Renal adverse reactions of tyrosine kinase inhibitors in the treatment of tumours: A Bayesian network meta-analysis

Xiong, Ying; Wang, Qinxuan; Liu, Yangyi; Wei, Jingwen; Chen, Xiaolei

doi:10.3389/fphar.2022.1023660

Cited by 8 publications

(14 citation statements)

References 86 publications

(93 reference statements)

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“…Downstream of VEGF receptor and ligand blockade, a variety of tyrosine kinase inhibitors exist that are integral to the machinery of cell cycle proliferation. As such, they are quite useful in prevention of the rapid and explosive growth of cancer cells, as well allow a selective toxicity towards rapidly dividing cells while effecting normally dividing cells less [8 ▪ ]. The renal risks mirror those of upstream VEGF inhibitors, but in reality, biopsy reports do demonstrate some unique predilections [8 ▪ ].…”

Section: Novel Onconephrology Approaches For More Novel Agentsmentioning

confidence: 99%

“…As such, they are quite useful in prevention of the rapid and explosive growth of cancer cells, as well allow a selective toxicity towards rapidly dividing cells while effecting normally dividing cells less [8 ▪ ]. The renal risks mirror those of upstream VEGF inhibitors, but in reality, biopsy reports do demonstrate some unique predilections [8 ▪ ]. Izzedine et al noted that TMA tends to be more common with VEGFi, but TKIs also can show TMA findings especially with chronic use.…”

Section: Novel Onconephrology Approaches For More Novel Agentsmentioning

confidence: 99%

“…Izzedine et al noted that TMA tends to be more common with VEGFi, but TKIs also can show TMA findings especially with chronic use. Biopsy series show that nephrotic syndrome can be seen on average more readily, than TMA [8 ▪ ,9 ▪▪ ,13,14 ▪▪ ,36 ▪ ,37,38]. Hypertension associated with tyrosine kinase inhibitors (TKIs) is also well reported as is new onset proteinuria similar to VEGFi.…”

Section: Novel Onconephrology Approaches For More Novel Agentsmentioning

confidence: 99%

“…Burton kinase inhibitors (BTKi) inhibit the Burton kinase gene present in B lymphocytes and by doing so allow modulation of these cells in malignant processes involving them. These agents are approved by US FDA for treatments of chronic lymphocytic lymphoma (CLL) and mantle cell lymphoma (MCL) [8 ▪ ,42,43]. There are also other investigations in to the role of these agents in multiple sclerosis as well as in hemolytic uremic syndrome.…”

Section: Novel Onconephrology Approaches For More Novel Agentsmentioning

confidence: 99%

“…A common organ system involved in complications of chemotherapy is the renal system. From the changes in serum electrolytes due to dying cancer cells, to interference in cellular repair in the glomerulus and to direct toxicity of renal endothelial and podocyte cells caused by anticancer treatments, every new therapy has surfaced potential toxicity beyond what was known from the basic antidividing cell side effects of antimetabolite chemotherapy [6,7 ▪▪ ,8 ▪ ].…”

Section: Introductionmentioning

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: Novel Onconephrology Approaches For More Novel Agentsmentioning

confidence: 99%

Section: Novel Onconephrology Approaches For More Novel Agentsmentioning

confidence: 99%

Section: Novel Onconephrology Approaches For More Novel Agentsmentioning

confidence: 99%

Section: Novel Onconephrology Approaches For More Novel Agentsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Onconephrology: mitigation of renal injury in chemotherapy administration

Selamet,

Ahdoot,

Salasnek

et al. 2023

Current Opinion in Nephrology &Amp; Hypertension

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Detection, Monitoring, and Mitigation of Drug-Induced Nephrotoxicity: A Pragmatic Approach

Antognini,

Portman,

Dong

et al. 2023

Ther Innov Regul Sci

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The kidneys play a pivotal role in elimination of most drugs; therefore, a comprehensive understanding of renal physiology and pathology is important for those involved in drug development. High filtration capacity and metabolic activity make the kidneys vulnerable to drug-induced nephrotoxicity (DIN). Acute DIN may manifest on a background of renal impairment that has resulted from underlying disease, previously administered nephrotoxic medications, congenital renal abnormalities, or the natural aging process. The ability of the kidneys to compensate for DIN depends on the degree of pre-insult renal function. Therefore, it can be difficult to identify. The discovery and development of novel biomarkers that can diagnose kidney damage earlier and more accurately than current clinical measures and may be effective in detecting DIN. The goal of this manuscript is to provide a pragmatic and evidence-based supportive guidance for the early identification and management of DIN during the drug development process for clinical trial participants of all ages. The overall objective is to minimize the impact of DIN on kidney function and to collect renal safety data enabling risk analysis and mitigation.

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Comparison of different estimated glomerular filtration rates for monitoring of kidney function in oncology patients

Vermassen,

Geboes,

Lumen

et al. 2024

Clinical Kidney Journal

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Background Tyrosine kinase inhibitors (TKIs) are associated with kidney function deterioration. A shift is ongoing towards glomerular filtration rate (GFR) equations based on other protein markers, such as cystatin C (CSTC) and β-trace protein (BTP). We evaluated various GFR equations for monitoring of kidney function in actively treated oncology patients. Methods We monitored 110 patients receiving a TKI. Blood and urine were collected during therapy. Serum analysis included creatinine (Cr), CSTC and BTP; for consequent GFR determination. Urine was analyzed for protein, albumin, immunoglobulin G and α-1-microglobulin. A similar analysis was done in a patient subgroup receiving immune checkpoint inhibitors (ICI) as prior or subsequent line of therapy. Results Cr remained constant during TKI treatment (P = 0.7753) whereas a significant decrease in CSTC (from week 2 onward, P < 0.0001) and BTP (at weeks 2 and 4, P = 0.0100) were noticed. Consequently, GFR estimations, using CSTC and/or BTP as biochemical parameter, showed an apparent increase in GFR, whereas this was not observed for Cr-related GFR estimations. As a result, the GFR gap (ΔGFR) was significantly different from week 2 onward between Cr-based and CSTC-based GFR and between BTP-based and CSTC-based GFR. Glomerular damage was noticed with significant increase in urine protein-to-creatinine ratio, albumin-to-creatinine ratio and immunoglobulin G (all P < 0.0001). No change in α-1-microglobulin was seen. ICI treatment had no effect on Cr (P = 0.2262), CSTC (P = 0.7341) and BTP concentrations (P = 0.3592). Conclusion GFR equations, in which CSTC is incorporated, fail to correctly estimate the GFR in oncology patients treated with TKIs. As TKI-treated patients show clear signs of glomerular injury, further assessment is needed on how to correctly monitor the kidney function in actively treated oncology patients.

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Renal adverse reactions of tyrosine kinase inhibitors in the treatment of tumours: A Bayesian network meta-analysis

Cited by 8 publications

References 86 publications

Onconephrology: mitigation of renal injury in chemotherapy administration

Onconephrology: mitigation of renal injury in chemotherapy administration

Detection, Monitoring, and Mitigation of Drug-Induced Nephrotoxicity: A Pragmatic Approach

Comparison of different estimated glomerular filtration rates for monitoring of kidney function in oncology patients

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