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Nephrotoxicity (kidney damage) is the primary dose-limiting side effect and is of major clinical concern. Cisplatin selectively accumulates into the proximal tubule via basolateral-to-apical transport, where it disrupts mitochondrial energetics and endoplasmic reticulum Ca 2+ homeostasis and stimulates reactive oxygen species and pro ...
Amifostine, approved by the FDA in 1995, which helps prevent kidney damage in patients undergoing cisplatin and carboplatin chemotherapy; Mesna, approved by the FDA in 1988, which helps prevent hemorrhagic cystitis (bladder bleeding) in patients undergoing cyclophosphamide or ifosfamide chemotherapy
Myelosuppression, diarrhoea, kidney failure, hypersensitivity, severe GI reactions (including perforation, ileus, colitis, etc.; all rare) and peripheral neuropathy Docetaxel: IV: As above. Breast cancer, non-small cell lung cancer, ovarian cancer, prostate cancer, squamous cell head and neck cancer and gastric cancer.
There are various forms, [2] and some drugs may affect kidney function in more than one way. Nephrotoxins are substances displaying nephrotoxicity. Nephrotoxicity should not be confused with some medications predominantly excreted by the kidneys needing their dose adjusted for the decreased kidney function (e.g., heparin, lithium).
The liver damage can consist of damage to liver cells, hepatic sinusoidal syndrome (obstruction of the veins in the liver), cholestasis (where bile does not flow from the liver to the intestine) and liver fibrosis. [127] [128] Nephrotoxicity (kidney damage) can be caused by tumor lysis syndrome and also due direct effects of drug clearance by ...
In her further research on cancer chemotherapy, she explored how cisplatin selectively kills proximal tubule cells, identified its metabolic pathway to a nephrotoxin, and showed that the metabolism in these cells is crucial for cisplatin-induced kidney damage, suggesting new targets for inhibition. [10]
Damage from oxygen radicals, inflammatory cells and molecules, edema, and other mechanisms mean that when oxygen flow is restored to the tissue, it can cause further damage to the kidney, potentially worsening prognosis. Despite this risk, the return of blood flow to the tissue is necessary for its survival, so clinical strategies focus on ...
There is a small amount of evidence supporting the use of sodium thiosulfate to counteract calciphylaxis, the calcification of blood vessels that may occur in hemodialysis patients with end-stage kidney disease. [15] [16] However, it has been claimed that this treatment may cause severe metabolic acidosis in some patients. [17] [18]