Research ArticleClinical Studies
Open Access

A Prospective Comparison of Azilsartan and Amlodipine for Bevacizumab-induced Hypertension and Proteinuria in Colorectal Cancer

SATORU NIHEI, HARUKI UJIIE, KAZUKI SAITO, TATSUKI IKEDA, JUNICHI ASAKA, MIZUNORI YAEGASHI, KOICHI ASAHI and KENZO KUDO
In Vivo January 2026, 40 (1) 465-473; DOI: https://doi.org/10.21873/invivo.14210

Abstract

Background/Aim: Bevacizumab (Bev) often induces hypertension and proteinuria. Optimal antihypertensive management in this setting remains unclear, and studies comparing angiotensin II receptor blockers (ARBs) and calcium channel blockers (CCBs) are limited. The objective of this study was to compare the effects of the ARB azilsartan and the CCB amlodipine on hypertension and proteinuria.

Patients and Methods: Patients with demonstrated systolic/diastolic blood pressure (SBP/DBP) ≥140/90 mmHg during Bev therapy for colorectal cancer were randomly assigned 1:1 to either the azilsartan group or the amlodipine group and were followed up for 18 weeks. The primary outcome was urinary protein-to-creatinine ratio (UPCR). Secondary outcomes included BP changes and achievement of target BP (<140/90 mmHg). After week six, the attending physician adjusted the antihypertensive medication as needed.

Results: Thirty patients were enrolled, and 26 (13 per group) completed 18 weeks of treatment. Mean baseline SBP was 156.8±9.2 mmHg in the azilsartan group and 158.0±9.4 mmHg in the amlodipine group. At week six, SBP decreased to 151.4±21.9 mmHg and 144.5±15.2 mmHg, respectively, with a significant reduction in the amlodipine group. At week 18, SBP was 136.5±12.9 mmHg vs. 138.7±14.9 mmHg. Target BP was achieved in 23% of patients at week six and in 40-50% at week 18, with no difference between groups. No significant difference in UPCR was observed at any time point. Subgroup analysis revealed that patients with proteinuria consistently had higher BP.

Conclusion: These findings emphasize that adequate BP control, rather than antihypertensive class, may be critical in managing Bev-induced proteinuria.

Keywords:

Introduction

Bevacizumab (Bev), a monoclonal antibody targeting vascular endothelial growth factor (VEGF), is widely used in the treatment of various solid tumors, including colorectal cancer, non-small cell lung cancer, and hepatocellular carcinoma. Inhibition of VEGF signaling suppresses tumor angiogenesis and prolongs survival (1), but frequently induces renal vascular adverse events such as hypertension and proteinuria (2-4). These events impede treatment continuation and directly impact patient prognosis and quality of life (5, 6), making their appropriate management a critical clinical challenge.

The fundamental mechanism of Bev-induced proteinuria is based on the fact that maintenance of glomerular endothelial functional integrity and glomerular filtration barrier podocyte-derived VEGF-A signaling through endothelial VEGF receptor 2; however, the mechanism is not fully elucidated (7, 8). Furthermore, VEGF inhibitors are theorized to induce hypertension through reduced synthesis of vasodilators (nitric oxide, prostacyclin), increased release of vasoconstrictors (endothelin-1), and thinning of microvascular endothelial cells (9, 10). This can impair renal hemodynamics and subsequently promote proteinuria (11).

In managing hypertension associated with diabetes or proteinuria, renin–angiotensin system inhibitors (RASIs) such as angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) are effective for suppressing proteinuria and are recommended in clinical guidelines as first-line therapy (12, 13). However, sufficient prospective clinical trial data are lacking to determine whether RASIs exert comparable efficacy in VEGF inhibitor-related hypertension and proteinuria. Furthermore, retrospective studies suggest inconsistent efficacy of RASIs (11, 14, 15). In contrast, dihydropyridine calcium channel blockers (CCBs) directly dilate peripheral vessels, leading to rapid reduction in blood pressure (BP), suggesting their potential efficacy against the abrupt BP elevations caused by VEGF inhibitors (16). Although CCBs are commonly used in clinical practice, few studies have prospectively evaluated their efficacy in hypertension and proteinuria associated with VEGF inhibitors. Consequently, there is currently no clear evidence guiding the choice between ARBs and CCBs for the prevention or treatment of VEGF inhibitor-related renal vascular adverse events, leaving treatment decisions to the discretion of the facility and physician.

The objective of this study was to prospectively evaluate the effects of the ARB azilsartan and the CCB amlodipine on BP and urinary protein excretion in patients with Bev-induced hypertension. Although small and conducted at a single-center, this study provides a foundation for evaluating the clinical appropriateness of antihypertensive drug selection for VEGF inhibitor-induced nephropathy.

Patients and Methods

Ethics. This study was conducted with approval from the Ethics Committee of Iwate Medical University School of Medicine (Approval Number: MH2018-584) and registered with the University Hospital Medical Information Network (UMIN Trial ID: UMIN000034880). The study was conducted in accordance with the Declaration of Helsinki and Japanese guidelines for research involving human subjects. Written informed consent was obtained from all participants prior to enrollment.

Study design and subjects. This study was a single-center, prospective, pilot, open-label trial conducted in the Outpatient Surgery Department of Iwate Medical University Hospital. Eligible participants were those with Bev-induced hypertension. The enrollment period was from February 2019 to May 2023.

Inclusion criteria were as follows: 1) patients diagnosed with colorectal cancer receiving treatment including Bev; 2) patients with systolic BP (SBP) and/or diastolic BP (DBP) ≥140/90 mmHg on at least two measurements; 3) patients aged ≥20 years.

Exclusion criteria were as follows: 1) patients with a history of antihypertensive medication use (RASIs, CCBs, diuretics, alpha blockers, beta blockers, etc.) within three months prior to enrollment; 2) patients with a history of diabetes; 3) patients with a history of serious cardiovascular disease such as stroke, heart failure, or myocardial infarction; 4) patients with an estimated glomerular filtration rate (eGFR) <30 ml/min/1.73 m2; 5) women who are pregnant, breastfeeding, or planning to become pregnant; 6) those deemed ineligible by the principal investigator.

In total, 30 patients were enrolled and randomly assigned 1:1 to either the azilsartan or amlodipine group for 18 weeks of treatment. Random assignment to the treatment groups was accomplished using a random number table that was generated in Excel (Microsoft, Redmond, WA, USA) before the initiation of the trial. Twenty-six patients completed the 18-week follow-up (Figure 1).

Figure 1.
Figure 1.

Flow diagram for the study.

Treatment. Patients received either azilsartan or amlodipine at standard doses for 18 weeks. Starting at week six, the treating physician could adjust the dose or add a new medication according to BP readings and clinical course. The additional medication was selected according to the group assignment, with the other drug serving as the control (amlodipine in the azilsartan group and azilsartan in the amlodipine group).

Primary endpoints and assessment. Follow-up visits were recorded at each Bev therapy cycle, which occurred every two to three weeks. The primary outcome was the urinary protein-to-creatinine ratio (UPCR) at weeks six and 18. Secondary outcomes included changes in SBP and DBP and the rate of achieving target BP <140/90 mmHg (17). The primary and secondary outcomes were evaluated at baseline and at weeks six and 18.

BP was measured during outpatient visits using standardized office BP protocols and an automated sphygmomanometer commonly used in clinical practice. Two measurements were taken with the patient seated and at rest, and the mean value was used. Urine samples were collected during outpatient visits and used for UPCR calculation. Twenty-four-hour urine collection was not included in the study design, and assessment was based on a single measurement.

Statistical analysis. As this study had an exploratory design, statistical power calculations and prior power analyses were not performed. Continuous variables were expressed as mean±standard deviation or median (interquartile range), and categorical variables as proportions (%). Data normality was assessed using the Shapiro–Wilk test. Between-group comparisons were performed with the paired t-test for normally distributed data and the Wilcoxon signed-rank test for non-normally distributed data. Comparisons of categorical variables employed the chi-square test or Fisher’s exact test. Two-way analysis of variance (ANOVA) was performed to compare BP trends between groups at baseline and weeks six and 18, with post-hoc multiple comparisons using the Bonferroni method. All analyses were two-sided, and p<0.05 was considered statistically significant. Statistical analyses were performed using IBM SPSS Statistics for Windows, version 27.0 (IBM, Armonk, NY, USA).

Results

A total of 30 patients were included in the study, but four patients dropped out. Ultimately, 26 patients (13 in each group) completed the trial (Figure 1). Table I summarizes the baseline characteristics of the study groups. The mean age was 68.4±9.0 years in the azilsartan group and 65.2±12.7 years in the amlodipine group. The mean duration of Bev administration was 10.8±2.4 weeks in the azilsartan group and 12.4±2.7 weeks in the amlodipine group. No significant differences were observed between the two groups in any baseline characteristic (Table I).

View this table:
Table I.

Baseline characteristics of the study groups.

Figure 2 shows the comparison of mean BP between the azilsartan and amlodipine groups at baseline, week six, and week 18. Both groups showed improvement in BP over time. At baseline, the mean SBP was 156.8±9.2 mmHg in the azilsartan group and 158.0±9.4 mmHg in the amlodipine group (p=0.710). At week six, the values were 151.4±21.9 mmHg and 144.5±15.2 mmHg (p=0.042), respectively; at week 18, they were 136.5±12.9 mmHg and 138.7±14.9 mmHg (p=0.501), respectively. The amlodipine group showed significantly lower values at week six (Figure 2A). Mean DBP was 94.0±10.9 mmHg and 95.5±13.8 mmHg at baseline (p=0.577), 92.5±13.7 mmHg and 87.5±11.8 mmHg at week six (p=0.073), and 84.8±11.1 mmHg and 84.2±10.8 mmHg at week 18 (p=0.802) (Figure 2B).

Figure 2.
Figure 2.

Comparison of blood pressure between the azilsartan and amlodipine groups. Systolic blood pressure (A) and diastolic blood pressure (B) at baseline, week six, and week 18. Data are shown as mean±standard deviation. *Azilsartan vs. amlodipine: p<0.05. SBP: Systolic blood pressure; DBP: diastolic blood pressure.

Table II summarizes BP control status during the 18-week follow-up. Changes in SBP and DBP at week six were greater in the amlodipine group than in the azilsartan group, but no significant difference was observed (p=0.232 and p=0.242, respectively). The proportion achieving the target BP of < 140/90 mmHg was 23.1% in both groups (p=1.000), with no significant difference. Regarding antihypertensive medication adjustments after week six, dose escalation was required in 46.2% of patients in the amlodipine group versus 38.5% in the azilsartan group (p=1.000). Conversely, the proportion of patients requiring initiation of an additional medication was 15.4% in the amlodipine group and 38.5% in the azilsartan group (p=0.378). No significant differences were observed between groups in changes in SBP and DBP at week 18, and in the proportion achieving target BP below 140/90 mmHg (Table II).

View this table:
Table II.

Blood pressure control status.

Figure 3 shows comparisons of the primary outcome (UPCR) at baseline, week six, and week 18. No significant differences between groups were observed at any time point (Figure 3). UPCR ≥0.5 g/gCr, classified as “severely elevated (A3)” in the KDIGO2024 guideline (18), was observed in eight patients overall (three in the azilsartan group, five in the amlodipine group). Furthermore, to examine the association between BP and proteinuria onset, a subgroup analysis comparing BP was performed after classifying patients into UPCR ≥0.5 g/gCr and <0.5 g/gCr groups (Figure 4). The results showed consistently elevated BP in the UPCR ≥0.5 g/gCr group. Both SBP and DBP were significantly higher at six weeks (p=0.003 and p<0.001, respectively). At week 18, DBP remained significantly elevated (p<0.001), and SBP showed a similar trend (p=0.112) (Figure 4A and B). No cases of Bev dose reduction or discontinuation due to hypertension or proteinuria were observed during the study.

Figure 3.
Figure 3.

Comparison of urinary protein-to-creatinine ratio between the azilsartan and amlodipine groups. Data are plotted as individual patient values at baseline, week six, and week 18, and presented as median (interquartile range) for each. No significant difference was observed between the two groups at any time point. UPCR: Urinary protein-to-creatinine ratio.

Figure 4.
Figure 4.

Comparison of blood pressure based on presence or absence of proteinuria status defined as urinary protein-to-creatinine ratio ≥0.5 g/gCr vs. <0.5 g/gCr. Systolic blood pressure (A) and diastolic blood pressure (B) at baseline, week six, and week 18. Data are shown as mean±standard deviation. *UPCR ≥0.5 g/gCr vs. <0.5 g/gCr: p<0.05. UPCR: Urinary protein-to-creatinine ratio; SBP: systolic blood pressure; DBP: diastolic blood pressure.

Discussion

This study provides one of the first prospective clinical evaluations comparing ARBs and CCBs for Bev-induced hypertension and proteinuria. Although no difference in the primary outcome (UPCR) was observed between groups at either six or 18 weeks, subgroup analysis revealed consistently higher BP in the proteinuria group compared to the non-proteinuria group. These findings align with those of previous reports, indicating that the degree of BP control, rather than the type of antihypertensive drug, is crucial for renal protection (11). However, these results should be interpreted with caution given the small sample size and limited statistical power.

Proteinuria induced by VEGF inhibitors is thought to result from both direct inhibition of VEGF leading to glomerular endothelial injury and indirect disruption of the glomerular filtration barrier secondary to hypertension, with both mechanisms likely interacting in a complex fashion. Basic research indicates that RASIs may prevent VEGF inhibitor-induced proteinuria in preclinical studies using rats treated with sunitinib (19, 20). Conversely, CCBs have been reported to improve BP but do not contribute to proteinuria suppression (19). Furthermore, retrospective clinical studies have also suggested that RASIs may be beneficial in reducing proteinuria (14, 15). However, no prospective trials have yet demonstrated the superiority of RASIs over other antihypertensive drugs, and this study likewise did not demonstrate such superiority. In particular, given that the mean SBP at the start of azilsartan or amlodipine was very high at 156–158 mmHg in the present study, the influence of BP on proteinuria was likely substantial, and may have masked any direct, drug-specific, renoprotective effects. Furthermore, the 18-week follow-up period may have been insufficient for evaluating proteinuria. Future studies incorporating earlier intervention and longer-term follow-up are necessary to more clearly verify the preventive effect of RASIs on proteinuria.

Regarding antihypertensive effects, the amlodipine group showed a greater BP reduction than the azilsartan group during the initial six weeks. Although first-line antihypertensive drugs generally have equivalent BP-lowering effects, the short-term impact on BP varies by agent, suggesting that CCBs alone or in combination are most effective for BP control (21, 22). As Bev-induced hypertension often develops abruptly, CCBs may be advantageous for initial management. However, this difference is transient and small, and considering multiple comparisons, statistical significance is difficult to establish. Therefore, rather than concluding superiority of amlodipine, it is more appropriate to limit the differences in antihypertensive effects observed in this study to propose only a hypothesis regarding drug selection in the early treatment phase.

Current recommendations for patients with diabetes or chronic kidney disease suggest initiating antihypertensive therapy at BP ≥140/90 mmHg, with a target of <130/80 mmHg (12, 13). The BP target set in this study (<140/90 mmHg) is considered appropriate for chemotherapy patients (17). However, the target achievement rate remained at only 23% at week six for both groups and stayed within the 40–50% range even at week 18. This was lower than the 66% achievement rate observed in Japanese patients undergoing antihypertensive therapy (23). These results suggest that VEGF inhibitor-induced hypertension may be refractory and distinct from conventional essential hypertension. Sufficient BP control is likely difficult with RASI or CCB monotherapy alone. Therefore, future research should also focus on the efficacy of combination therapy from the perspective of strict BP management.

Study limitations. First, as a small, single-center, prospective, pilot, open-label study, it cannot exclude confounding factors related to patient background or physician judgment. Furthermore, BP assessment relied solely on clinic measurements, without accounting for circadian variation or discrepancies with home BP readings. Moreover, UPCR assessment relied on a single urine sample rather than 24-hour urine collection, limiting consistency. Although statistical analysis used a two-way ANOVA with Bonferroni correction, the limited sample size reduced statistical power. Therefore, it is crucial to recognize that this analysis remains exploratory.

Conclusion

Although no significant difference in the primary outcome (UPCR) was observed between azilsartan and amlodipine groups, subgroup analysis demonstrated an association between BP and the development of proteinuria. This finding supports prior research indicating that the quality of BP management is more important than the type of antihypertensive drug. However, as this study was small, single-center, and open-label, caution is warranted in interpreting the results, and they should not be generalized. Future large-scale randomized trials are necessary to clarify optimal initial BP-lowering strategies and their implications for long-term renal outcomes.

Acknowledgements

The Authors sincerely thank all those who participated in this study.

Footnotes

  • Authors’ Contributions

    Conceptualization: SN. Data curation: SN, KS and TI. Formal analysis: SN and HU. Investigation: SN, HU, KS, TI and MY. Methodology: SN, HU and KK. Project administration: SN. Software: SN. Supervision: KK. Validation: KK. Visualization, Writing - original draft: SN. Writing – review and editing: SN, HU, KS, TI, MY, KA and KK. All Authors have read and agreed to the published version of the manuscript.

  • Conflicts of Interest

    The Authors declare that they have no conflicts of interest in relation to this study.

  • Funding

    No funding was received for this study.

  • Artificial Intelligence (AI) Disclosure

    No artificial intelligence (AI) tools were used in the preparation or writing of this manuscript.

  • Received October 2, 2025.
  • Revision received October 21, 2025.
  • Accepted October 22, 2025.

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY-NC-ND) 4.0 international license (https://creativecommons.org/licenses/by-nc-nd/4.0).

References

  1. ↵
    1. Garcia J,
    2. Hurwitz HI,
    3. Sandler AB,
    4. Miles D,
    5. Coleman RL,
    6. Deurloo R,
    7. Chinot OL
    : Bevacizumab (Avastin®) in cancer treatment: A review of 15 years of clinical experience and future outlook. Cancer Treat Rev 86: 102017, 2020. DOI: 10.1016/j.ctrv.2020.102017
    OpenUrlCrossRefPubMed
  2. ↵
    1. Zhu X,
    2. Wu S,
    3. Dahut WL,
    4. Parikh CR
    : Risks of proteinuria and hypertension with bevacizumab, an antibody against vascular endothelial growth factor: systematic review and meta-analysis. Am J Kidney Dis 49(2): 186-193, 2007. DOI: 10.1053/j.ajkd.2006.11.039
    OpenUrlCrossRefPubMed
    1. Izzedine H,
    2. Ederhy S,
    3. Goldwasser F,
    4. Soria JC,
    5. Milano G,
    6. Cohen A,
    7. Khayat D,
    8. Spano JP
    : Management of hypertension in angiogenesis inhibitor-treated patients. Ann Oncol 20(5): 807-815, 2009. DOI: 10.1093/annonc/mdn713
    OpenUrlCrossRefPubMed
  4. ↵
    1. Mir O,
    2. Coriat R,
    3. Cabanes L,
    4. Ropert S,
    5. Billemont B,
    6. Alexandre J,
    7. Durand JP,
    8. Treluyer JM,
    9. Knebelmann B,
    10. Goldwasser F
    : An observational study of bevacizumab-induced hypertension as a clinical biomarker of antitumor activity. Oncologist 16(9): 1325-1332, 2011. DOI: 10.1634/theoncologist.2010-0002
    OpenUrlAbstract/FREE Full Text
  5. ↵
    1. Wu S,
    2. Kim C,
    3. Baer L,
    4. Zhu X
    : Bevacizumab increases risk for severe proteinuria in cancer patients. J Am Soc Nephrol 21(8): 1381-1389, 2010. DOI: 10.1681/ASN.2010020167
    OpenUrlAbstract/FREE Full Text
  6. ↵
    1. Ranpura V,
    2. Pulipati B,
    3. Chu D,
    4. Zhu X,
    5. Wu S
    : Increased risk of high-grade hypertension with bevacizumab in cancer patients: a meta-analysis. Am J Hypertens 23(5): 460-468, 2010. DOI: 10.1038/ajh.2010.25
    OpenUrlCrossRefPubMed
  7. ↵
    1. Eremina V,
    2. Jefferson JA,
    3. Kowalewska J,
    4. Hochster H,
    5. Haas M,
    6. Weisstuch J,
    7. Richardson C,
    8. Kopp JB,
    9. Kabir MG,
    10. Backx PH,
    11. Gerber HP,
    12. Ferrara N,
    13. Barisoni L,
    14. Alpers CE,
    15. Quaggin SE
    : VEGF inhibition and renal thrombotic microangiopathy. N Engl J Med 358(11): 1129-1136, 2008. DOI: 10.1056/NEJMoa0707330
    OpenUrlCrossRefPubMed
  8. ↵
    1. Estrada CC,
    2. Maldonado A,
    3. Mallipattu SK
    : Therapeutic inhibition of VEGF signaling and associated nephrotoxicities. J Am Soc Nephrol 30(2): 187-200, 2019. DOI: 10.1681/ASN.2018080853
    OpenUrlAbstract/FREE Full Text
  9. ↵
    1. Camarda N,
    2. Travers R,
    3. Yang VK,
    4. London C,
    5. Jaffe IZ
    : VEGF receptor inhibitor-induced hypertension: emerging mechanisms and clinical implications. Curr Oncol Rep 24(4): 463-474, 2022. DOI: 10.1007/s11912-022-01224-0
    OpenUrlCrossRefPubMed
  10. ↵
    1. Nihei S,
    2. Asaka J,
    3. Takahashi H,
    4. Kudo K
    : Bevacizumab increases endothelin-1 production via forkhead box protein O1 in human glomerular microvascular endothelial cells in vitro. Int J Nephrol 2021: 8381115, 2021. DOI: 10.1155/2021/8381115
    OpenUrlCrossRefPubMed
  11. ↵
    1. Nihei S,
    2. Asaka J,
    3. Yaegashi M,
    4. Asahi K,
    5. Kudo K
    : Effect of blood pressure control on the risk of proteinuria during bevacizumab treatment in patients with colorectal cancer: a single-center retrospective cohort study. J Pharm Health Care Sci 10(1): 51, 2024. DOI: 10.1186/s40780-024-00372-8
    OpenUrlCrossRefPubMed
  12. ↵
    1. Writing Committee Members,
    2. Jones DW,
    3. Ferdinand KC,
    4. Taler SJ,
    5. Johnson HM,
    6. Shimbo D,
    7. Abdalla M,
    8. Altieri MM,
    9. Bansal N,
    10. Bello NA,
    11. Bress AP,
    12. Carter J,
    13. Cohen JB,
    14. Collins KJ,
    15. Commodore-Mensah Y,
    16. Davis LL,
    17. Egan B,
    18. Khan SS,
    19. Lloyd-Jones DM,
    20. Melnyk BM,
    21. Mistry EA,
    22. Ogunniyi MO,
    23. Schott SL,
    24. Smith SC Jr.,
    25. Talbot AW,
    26. Vongpatanasin W,
    27. Watson KE,
    28. Whelton PK,
    29. Williamson JD
    : 2025 AHA/ACC/AANP/AAPA/ABC/ACCP/ACPM/AGS/AMA/ASPC/NMA/PCNA/SGIM guideline for the prevention, detection, evaluation and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation 152(11): e114-e218, 2025. DOI: 10.1161/CIR.0000000000001356
    OpenUrlCrossRef
  13. ↵
    1. Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group
    : KDIGO 2024 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int 105(4S): S117-S314, 2024. DOI: 10.1016/j.kint.2023.10.018
    OpenUrlCrossRefPubMed
  14. ↵
    1. Nihei S,
    2. Sato J,
    3. Harada T,
    4. Kuyama S,
    5. Suzuki T,
    6. Waga N,
    7. Saito Y,
    8. Kisara S,
    9. Yokota A,
    10. Okada K,
    11. Tsuchiya M,
    12. Terui K,
    13. Tadokoro Y,
    14. Chiba T,
    15. Kudo K,
    16. Oizumi S,
    17. Inoue A,
    18. Morikawa N
    : Antiproteinuric effects of renin–angiotensin inhibitors in lung cancer patients receiving bevacizumab. Cancer Chemother Pharmacol 81(6): 1051-1059, 2018. DOI: 10.1007/s00280-018-3580-1
    OpenUrlCrossRefPubMed
  15. ↵
    1. Hirai T,
    2. Shuji Y,
    3. Takiyama M,
    4. Hanada K,
    5. Itoh T
    : Renin–angiotensin system inhibitors for countering proteinuria induced by angiogenesis inhibitors: a retrospective observational analysis. Cancer Chemother Pharmacol 84(1): 195-202, 2019. DOI: 10.1007/s00280-019-03876-5
    OpenUrlCrossRefPubMed
  16. ↵
    1. Mir O,
    2. Coriat R,
    3. Ropert S,
    4. Cabanes L,
    5. Blanchet B,
    6. Camps S,
    7. Billemont B,
    8. Knebelmann B,
    9. Goldwasser F
    : Treatment of bevacizumab-induced hypertension by amlodipine. Invest New Drugs 30(2): 702-707, 2012. DOI: 10.1007/s10637-010-9549-5
    OpenUrlCrossRefPubMed
  17. ↵
    1. Maitland ML,
    2. Bakris GL,
    3. Black HR,
    4. Chen HX,
    5. Durand JB,
    6. Elliott WJ,
    7. Ivy SP,
    8. Leier CV,
    9. Lindenfeld J,
    10. Liu G,
    11. Remick SC,
    12. Steingart R,
    13. Tang WH, Cardiovascular Toxicities Panel, Convened by the Angiogenesis Task Force of the National Cancer Institute Investigational Drug Steering Committee
    : Initial assessment, surveillance, and management of blood pressure in patients receiving vascular endothelial growth factor signaling pathway inhibitors. J Natl Cancer Inst 102(9): 596-604, 2010. DOI: 10.1093/jnci/djq091
    OpenUrlCrossRefPubMed
  18. ↵
    1. Kidney Disease: Improving Global Outcomes (KDIGO) Lupus Nephritis Work Group
    : KDIGO 2024 Clinical Practice Guideline for the management of LUPUS NEPHRITIS. Kidney Int 105(1S): S1-S69, 2024. DOI: 10.1016/j.kint.2023.09.002
    OpenUrlCrossRefPubMed
  19. ↵
    1. Lankhorst S,
    2. Kappers MH,
    3. Van Esch JH,
    4. Smedts FM,
    5. Sleijfer S,
    6. Mathijssen RH,
    7. Baelde HJ,
    8. Danser AJ,
    9. Van Den Meiracker AH
    : Treatment of hypertension and renal injury induced by the angiogenesis inhibitor sunitinib: preclinical study. Hypertension 64(6): 1282-1289, 2014. DOI: 10.1161/HYPERTENSIONAHA.114.04187
    OpenUrlCrossRef
  20. ↵
    1. Imai S,
    2. Miyake H,
    3. Fujisawa M
    : Acceleration of proteinuria without significant impact on renal function and its protection by angiotensin II receptor blocker in rats treated with axitinib. Target Oncol 11(3): 309-315, 2016. DOI: 10.1007/s11523-015-0393-6
    OpenUrlCrossRefPubMed
  21. ↵
    1. Nardin C,
    2. Rattazzi M,
    3. Pauletto P
    : Blood pressure variability and therapeutic implications in hypertension and cardiovascular diseases. High Blood Press Cardiovasc Prev 26(5): 353-359, 2019. DOI: 10.1007/s40292-019-00339-z
    OpenUrlCrossRefPubMed
  22. ↵
    1. Levi-Marpillat N,
    2. Macquin-Mavier I,
    3. Tropeano A,
    4. Parati G,
    5. Maison P
    : Antihypertensive drug classes have different effects on short-term blood pressure variability in essential hypertension. Hypertens Res 37(6): 585-590, 2014. DOI: 10.1038/hr.2014.33
    OpenUrlCrossRefPubMed
  23. ↵
    1. Fujishima S,
    2. Kodama S,
    3. Tsuchihashi T
    : Achievement rate of blood pressure <140/90 mmHg and <130/80 mmHg in subjects with hypertension; findings from a Japanese health checkup in 2017. Clinical and Experimental Hypertension 42(7): 648-655, 2020. DOI: 10.1080/10641963.2020.1764017
    OpenUrlCrossRefPubMed
Back to top

In this issue

Print
Download PDF
Article Alerts
Email Article
Citation Tools
Reprints and Permissions
A Prospective Comparison of Azilsartan and Amlodipine for Bevacizumab-induced Hypertension and Proteinuria in Colorectal Cancer
SATORU NIHEI, HARUKI UJIIE, KAZUKI SAITO, TATSUKI IKEDA, JUNICHI ASAKA, MIZUNORI YAEGASHI, KOICHI ASAHI, KENZO KUDO
In Vivo Jan 2026, 40 (1) 465-473; DOI: 10.21873/invivo.14210
Twitter logo Facebook logo Mendeley logo

Jump to section

Keywords