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 ...

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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.

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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.

It remains uncertain whether intensive control of blood pressure (BP) results in a lower risk of atrial fibrillation (AF) in patients with hypertension. Using data from SPRINT (Systolic Blood Pressure Intervention Trial), which enrolled participants with hypertension at increased risk of cardiovascular disease, we examined whether intensive BP lowering (target systolic BP [SBP] <120 mm Hg), compared with standard BP lowering (target SBP<140 mm Hg), results in a lower risk of AF. This analysis included 8022 participants (4003 randomized to the intensive arm and 4019 to standard BP arm) who were free of AF at the time of enrollment and with available baseline and follow-up electrocardiographic data. AF was ascertained from standard 12-lead electrocardiograms recorded at biannual study examinations and an exit visit. During up to 5.2 years of follow-up and a total of 28 322 person-years, 206 incident AF cases occurred; 88 in the intensive BP-lowering arm and 118 in the standard BP-lowering arm. Intensive BP lowering was associated with a 26% lower risk of developing new AF (hazard ratio, 0.74 [95% CI, 0.56–0.98]; P =0.037). This effect was consistent among prespecified subgroups of SPRINT participants stratified by age, sex, race, SBP tertiles, prior cardiovascular disease, and prior chronic kidney disease when interactions between treatment effect and these subgroups were assessed using Hommel adjusted P values. In conclusion, intensive treatment to a target of SBP <120 mm Hg in patients with hypertension at high risk of cardiovascular disease has the potential to reduce the risk of AF. Registration— URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01206062.

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Prospective studies indicate that hyperaldosteronism is found in 20% of patients with resistant hypertension (RHTN). A small number of observational studies in normotensive and hypertensive patients suggest a correlation between aldosterone levels and obesity while others could not confirm these findings. The correlation between aldosterone levels and body mass index (BMI) in patients with RHTN has not been previously investigated. Our objective was to determine if BMI is positively correlated with plasma aldosterone concentration (PAC), plasma renin activity (PRA), aldosterone-renin ratio (ARR), and 24-hour urinary aldosterone (24-hr UAldo) African-American (AA) and Caucasian patients. We performed a cross-sectional analysis of a large diverse cohort (n=2170) with RHTN. The relation between PAC, PRA, ARR, 24-hr UAldo and BMI was investigated for the entire cohort, by gender, and race (65.3% Caucasian, 40.3% men). We demonstrate that PAC and ARR were significantly correlated to BMI (p<0.0001) across the first three quartiles, but not from the 3rd to 4th quartile of BMI. PRA was not correlated with BMI. 24-hr UAldo was positively correlated across all quartiles of BMI for the cohort (p<0.0001) and when analyzed by gender (men p<0.0001; women p=0.0013) and race (p<0.05), and stronger for men compared to women (r=0.19, p<0.001 versus r=0.05, p=0.431, p=0.028) regardless of race. In both AA and Caucasian patients, aldosterone levels were positively correlated to increasing BMI, with the correlation being more pronounced in AA and Caucasian men. These findings suggest that obesity, particularly the abdominal obesity typical of men, contributes to excess aldosterone in patients with RHTN.