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While preventing AKI is not always feasible (in part because many patients present to the hospital with ongoing AKI), mitigating its consequences is within closer reach, with blockade of the renin-angiotensin-aldosterone system (RAAS) after AKI appearing to be one of the most promising approaches. The authors reported a similar risk of AKI in the year following discharge of patients with AKI and treated with ACEi/ARB or not treated. Hsu CY, Liu KD, Yang J, et al: Renin-angiotensin system blockade after acute kidney injury (AKI) and risk of recurrent AKI. [Extracted from the article]

Introduction: Vascular endothelial growth factor inhibition (VEGFi) in cancer treatment is associated with hypertension. Imbalance between the renin-angiotensin-aldosterone system (RAAS) and VEGF may contribute to VEGFi associated hypertension. We hypothesized that RAAS blockade at the time of VEGFi attenuates increases in blood pressure. Methods: Using de-identified medical records from 1085 outpatients with cancer on VEGFi, we extracted demographic, oncologic, anti-hypertensive medication exposure and comorbidity data between 2003-2017. Baseline blood pressure was estimated as the average of all outpatient blood pressures collected during 12-6 weeks prior to VEGFi. Response blood pressure was estimated as the average blood pressure collected from 0-6 weeks after VEGFi. We used non-parametric methods and adjusted regression models to assess associations in BP change between patients taking or not taking ACEi/ARB. Results: Patients where 48% male, 88% Caucasian, and had mean age of 64+13 years. Patients using ACEi/ARB therapy were older with a lower GFR, lower prevalence of hypertension, and a higher prevalence of diabetes and hyperlipidemia compared with patients not using ACEi/ARB therapy (Table 1). We observed a 2.6 + 16mmHg reduction in systolic blood pressure among patients exposed to ACEi/ARB prior to VEGFi compared with 1 + 15mmHg reduction in patients not exposed to an ACEi/ARB. ACEi/ARB exposure was associated with a reduction in BP at 6 weeks even after adjusting for age, gender, BMI, GFR, hyperlipidemia, hypertension, and diabetes (-3.3mmHg [95% CI -5.5, -1.1]; p =0.005). Conclusions: Our results suggest a protective effect of pre-VEGFi exposure to ACEi/ARB on blood pressure response. Future studies are warranted to determine whether RAAS blockade should be initiated prophylactically in patients receiving VEGFi. [ABSTRACT FROM AUTHOR]