Acute Renal Failure after Analgesic Drugs Including Paracetamol (Acetaminophen)

Björck, S; Svalander, Christian; Aurell, Mattias

doi:10.1159/000184985

Cited by 42 publications

(23 citation statements)

References 15 publications

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“…The necrosis may be because of direct toxic action on the vascular wall or because of impaired oxygen delivery caused by injury of the capillary wall [45]. The granular material in the cell lumens has been postulated to be an accumulation of cellular material denatured as a result of the toxic action of APAP or its metabolites, or intracellular calcium accumulation [46].…”

Section: Discussionmentioning

confidence: 99%

Melatonin prevents acetaminophen-induced nephrotoxicity in rats

İlbey¹,

Özbek²,

Çekmen³

et al. 2009

Int Urol Nephrol

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Nephrotoxicity is a major complication of acetaminophen (APAP), a widely used analgesic and antipyretic drug, and there is no specific treatment for APAP-induced renal damage. It has been reported that reactive oxygen metabolites or free radicals are important mediators of APAP toxicity. In this study, the protective role of melatonin (MLT) on APAP-induced nephrotoxicity was investigated in rats. For this purpose, nephrotoxicity was induced in male Wistar albino rats by intraperitoneal (i.p.) administration of a single dose of 1,000 mg/kg APAP. Some of these rats also received i.p. melatonin (10 mg/kg) 20 min after administration of APAP. The rats were sacrificed 24 h after administration of APAP. Urea and creatinine levels were measured in the blood, and levels of malondialdehyde (MDA) and glutathione (GSH), and glutathione peroxidase (GSH-Px), catalase (CAT), and superoxide dismutase (SOD) activity were determined in renal tissue. Serum urea and creatinine levels increased significantly as a result of APAP nephrotoxicity. A significant increase in MDA and decreases in GSH level and GSH-Px, CAT, and SOD activity indicated that APAP-induced renal damage was mediated through oxidative stress. Significant beneficial changes were noted in serum and tissue oxidative stress indicators in rats treated with MLT. These biochemical observations were supplemented by histopathological examination of kidney sections, which revealed that MLT also reduced the severity of APAP-induced histological alterations in the kidney. These results indicate that administration of APAP causes oxidative stress to renal tissue and that MLT protects against the oxidative damage associated with APAP.

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Section: Discussionmentioning

confidence: 99%

Melatonin prevents acetaminophen-induced nephrotoxicity in rats

İlbey¹,

Özbek²,

Çekmen³

et al. 2009

Int Urol Nephrol

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“…Both medications are analgesicantipyretics and their effects result from inhibition of prostaglandin synthesis, although to a lesser extent than other NSAID [7]. This may explain why ARF is rare after treatment with recommended doses of paracetamol [8]. Acute renal failure has been reported after paracetamol intoxication and may occur without signs of fulminant liver failure [9].…”

Section: Discussionmentioning

confidence: 99%

Acute renal failure, associated with non-steroidal anti-inflammatory drugs in healthy children

et al. 2005

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Seven patients aged 13 to 17.5 years developed acute renal failure after treatment with a variety of non-steroidal anti-inflammatory drugs (NSAID): naproxen, diclofenac, ibuprofen, dipyrone and paracetamol. Six of the patients used more than one kind of NSAID. None of the patients had previous history of renal disease or concomitant treatment with other drugs. The time interval between NSAID administration to the emergence of symptoms ranged from 1 to 4 days. The most common presenting symptoms were flank pain (4 patients), abdominal pain (3 patients) and vomiting (3 patients). All patients had normal urine output. Microscopic hematuria and proteinuria were found in 5 patients and leukocyturia in 2. Serum creatinine ranged from 1.3 to 8.3 mg% at presentation. Kidney biopsy was performed in 3 patients and showed findings consistent with mild interstitial inflammation in 1 patient, and normal renal tissue in 2. All patients were treated with intravenous fluids, 1 received corticosteroids. Renal function completely normalized in all patients within 7 to 16 days.

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“…At the tissue level, these toxins affect the proximal tubule most commonly, although disease may be more diffuse. Light microscopy of renal biopsies in patients with acetaminophen toxicity and renal insufficiency demonstrate tubular epithelial cell necrosis in both proximal and distal parts of the tubules [16]. In some cases, light microscopy demonstrates normal glomeruli and vessels, but with debris and damage to the basement membrane.…”

Section: Histopathologymentioning

confidence: 99%

“…There is no deposition of immunoglobulins or complement on fluorescent microscopy. Electron microscopy is significant for the loss of the tubular brush border with tubular swelling and distortion of mitochondrial organization [16,17].…”

Section: Histopathologymentioning

confidence: 99%

Acetaminophen-induced nephrotoxicity: Pathophysiology, clinical manifestations, and management

2008

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Acetaminophen-induced liver necrosis has been studied extensively, but the extrahepatic manifestations of acetaminophen toxicity are currently not described well in the literature. Renal insufficiency occurs in approximately 1-2% of patients with acetaminophen overdose. The pathophysiology of renal toxicity in acetaminophen poisoning has been attributed to cytochrome P-450 mixed function oxidase isoenzymes present in the kidney, although other mechanisms have been elucidated, including the role of prostaglandin synthetase and N-deacetylase enzymes. Paradoxically, glutathione is considered an important element in the detoxification of acetaminophen and its metabolites; however, its conjugates have been implicated in the formation of nephrotoxic compounds. Acetaminophen-induced renal failure becomes evident after hepatotoxicity in most cases, but can be differentiated from the hepatorenal syndrome, which may complicate fulminant hepatic failure. The role of N-acetylcysteine therapy in the setting of acetaminophen-induced renal failure is unclear. This review will focus on the pathophysiology, clinical features, and management of renal insufficiency in the setting of acute acetaminophen toxicity.Case: A 47-year-old female was found lethargic at home and brought by ambulance to an emergency department. History from family members suggested an inadvertent acetaminophen overdose, and she had last been seen a few hours earlier. She reportedly ingested 18 tablets of 500 mg acetaminophen (APAP) over the previous two days because she had run out of her prescription pain medication. Her past medical history was significant for fibromyalgia, arthritis, and a prior gastric bypass procedure. She had no history of alcohol abuse or renal insufficiency. She was lethargic. Vital signs: BP 128/96 mmHg, pulse 112/min, respirations 32/min; pulse oximetry 98% on 2L nasal cannula oxygen. Laboratory studies: BUN 9 mg/dL, creatinine 0.9 mg/dl, acetaminophen 12 mcg/mL, AST 5409 u/L and ALT 1085 u/L. A urinalysis was negative for blood with trace protein and ketones. A urine drug screen was positive for marijuana and opioid metabolites. At the initial hospital, she was treated with N-acetylcysteine (NAC) orally. Subsequently, she developed fulminant hepatic failure with elevated transaminases, hypoglycemia, and coagulopathy (Tables 1A and 1B). She was transferred

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Acute Renal Failure after Analgesic Drugs Including Paracetamol (Acetaminophen)

Cited by 42 publications

References 15 publications

Melatonin prevents acetaminophen-induced nephrotoxicity in rats

Melatonin prevents acetaminophen-induced nephrotoxicity in rats

Acute renal failure, associated with non-steroidal anti-inflammatory drugs in healthy children

Acetaminophen-induced nephrotoxicity: Pathophysiology, clinical manifestations, and management

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