Chemotherapy-associated renal dysfunction

Sahni, Vaibhav; Choudhury, Devasmita; Ahmed, Ziauddin

doi:10.1038/nrneph.2009.97

Cited by 157 publications

(106 citation statements)

References 142 publications

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“…Leucovorin will restore reduced folate, which has dropped due to high doses of methotrexate. After conversion into its active metabolite, 5-methyltetrahidrofolate, it will help to reduce toxicity that may result from high doses of methotrexate (Sahnl et al 2009).…”

Section: Discussionmentioning

confidence: 99%

Methotrexate Use Is Safe in Children With Acute Lymphoblastic Leukemia

Utomo¹,

Yulistiani²,

Zairina³

et al. 2017

FMI

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Section: Discussionmentioning

confidence: 99%

Methotrexate Use Is Safe in Children With Acute Lymphoblastic Leukemia

Utomo¹,

Yulistiani²,

Zairina³

et al. 2017

FMI

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“…It is reserved for use when methotrexate levels are toxic, and there is significant risk for systemic toxicity (45). High-flux hemodialysis clears the plasma of methotrexate fairly well (76%) but is associated with immediate postdialysis plasma rebound (1,2). It may have a role when severe AKI is present, but it may become unnecessary with the availability of glucarbidase.…”

Section: Tubules: Crystal Nephropathy Methotrexatementioning

confidence: 99%

“…In fact, nearly 60% of patients with cancer have some form of renal disease (1,2). Direct malignant effects include myeloma-related kidney injury, infiltration of the renal parenchyma as seen with leukemias and lymphomas, urinary tract obstruction from various cancers, and secondary glomerulopathies (2).…”

Section: Renal Susceptibility To Chemotherapeutic Agentsmentioning

confidence: 99%

“…These effects include the clinical and histopathologic manifestations of renal toxicity (1)(2)(3)(4)(5)(6). Clinicians should also be well versed in preventive measures available for the various chemotherapy regimens, as well as effective treatment options for nephrotoxic consequences (1)(2)(3)(4)(5)(6).…”

Section: Introductionmentioning

confidence: 99%

“…Those patients previously considered therapy failures are now deriving significant benefit with decreased tumor progression and increased survival, often with less severe adverse systemic drug effects. Despite this positive advancement in chemotherapeutics for various malignancies, drug nephrotoxicity remains a complication and sometimes limits life-saving therapy (1)(2)(3).…”

Section: Introductionmentioning

confidence: 99%

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Onco-Nephrology

Perazella

2012

Clinical Journal of the American Society of Nephrology

268

197

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SummaryDespite dramatic improvements in patient survival and drug tolerability, nephrotoxicity remains an important complication of chemotherapy. Adverse renal effects occur because of innate drug toxicity and a number of patient-and drug-related factors. To provide cutting edge care for these patients, nephrologists and oncologists must be familiar with the nephrotoxicity of these drugs, particularly their associated clinical and laboratory manifestations. Rapid diagnosis, targeted treatment, and supportive care are critical to improving care for these patients. Unfortunately, some patients who develop nephrotoxicity will be left with long-term complications such as chronic tubulopathies and CKD. Onco-Nephrology is a new area that is rapidly expanding and requires a close working relationship between oncologists and nephrologists.

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Panax notoginseng saponins ameliorate cisplatin‐induced mitochondrial injury via the HIF‐1α/mitochondria/ROS pathway

Liang

Yang

et al. 2019

FEBS Open Bio

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Cisplatin is a major antineoplastic drug that is used to treat solid tumors, but its use is restricted by its nephrotoxicity. Such cisplatin‐induced nephrotoxicity (CIN) is believed to occur primarily through mitochondrial damage and reactive oxygen species (ROS) generation. Our previous studies have indicated that Panax notoginseng saponins (PNSs) mitigate CIN by enhancing hypoxia‐inducible factor 1α (HIF‐1α)‐induced mitochondrial autophagy. In this study, the role of the HIF‐1α/mitochondria/ROS pathway in PNSs protection against CIN was investigated using a rat model. A CIN model was generated by giving rats intraperitoneal injections with cisplatin (a single dose) and then treating them with or without 2‐methoxyestradiol (HIF‐1α inhibitor) and PNSs. We then measured ROS levels, superoxide dismutase, glutathione, catalase malondialdehyde and nitric oxide (to evaluate oxidative stress) and ATP, mitochondrial membrane potential and mitochondrial permeability transition pore opening (to evaluate mitochondrial function) in kidneys at different time points. We observed that PNSs remarkably reduced the levels of ROS, malondialdehyde and nitric oxide, as well as the opening of mitochondrial permeability transition pore, which is increased by cisplatin and further increased by HIF‐1α inhibition. In addition, PNSs increased the levels of superoxide dismutase, catalase and glutathione, as well as ATP and mitochondrial membrane potential in renal tissues; these are all reduced by cisplatin and further reduced by HIF‐1α inhibition. In conclusion, we demonstrate here that PNSs protects against mitochondrial damage induced by cisplatin through HIF‐1α/mitochondria/ROS.

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Chemotherapy-associated renal dysfunction

Cited by 157 publications

References 142 publications

Methotrexate Use Is Safe in Children With Acute Lymphoblastic Leukemia

Methotrexate Use Is Safe in Children With Acute Lymphoblastic Leukemia

Onco-Nephrology

Panax notoginseng saponins ameliorate cisplatin‐induced mitochondrial injury via the HIF‐1α/mitochondria/ROS pathway

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