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An Overview of Drug-Induced Nephropathies *
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Jean Paul Fillastre, Michel Godin
Radiocontrast material may be an important cause of acute renal failure. The true incidence of acute renal failure in the entire population at risk cannot be established since incidences vary, depending on the population studied and the criteria used to diagnose nephrotoxicity. It may be less than 0.5% in apparently healthy subjects, but can affect a great number of elderly subjects with diabetes, arteriosclerosis, and chronic renal failure. The list of risk factors purported to predispose to radiocontrast-induced acute renal failure is long, but very frequently, underlying renal insufficiency and the presence of diabetes mellitus are the two major risk factors. Despite some case reports documenting multiple myeloma as a high-risk state for the development of acute renal failure, the overall risk for this complication is relatively small.
Pharmacology
Published in Bhaskar Punukollu, Michael Phelan, Anish Unadkat, MRCPsych Part 1 In a Box, 2019
Bhaskar Punukollu, Michael Phelan, Anish Unadkat
In toxicity: CNS effects – muscle weakness, ataxia, tremor (coarse), drowsiness. Gl upset – nausea, diarrhoea, anorexia. Disorientation and seizures, coma and death can occur if levels go above 2 mmol/L. Long term treatment may lead to nephrotoxicity. Small reduction in glomerular filtration rate is seen in 20% of patients – usually benign. Very small number of patients may develop interstitial nephritis. Lithium can also cause nephrogenic diabetes insipidus which may be irreversible after long term treatment (>15 years).
EFFECT OF Plectranthus wightii METHANOL EXTRACT AGAINST GENTAMICIN-INDUCED NEPHROTOXICITY IN RAT
Published in V. R. Mohan, A. Doss, P. S. Tresina, Ethnomedicinal Plants with Therapeutic Properties, 2019
K. Subramonian, A. Saravana Ganthi, M. Padma Sorna Subramanian, S. L. Subha
Nephrotoxicity is one of the most common kidney problems. It occurs when a body is exposed to a drug or toxin (Porter, 1981). A number of therapeutic agents can adversely affect the kidney resulting in acute renal failure, chronic interstitial nephritis, and nephritic syndrome because there is an increasing number of potent therapeutic drugs such as aminoglycoside antibiotics, NSAIDs, and chemotherapeutic agents that have been added to the therapeutic arsenal in recent years. Exposure to chemical reagents such as ethylene glycol, carbon tetrachloride, sodium oxalate, and heavy metals such as lead, mercury, cadmium, and arsenic also induces nephrotoxicity. Prompt recognition of the disease and cessation of responsible drugs are usually the only necessary therapy. Nephroprotective agents are the substances which possess protective activity against nephrotoxicity.
Further insights into the impact of rebamipide on gentamicin-induced nephrotoxicity in rats: modulation of SIRT1 and β-catenin/cyclin D1 pathways
Published in Drug and Chemical Toxicology, 2023
Heba S. Zaky, Somaia A. Abdel-Sattar, Albatoul Allam, Hebatalla I. Ahmed
Gentamicin (GM) is an effective antibiotic administered to treat acute and life-threatening infections caused by Gram-negative microorganisms (Ahmed and Mohamed 2019). To date, GM is used despite its negative side effects, such as nephrotoxicity and ototoxicity (Mahi-Birjand et al.2020). Nephrotoxicity is primarily caused by the accumulation of the drug in the proximal tubular cells (Lopez-Novoa et al.2011, Randjelovic et al.2017). The drug causes a variety of adverse effects in these cells, including excessive oxidative stress, inflammation, apoptosis, and phospho-lipidosis, in addition to mitochondrial dysfunction. These events may eventually cause tubular dysfunction, cell death, and decreased glomerular filtration rate (GFR) (Martínez-Salgado et al.2007, Lopez-Novoa et al.2011, Abd-Elhamid et al.2018). As a result, medications that control oxidative stress, inflammation, and apoptosis could be used to prevent GM-induced nephrotoxicity (Famurewa et al.2020).
Rivaroxaban-loaded SLNs with treatment potential of deep vein thrombosis: in-vitro, in-vivo, and toxicity evaluation
Published in Pharmaceutical Development and Technology, 2023
Xuemei Luo, Aiman Saleem, Uswa Shafique, Sadia Sarwar, Kalim Ullah, Muhammad Imran, Alam Zeb, Fakhar ud Din
Cytotoxicity study revealed that the RXB-SLNs displayed higher cell viability demonstrating that the formulation was safe to the normal cells. The results were in accordance with the cytotoxicity profile of blank SLNs. According to ISO 10993:5, a sample must have a limit value of 70% or less in order to be considered toxic to HEK cells. Even though the cell viability of blank-SLNs was around 99% as compared to the 96% of RXB-SLNs, our results showed that cell viability was well above the specified limit, portraying the safety of RXB-SLNs to the kidney tissue (Figure 6) (ISO 2009). As previously mentioned, approximately 67% of the administered RXB dose is eliminated through the kidneys intact. Due to the RXB-SLNs’ lower toxicity profile, any kidney tissue damage may be prevented, mitigating the drug’s adverse systemic effects (Fordyce et al. 2016). Advanced nephrotoxicity evaluation techniques may need to be used to further assess these findings.
Curcumin protects rats against gentamicin-induced nephrotoxicity by amelioration of oxidative stress, endoplasmic reticulum stress and apoptosis
Published in Pharmaceutical Biology, 2022
Pongrapee Laorodphun, Rada Cherngwelling, Aussara Panya, Phatchawan Arjinajarn
Nephrotoxicity can be a result of hemodynamic changes due to toxic effect of medications and chemicals. Most drugs found to cause nephrotoxicity exert toxic effects by one or more common pathogenic mechanisms (Al-Naimi et al. 2019). Gentamicin (GM) is an aminoglycoside antibiotic used in the treatment of serious infections which caused by Gram-negative bacteria (Balakumar et al. 2010). Although GM is the most frequently used aminoglycoside because of its broad-spectrum activity, rapid bactericidal action and low cost, serious side effects such as nephrotoxicity have limited the clinical use of the drug (Edson and Terrell 1999; Lopez-Novoa et al. 2011). Several reports indicated that up to 30% of patients who received GM for more than seven days showed signs of nephrotoxicity characterized by increases in the serum level of creatinine and blood urea nitrogen (BUN), with a decrease in renal clearance, changes in body weight and urine volume and severe proximal renal tubular necrosis, which eventually result in renal dysfunction and failure (Soliman et al. 2007; Abdel-Raheem et al. 2009).