mann Whitney and chi-square tests.Results: Seventy patients were studied (17 men, 53 women), age 37 years (23-45 years). The stated acetaminophen dose was 15 g (8-20 g), and interval between ingestion and presentation was 4.6 hours (4.1-7.9 hours). Urinary albumin concentrations were 8 mg/L (0-12 mg/L) in the mild group, 12 mg/L (5-25 mg/L) in the moderate group, and 11 mg/L (6-22 mg/L) in the severe group. Total protein concentrations were 90 mg/L (50-183 mg/L), 70 mg/L (40 to 130 mg/L), and 110 mg/L (75-205 mg/L), respectively. The proportions of patients who had urine albumin:creatinine ratio Ͼ3 mg/mmol were 20.8%, 23.5%, and 21.2%, respectively. None of the patients developed acute renal failure.
Conclusions:No relationship was found between the extent of acute acetaminophen exposure and proteinuria. Further work is required to examine whether urinary protein excretion is altered in patients who subsequently develop acute renal failure following acetaminophen overdose.
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