IMPORTANCE Acute kidney injury (AKI) occurs in up to half of patients hospitalized with coronavirus disease 2019 (COVID-19). The longitudinal effects of COVID-19-associated AKI on kidney function remain unknown. OBJECTIVE To compare the rate of change in estimated glomerular filtration rate (eGFR) after hospital discharge between patients with and without COVID-19 who experienced in-hospital AKI. DESIGN, SETTING, AND PARTICIPANTS A retrospective cohort study was conducted at 5 hospitals in Connecticut and Rhode Island from March 10 to August 31, 2020. Patients who were tested for COVID-19 and developed AKI were screened, and those who survived past discharge, did not require dialysis within 3 days of discharge, and had at least 1 outpatient creatinine level measurement following discharge were included. EXPOSURES Diagnosis of COVID-19. MAIN OUTCOMES AND MEASURES Mixed-effects models were used to assess the association between COVID-19-associated AKI and eGFR slope after discharge. The secondary outcome was the time to AKI recovery for the subgroup of patients whose kidney function had not returned to the baseline level by discharge. RESULTS A total of 182 patients with COVID-19-associated AKI and 1430 patients with AKI not associated with COVID-19 were included. The population included 813 women (50.4%); median age was 69.7 years (interquartile range, 58.9-78.9 years). Patients with COVID-19-associated AKI were more likely to be Black (73 [40.1%] vs 225 [15.7%]) or Hispanic (40 [22%] vs 126 [8.8%]) and had fewer comorbidities than those without COVID-19 but similar rates of preexisting chronic kidney disease and hypertension. Patients with COVID-19-associated AKI had a greater decrease in eGFR in the unadjusted model (−11.3; 95% CI,-22.1 to −0.4 mL/min/1.73 m 2 /y; P = .04) and after adjusting for baseline comorbidities (−12.4; 95% CI,-23.7 to −1.2 mL/min/1.73 m 2 /y; P = .03). In the fully adjusted model controlling for comorbidities, peak creatinine level, and in-hospital dialysis requirement, the eGFR slope difference persisted (−14.0; 95% CI,-25.1 to −2.9 mL/min/1.73 m 2 /y; P = .01). In the subgroup of patients who had not achieved AKI recovery by discharge (n = 319), COVID-19-associated AKI was associated with decreased kidney recovery during outpatient follow-up (adjusted hazard ratio, 0.57; 95% CI, 0.35-0.92). CONCLUSIONS AND RELEVANCE In this cohort study of US patients who experienced in-hospital AKI, COVID-19-associated AKI was associated with a greater rate of eGFR decrease after discharge compared with AKI in patients without COVID-19, independent of underlying comorbidities or AKI (continued) Key Points Question What is the association between coronavirus disease 2019 (COVID-19) in patients with acute kidney injury and the longitudinal trajectory of estimated glomerular filtration rate? Findings In this cohort study of 1612 patients with acute kidney injury monitored after their index hospitalization, estimated glomerular filtration rate declined by 11.3 mL/min/ 1.73 m 2 per year faster in patients ...
Background It is currently unknown whether intensive blood pressure (BP) lowering beyond that recommended would lead to more lowering of the risk of Left ventricular hypertrophy (LVH) in patients with hypertension, and whether reducing the risk of LVH explains the reported cardiovascular disease (CVD) benefits of intensive BP lowering in this population. Methods This analysis included 8,164 participants (mean age 67.9 years, 35.3% women, 31.2% blacks) with hypertension but no diabetes from the Systolic Blood Pressure Intervention (SPRINT) Trial; 4,086 randomly assigned to intensive BP lowering (target systolic BP<120mmHg) and 4,078 assigned to standard BP lowering (target systolic BP <140mmHg). Progression and regression of LVH as defined by Cornell voltage criteria derived from standard 12-lead electrocardiograms recorded at baseline and biannually were compared between treatment arms during a median follow-up of 3.81 years. The effect of intensive (vs. standard) BP lowering on the SPRINT primary CVD outcome (a composite of myocardial infarction, acute coronary syndrome, stroke, heart failure, and CVD death) was compared before and after adjusting for LVH as a time-varying covariate. Results Among SPRINT participants without baseline LVH (n=7,559), intensive (vs. standard) BP lowering was associated with a 46% lower risk of developing LVH (HR=0.54, 95%CI: 0.43 to 0.68). Similarly, among SPRINT participants with baseline LVH (n=605, 7.4%), those assigned to the intensive (vs. standard) BP lowering were 66% more likely to regress/improve their LVH (HR=1.66, 95%CI: 1.31 to 2.11). Adjustment for LVH as a time-varying covariate did not substantially attenuate the effect of intensive BP therapy on CVD events (HR (95%CI) of intensive vs. standard BP lowering on CVD: 0.76(0.64,0.90) and 0.77(0.65,0.91) before and after adjusting for LVH as a time-varying covariate, respectively). Conclusions Among patients with hypertension but no diabetes, intensive BP lowering (target systolic BP<120 mmHg), compared with standard BP lowering (target systolic BP<140 mmHg), resulted in lower rates of developing new LVH in those without LVH, and higher rates of regression of LVH in those with existing LVH. This favorable effect on LVH did not explain most of the reduction in CVD events associated with intensive BP lowering in the SPRINT trial.
The renin-angiotensin-aldosterone system (RAAS) plays a fundamental role in the physiology of blood pressure control and the pathophysiology of hypertension (HTN) with effects on vascular tone, sodium retention, oxidative stress, fibrosis, sympathetic tone, and inflammation. Fortunately, RAAS blocking agents have been available to treat HTN since the 1970s and newer medications are being developed. In this review, we will (1) examine new anti-hypertensive medications affecting the RAAS, (2) evaluate recent studies that help provide a better understanding of which patients may be more likely to benefit from RAAS blockade, and (3) review three recent pivotal randomized trials that involve newer RAAS blocking agents and inform clinical practice.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.