Diclofenac-Associated Acute Renal Failure

Rossi, Eugenio; Ferraccioli, G.; Cavalieri, F; Menta, R.; Dall'Aglio, P; Migone, L

doi:10.1159/000183528

Cited by 20 publications

(4 citation statements)

References 13 publications

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“…Indeed, these drugs are potent nonselective inhibitors of the cyclooxygenases 1 and 2 (COX1 and COX2) used for the treatment of chronic inflammatory diseases such as osteoarthritis and rheumatoid arthritis. As many other nonselective COX inhibitors, the most significant side effects induced by diclofenac and indomethacin are GI complications such as bleeding and ulceration, hypersensitivity reactions (e.g., anaphylaxis, skin eruptions, and bronchospasms), and kidney injury (Rossi et al 1985;Richy et al 2004;Gonzalez et al 2009;Castellsague et al 2012;Wallace 2012). These drugs can also induce hepatotoxicity, mostly cytolytic hepatitis and cholestasis (Banks et al 1995;Biour et al 2004;Wang et al 2013a).…”

Section: Diclofenac and Indomethacinmentioning

confidence: 99%

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Role of endoplasmic reticulum stress in drug‐induced toxicity

Foufelle

Fromenty

2016

Pharmacology Res & Perspec

194

161

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Drug‐induced toxicity is a key issue for public health because some side effects can be severe and life‐threatening. These adverse effects can also be a major concern for the pharmaceutical companies since significant toxicity can lead to the interruption of clinical trials, or the withdrawal of the incriminated drugs from the market. Recent studies suggested that endoplasmic reticulum (ER) stress could be an important event involved in drug liability, in addition to other key mechanisms such as mitochondrial dysfunction and oxidative stress. Indeed, drug‐induced ER stress could lead to several deleterious effects within cells and tissues including accumulation of lipids, cell death, cytolysis, and inflammation. After recalling important information regarding drug‐induced adverse reactions and ER stress in diverse pathophysiological situations, this review summarizes the main data pertaining to drug‐induced ER stress and its potential involvement in different adverse effects. Drugs presented in this review are for instance acetaminophen (APAP), arsenic trioxide and other anticancer drugs, diclofenac, and different antiretroviral compounds. We also included data on tunicamycin (an antibiotic not used in human medicine because of its toxicity) and thapsigargin (a toxic compound of the Mediterranean plant Thapsia garganica) since both molecules are commonly used as prototypical toxins to induce ER stress in cellular and animal models.

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Section: Diclofenac and Indomethacinmentioning

confidence: 99%

“…As many other nonselective COX inhibitors, the most significant side effects induced by diclofenac and indomethacin are GI complications such as bleeding and ulceration, hypersensitivity reactions (e.g., anaphylaxis, skin eruptions, and bronchospasms), and kidney injury (Rossi et al. 1985; Richy et al. 2004; Gonzalez et al.…”

Section: Introductionmentioning

confidence: 99%

Role of endoplasmic reticulum stress in drug‐induced toxicity

Foufelle

Fromenty

2016

Pharmacology Res & Perspec

194

161

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“…> 50 ml/min; reduction from 164 to 74 ml/min). However, it is important to note that from 7 days after the first course until 4 weeks after the second course of lometrexol this patient also received diclofenac, a non steroidal anti-flammatory drug (NSAID), which can effect renal function and cause acute renal failure [16]. Although it appears that NSAIDs have little effect on the GFR in normal controls [17], in high renin states including cirrhosis, NSAID treatment was found to decrease GFR [18].…”

Section: Discussionmentioning

confidence: 99%

A Phase I clinical study of the antipurine antifolate lometrexol (DDATHF) given with oral folic acid

et al. 1996

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Lometrexol is an antifolate which inhibits glycinamide ribonucleotide formyltransferase (GARFT), an enzyme essential for de novo purine synthesis. Extensive experimental and limited clinical data have shown that lometrexol has activity against tumours which are refractory to other drugs, notably methotrexate. However, the initial clinical development of lometrexol was curtailed because of severe and cumulative antiproliferative toxicities. Preclinical murine studies demonstrated that the toxicity of lometrexol can be prevented by low dose folic acid administration, i.e. for 7 days prior to and 7 days following a single bolus dose. This observation prompted a Phase I clinical study of lometrexol given with folic acid supplementation which has confirmed that the toxicity of lometrexol can be markedly reduced by folic acid supplementation. Thrombocytopenia and mucositis were the major toxicities. There was no clear relationship between clinical toxicity and the extent of plasma folate elevation. Associated studies demonstrated that lometrexol plasma pharmacokinetics were not altered by folic acid administration indicating that supplementation is unlikely to reduce toxicity by enhancing lometrexol plasma clearance. The work described in this report has identified for the first time a clinically acceptable schedule for the administration of a GARFT inhibitor. This information will facilitate the future evaluation of this class of compounds in cancer therapy.

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“…This may explain that co-administration of CIP could attenuate enterohepatic circulation of DCF and alleviated DCF-induced enteropathy. Sever hepatic injuries and nephrotoxicity have been reported to be induced by DCF and by CIP as well [35][36][37][38]. On the other hands, DCF causes dose-dependent significant increase in renal and hepatic fibroses [39] but CIP does not [40,41], however, the molecular mechanism is not yet fully explored.…”

Section: Figure 4kidney Tissues Of Group a Show Normal Glomeruli (White Arrows) Normal Renal Tubules (Black Arrows) With Intact Well Orgamentioning

confidence: 99%

Hepatorenal Effects of Diclofenac and Ciprofloxacin in Rats

Abdelgadir

Alzaidi

Ramady³

et al. 2021

AJFSFM

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The toxic effect of diclofenac (DCF) sodium and Ciprofloxacin (CIP) on gene expression of cytochrome P450 oxidase (CYPs) and the histology of liver and kidney of male albino rat has been evaluated in this study. DCF and CIP were chosen since they are inhibitors for specific CYP enzymes. Thirty-five adult male albino rats were divided into 7 groups of 5 animals each (A, B, C, D, E, F and G) and were treated orally with drugs for 21 consecutive days. Group A served as the control while B and C were treated with 5.3, 10.6 mg/kg body weight (bw) DCF sodium and groups D and E were treated with 40 and 80 mg/kg bw CIP, respectively. Groups F and G were treated with a mixture of the low and the high doses of both drugs, respectively. Both drugs significantly downregulated the mRNA expression of CYP1a2, CYP3a4 and CYP2c9. They caused hepatorenal histological changes. In the liver, massive fibrosis, necrosis, inflammatory cell infiltration with hemorrhages and hydrophilic degeneration have been observed. A massive tissue injury with glomerular and tubular damages due to sever necrosis, degeneration of concomitant inflammatory cells and blood vessels congestion have been shown in renal tissues. Although DCF and CIP are still used as therapeutic drugs, their use should be limited as their chronic administration induces a toxic effect on human health.

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Diclofenac-Associated Acute Renal Failure

Cited by 20 publications

References 13 publications

Role of endoplasmic reticulum stress in drug‐induced toxicity

Role of endoplasmic reticulum stress in drug‐induced toxicity

A Phase I clinical study of the antipurine antifolate lometrexol (DDATHF) given with oral folic acid

Hepatorenal Effects of Diclofenac and Ciprofloxacin in Rats

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