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Role of Transport in Chemically-Induced Nephrotoxicity *
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Several physiological factors have been suggested as explanations for the sensitivity of the kidney to the toxic effects of chemicals. Many have cited the high renal blood flow (approximately 25% of the cardiac output) to be a primary consideration. The high renal blood flow can be responsible for the delivery of large quantities of any substance present in the blood. The kidney might be in a position to accumulate large quantities of the chemical if it can readily cross the various biological membranes. The accumulation by passive means of large quantities of potentially nephrotoxic compounds might lead to high intracellular concentrations which could disrupt renal function.
Antiviral therapeutics for viral infections of the central nervous system
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Foscarnet has been associated with significant renal toxicity, and dose adjustments are necessary when the creatinine clearance is ≤1.4 mL min−1 kg−1. Prehydration with saline has been shown to reduce the incidence of nephrotoxicity, as has avoidance of concurrent nephrotoxic therapy [39,40]. Nephrotoxicity and electrolyte disturbances are the major side effects associated with foscarnet. Serum creatinine elevations of up to three-fold are observed in about half of recipients. Risk factors for renal dysfunction include preexisting renal disease and concurrent use of other nephrotoxic drugs. In addition, factors such as hydration status and manner of infusion also affect nephrotoxicity [41]. Renal toxic effects are typically reversible within 2–4 weeks of discontinuing therapy. Foscarnet is a chelating agent that can cause significant electrolyte abnormalities, including hypo- and hypercalcemia and hypo- and hyperphosphatemia [42]. Hypocalcemia is seen in up to a third of patients, and can result in seizures, tetany, and arrhythmias. Hypomagnesemia and hypokalemia can also occur in some patients. CNS side effects include headache, seizures, hallucinations, tremors, and neuropathies. Other adverse effects include fever, nausea, vomiting, hepatic dysfunction, and cytopenias [1].
Contrast enhancement agents and radiopharmaceuticals
Published in A Stewart Whitley, Jan Dodgeon, Angela Meadows, Jane Cullingworth, Ken Holmes, Marcus Jackson, Graham Hoadley, Randeep Kumar Kulshrestha, Clark’s Procedures in Diagnostic Imaging: A System-Based Approach, 2020
A Stewart Whitley, Jan Dodgeon, Angela Meadows, Jane Cullingworth, Ken Holmes, Marcus Jackson, Graham Hoadley, Randeep Kumar Kulshrestha
There is action that can be taken to minimise the risks of CIN to the patient: Use of a small volume of low-osmolar or iso-osmolar non-ionic contrast agent.Use of volume repletion (saline/sodium bicarbonate).Review of patient medications and stopping nephrotoxic drugs if necessary.Use of a method of pharmacotherapy.If deemed necessary by a clinician, the patient can be referred for haemofiltration.
Acute kidney injury in COVID 19 – an update on pathophysiology and management modalities
Published in Archives of Physiology and Biochemistry, 2023
Manoj Khokhar, Purvi Purohit, Dipayan Roy, Sojit Tomo, Ashita Gadwal, Anupama Modi, Mithu Banerjee, Praveen Sharma
Several emerging novel AKI biomarkers like kidney injury molecule 1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), IL-18, cystatin C, and liver-type fatty acid-binding protein (L-FABP) have yet to be explored for their usefulness in diagnosing and early management of AKI in COVID-19 (Alge and Arthur 2015). Various nephrotoxic drugs prescribed in the initial stage of SARS-CoV-2 infection should be advised with caution, keeping in view the risk-benefit ratio and increased incidence of AKI. Some of the nephrotoxic drugs used includes (NSAIDs), antibacterial drugs (Quinolones, Aminoglycosides, Rifampin, Sulphonamides, Vancomycin), antiviral therapy (Adefovir, cidofovir, tenofovir Indinavir, Acyclovir), and traditional medicine (Chinese herbals with aristocholic acid) (Naughton 2008). Early diagnosis of COVID-19 associated AKI and initiation of treatment, including adequate hemodynamic support, therapeutic management, and avoidance of nephrotoxic drugs may help to improve the prognosis of these patients (Gabarre et al.2020, p. 19). Loop diuretics should not be used directly for the treatment of AKI but can be used for fluid balance management (Selby et al.2020).
Does snake envenoming cause chronic kidney disease? A cohort study in rural Sri Lanka
Published in Clinical Toxicology, 2023
Subodha Waiddyanatha, Anjana Silva, Kosala Weerakoon, Sisira Siribaddana, Geoffrey K. Isbister
AKI during the acute stage of envenoming occurs in bites by some true vipers, pit vipers, and Australasian elapids [4]. No specific direct nephrotoxin has been identified, but there is some evidence for a primary nephrotoxin [4–6]. Secondary mechanisms such as hypotension and thrombotic microangiopathy are thought to be the more likely mechanisms of AKI in envenomed humans. AKI in snake envenoming is managed with or without renal replacement therapy after antivenom. However, up to 72% of the patients by three months and 52% by one year have ongoing renal dysfunction, with reports of subsequent progression to chronic kidney disease (CKD) [3,4,7–12]. Most of these reports are of envenomings by viperine snakes, Russell’s viper (Daboia russelii), and Hump-nosed vipers (Hypnale spp.) in Sri Lanka and India.
Nephrotoxicity induced by natural compounds from herbal medicines – a challenge for clinical application
Published in Critical Reviews in Toxicology, 2022
Jinqiu Rao, Ting Peng, Na Li, Yuan Wang, Caiqin Yan, Kai Wang, Feng Qiu
The biomarkers released directly into the blood or urine by the kidneys in response to injury may be better early markers of drug-induced kidney toxicity. Screening for early nephrotoxicity markers by multi-omics techniques (such as metabolomics) has become a popular method (Mussap et al. 2014). Urinary albumin and urinary protein, as well as kidney injury molecule-1 (KIM-1), β2-microglobulin (β2-M), cystatin C (CysC), agglomerin, and trefoilfactor-3 (TFF-3), have been accepted by the Ministry of Food and the European Medicines Agency as highly sensitive and specific urine biomarkers, which can be used to monitor drug-induced renal injury individually in preclinical studies and clinical trials (Westhuyzen et al. 2003). The combined use of functional and damaging markers may promote the development of biomarkers of drug nephrotoxicity. Early detection of nephrotoxicity induced by drugs using kidney specific biomarkers may reduce the incidence of nephrotoxic drug use in clinical research.