Articles tagged with Renal Toxicity
A recent study published in Cell Biology and Toxicology found that high concentrations of nanoplastics can cause damage to kidney cells, leading to changes in cell shape, survival, and function. The research highlights the need for more investigations into the long-term risks of nanoplastic exposure on human health.
A new study by the University of Arizona found that heat exposure and toxic metal exposure can increase signs of kidney injury in agricultural workers. The study suggests that providing mandatory breaks, water, electrolyte replacement, and restrooms nearby can help prevent heat-related illnesses and kidney damage.
Researchers analyzed data from over 700 patients with kidney injury and found that glucarpidase treatment improved kidney recovery rates. Glucarpidase rapidly clears methotrexate from the blood, reducing the risk of kidney toxicity.
Researchers at Boston Medical Center have identified six new biomarkers that could detect kidney injury faster and with more sensitivity. These biomarkers can be measured in the urine and may offer a more sensitive approach than existing standards for monitoring kidney health.
Researchers have found a compound that can prevent cisplatin-induced renal toxicity and improve the outcomes of cancer treatment. The aromatic ketone 2',4',6'-trihydroxyacetophenone (THA) inhibits the CCBL1-mediated metabolism of cisplatin, reducing its toxic effects without affecting its potency.
A neglected 80-year-old antibiotic, nourseothricin, has been found to be effective against multi-drug resistant bacterial infections. The improvement in purification of the streptothricins has overcome original toxicity concerns, making it a promising agent for treating difficult-to-treat infections.
Researchers at Georgia Health Sciences University have identified PKC-delta as a critical regulator of cisplatin-mediated kidney toxicity. Inhibiting this protein not only protected the kidneys but also enhanced the antitumor effects of cisplatin in mouse tumor models.