Preloading magnesium attenuates cisplatin-associated nephrotoxicity: pilot randomized controlled trial (PRAGMATIC study)

Suppadungsuk, Supawadee; Phitakwatchara, Wallaya; Reungwetwattana, Thanyanan; Pathumarak, A.; Phakdeekitcharoen, Bunyong; Kitiyakara, Chagriya; Srisuwarn, Praopilad; Davenport, Andrew; Nongnuch, Arkom

doi:10.1016/j.esmoop.2021.100351

Cited by 11 publications

(8 citation statements)

References 19 publications

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“…Careful use of renal replacement therapy also considered in cases where the patient already has acute kidney injury to prevent high serum peak levels of cisplatin. It is also important to note that severe sodium wasting can also be seen in Cisplatin 27,28]. The PRAGMATIC trial, showed that magnesium loading attenuates Cisplatin toxicity and increases cumulative cisplatin dose used until AKI was detected [28].…”

Section: Carboplatin/cisplatinmentioning

confidence: 99%

“…Careful use of renal replacement therapy also considered in cases where the patient already has acute kidney injury to prevent high serum peak levels of cisplatin. It is also important to note that severe sodium wasting can also be seen in Cisplatin induced nephrotoxicity [23 ▪ ,24 ▪▪ ,25,26 ▪ ,27,28].…”

Section: Reviewmentioning

confidence: 99%

“…A new trial has been designed to answer the question of whether magnesium supplementation can prevent cisplatin toxicity [23 ▪ ,24 ▪▪ ,25,26 ▪ ,27,28]. The PRAGMATIC trial, showed that magnesium loading attenuates Cisplatin toxicity and increases cumulative cisplatin dose used until AKI was detected [28].…”

Section: Reviewmentioning

confidence: 99%

Section: Reviewmentioning

confidence: 99%

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Onconephrology: mitigation of renal injury in chemotherapy administration

Selamet,

Ahdoot,

Salasnek

et al. 2023

Current Opinion in Nephrology &Amp; Hypertension

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Purpose of review Onconephrology was first coined as a name for the intersection of cancer medicine and nephrology in the early 2010s. It was recognized then that beyond and understanding of kidney physiology, a new generation of nephrologists skilled in both molecular biology and precision medicine were needed to deal with the challenges of emerging cancer therapies. Stem cell transplants, biologic agents, adjuvants blocking basic cellular signaling pathways, immunotherapy were found to promote novel anticancer outcomes, but also to pose new risks to the kidneys. The field rapidly overlapped with emerging expertise in vascular glomerular disease, glomerular disease, and the same biologic agents now applied to auto immune systemic and kidney diseases. Recent findings Many categories of chemotherapeutic agents have been discovered to have adverse renal side effects. In this review, we address classic chemotherapeutic nephrotoxicity and oncologic clinical situations leading to acute kidney injury. We also review the frontiers of nephrotoxicity reported with cell cycle inhibitors, diverse classes of tyrosine kinase inhibitors, immune checkpoint inhibitors, chimeric antigen receptor T-cell therapy, anticancer vaccines, and thrombotic microangiopathies triggered by malignancy and chemotherapy. The aim will be to focus on published strategies to mitigate nephrotoxicity. Summary As onconephrology expands into its own field, it gives birth to new subdisciplines. An understanding that patient populations want the benefits of chemotherapy without the renal (and other) systemic toxicities is emerging. A need to develop a new class of molecular and genetic experts in onconephrology to mitigate nephrotoxicity from chemotherapy is apparent and urgent.

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Section: Carboplatin/cisplatinmentioning

confidence: 99%

“…Careful use of renal replacement therapy also considered in cases where the patient already has acute kidney injury to prevent high serum peak levels of cisplatin. It is also important to note that severe sodium wasting can also be seen in Cisplatin induced nephrotoxicity [23 ▪ ,24 ▪▪ ,25,26 ▪ ,27,28].…”

Section: Reviewmentioning

confidence: 99%

Section: Reviewmentioning

confidence: 99%

Section: Reviewmentioning

confidence: 99%

See 2 more Smart Citations

Onconephrology: mitigation of renal injury in chemotherapy administration

Selamet,

Ahdoot,

Salasnek

et al. 2023

Current Opinion in Nephrology &Amp; Hypertension

View full text Add to dashboard Cite

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“…Besides that, AKI is also highly involved in those patients with cancer who are subjects administering chemotherapeutic drugs such as cisplatin [ 2 , 7 – 9 ]. Of note, cisplatin is an agent which is metabolized through the kidney [ 10 ], and could trigger AKI at high incidence [ 9 , 11 ]. However, the therapeutic strategies for AKI are still in blank nowadays.…”

Section: Introductionmentioning

confidence: 99%

Annexin A2 plays a key role in protecting against cisplatin-induced AKI through β-catenin/TFEB pathway

et al. 2022

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Acute kidney injury (AKI) is in high prevalence in the world. However, the therapeutic strategies for AKI are still in mystery. Studies have shown to improve autophagy and lysosomal function could inhibit AKI. But their modulators need to be explored in detail. Annexin A2 (ANXA2) is a phospholipid-binding protein involving in organelle membrane integrity function, suggesting its important role in autophagy and lysosome homeostasis. It implicates ANXA2 potentially protects against AKI. However, this has not been elucidated. Herein, we found that ANXA2 is increased in renal tubules in cisplatin-induced AKI mice. Ectopic expression of ANXA2 improved lysosomal functions and enhanced autophagic flux, further protecting against renal tubular cell apoptosis and kidney injury. Conversely, knockdown of ANXA2 inhibited lysosomal function and autophagy, which aggravated the progression of AKI. Transcriptome sequencing revealed β-catenin signaling is highly responsible for this process. In vitro, we found ANXA2 induced β-catenin activation, further triggering T-cell factor-4 (TCF4)-induced transcription factor EB (TFEB). Furthermore, TFEB promoted lysosome biogenesis to enhance autophagic flux, resulting in the alleviation of AKI. Our new findings underline ANXA2 is a new therapeutic potential for AKI through modulating autophagy and lysosomal function. The underlying mechanism is associated with its inductive effects on β-catenin/TFEB pathway.

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Magnesium supplementation therapy to prevent cisplatin-induced acute nephrotoxicity in pediatric cancer: a randomized phase-2 trial

Matsui,

Makimoto,

Chin

et al. 2024

Int J Clin Oncol

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Background:The present study aimed to examine the effect of magnesium (Mg) supplementation on cisplatin-induced nephrotoxicity (CIN) in pediatric cancer patients. Methods:The present phase II, open-label, multicenter, randomized controlled trial enrolled patients aged less than 20 years who were scheduled to receive cisplatin-containing chemotherapy and randomly allocated them at a ratio of 1:1 to a Mg supplementation arm with even-numbered chemotherapy courses (arm AB) or another arm with odd-numbered courses (arm BA). Analysis objects were reconstructed into two groups depending on whether the chemotherapy course had Mg supplementation (group B) or not (group A). The primary outcome was the proportion of chemotherapy courses resulting in elevating serum creatinine per chemotherapy course. The secondary outcomes included e cacies evaluated using other biomarkers and the safety of the Mg supplementation. Results:Twenty-eight patients were randomly allocated to either group (16 to arm AB and 12 to arm BA). The baseline characteristics of the groups were similar. There was no signi cant difference in elevated serum creatinine between the groups (group A: 10% vs. group B: 6%; P = 0.465), nor was any signi cant difference observed in other biomarkers during any chemotherapy course. The Mg value during chemotherapy was signi cantly higher in group B than in group A. No adverse events related to magnesium administration were observed. Conclusions:The study design, which treated a single chemotherapy course as a study object, failed to detect a statistically signi cant bene t of Mg supplementation for preventing CIN in pediatric cancer patients. Trial registrationJRCT (https://jrct.niph.go.jp/) Identi er UMIN000029215 jRCTs031180251.

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Preloading magnesium attenuates cisplatin-associated nephrotoxicity: pilot randomized controlled trial (PRAGMATIC study)

Cited by 11 publications

References 19 publications

Onconephrology: mitigation of renal injury in chemotherapy administration

Onconephrology: mitigation of renal injury in chemotherapy administration

Annexin A2 plays a key role in protecting against cisplatin-induced AKI through β-catenin/TFEB pathway

Magnesium supplementation therapy to prevent cisplatin-induced acute nephrotoxicity in pediatric cancer: a randomized phase-2 trial

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