Abstract
Renal cell carcinoma (RCC) is one of the most common kidney malignancies. An upgraded comprehension of the molecular biology implicated in the development of cancer has stimulated an increase in research and development of innovative antitumor therapies. The aim of the study was to analyze the medical literature for hypertension and renal toxicities as the adverse events of the vascular endothelial growth factor (VEGF) signaling pathway inhibitor (anti-VEGF) therapy. Relevant studies were identified in PubMed and ClinicalTrials.gov databases. Eligible studies were phase III and IV prospective clinical trials, meta-analyses and retrospective studies that had described events of hypertension or nephrotoxicity for patients who received anti-VEGF therapy. A total of 48 studies were included in the systematic review. The incidence of any grade hypertension ranged from 17% to 49.6%. Proteinuria and increased creatinine levels were ascertained in 8% to 73% and 5% to 65.6% of patients, respectively. These adverse events are most often mild in severity but may sometimes lead to treatment discontinuation. Nephrotoxicity and hypertension are related to multiple mechanisms; however, one of the main disturbances in those patients is VEGF inhibition. There is a significant risk of developing hypertension and renal dysfunction among patients receiving anti-VEGF treatment; however, there is also some evidence that these side effects may be used as biomarkers of response to antiangiogenic agents.
Highlights
Renal cell carcinoma (RCC) is one of the most frequent kidney malignancies and the development of RCC metastases is a major cause of tumor-associated deaths
In the Qi et al study, the frequency of all-grade hypertension associated with pazopanib was notably higher than that of sorafenib and sunitinib, whereas the incidence of high-grade hypertension linked with pazopanib was comparable to that of sorafenib and sunitinib, and, in the Hall et al study, sorafenib was connected with the largest risk of the development of hypertension [24,27]
Rini et al reported that systolic blood pressure (BP) ≥140 mmHg and diastolic BP ≥90 mmHg in patients treated with sunitinib were associated with notably better results than patients with lower systolic and diastolic BP; Goldstein et al detected that for week 4 and week 12, there were no significant associations between progression-free survival (PFS) and SBP increase in patients treated with sunitinib or pazopanib [89,90]
Summary
Renal cell carcinoma (RCC) is one of the most frequent kidney malignancies and the development of RCC metastases is a major cause of tumor-associated deaths. The morbidity of RCC has increased and RCC is one of the most common cancers; the therapeutic opportunities for metastatic renal cell carcinoma (mRCC) has been rapidly developing [1]. Inhibition of the vascular endothelial growth factor (VEGF) pathways has been one of the most successful directions to date in rearranging scientific discoveries to clinical benefit for the treatment of malignancies. Specific cells that express VEGF include progenitor endothelial cells, endothelial cells (EC), podocytes, fibroblasts, macrophages, and certain tumor types. The proangiogenic effect of VEGF is mediated primarily through receptor tyrosine kinases (RTKs) defined as vascular endothelial growth factor receptor 2 (VEGFR-2) on endothelial cells.
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