Search

Introduction and Objective: The COVID-19 pandemic and worldwide quarantine resulted in major changes in individual lifestyles. In New York State, March 16, 2020, marked the end of in-restaurant dining and a reported shift to more cooking at home. We investigated the 24-hour urine of patients with known history of nephrolithiasis to see if changes during COVID-19 pandemic altered the risk of stone disease. Methods: Retrospectively, patients with history of nephrolithiasis seen for an outpatient visit from April 1, 2020, to December 31, 2020, were studied. All patients had a 24-hour urine study "pre-COVID" defined as before March 16, 2020, "during-COVID" from March 16, 2020, to December 31, 2020; if available, "post-COVID" from January 1, 2021, to October 31, 2022, was also included. Mean study values were compared using paired, two-tailed t -tests. Results: Ninety-three patients ( M  = 54, F  = 39) with a mean age of 60 years were evaluated. Twenty-four-hour urine revealed a significant reduction in urinary sodium (uNa) levels from pre-COVID (166.15 ± 7.51 mEq/L) compared with during-COVID (149.09 ± 7.55 mEq/L) ( p  = 0.015) and urinary calcium (uCa) levels from pre-COVID (214.18 ± 13.05 mg) compared with during-COVID (191.48 ± 13.03 mg) ( p  = 0.010). Post-COVID 24-hour urine ( N  = 73) levels for uNa (138.55 ± 6.83 mEq/L, p  = 0.0035) and uCa (185.33 ± 12.61 mg, p  = 0.012) remained significantly reduced compared with pre-COVID values, but with no difference compared with during-COVID values. Upon age stratification, this significance was found only in patients younger than 65. There were no significant differences in 24-hour urine total volume, magnesium, or citrate levels. Conclusions: During the COVID-19 lockdown, dietary choices limited to home-cooked meals allowed patients to better identify their food choices. This study demonstrates that home-cooked meals improved urinary parameters minimizing lithogenic risk factors for stone formation, including hypernatriuria and hypercalciuria. That these changes persisted into the post-COVID period may indicate improved dietary practices after the lockdown ended.

Objectives: To compare impact of day or on-call team, pediatric or adult attending, and patient age on testicular torsion management and outcomes., Methods: A retrospective study of patients with testicular torsion between 2012 and 2022 at a single institution was conducted. Variables impacting management time were assessed using univariate analyses., Results: One hundred and thirty-four patients were included: 49 underwent orchiectomies and 84 underwent orchiopexies. There was no significant difference between efficiency of on-call vs day team regarding time to ultrasound or time to operating room (OR). There were no significant differences between pediatric vs adult attending surgeons for time to surgery, intraoperative length of surgery, or testicular salvage rates. However, when patients were stratified by age greater or younger than 18years, older patients had significantly longer symptom duration (91.9 vs 20.0 minutes, P = .005), time to receive an ultrasound from emergency room registration (152 vs 87 minutes, P < .001), time to OR from emergency room registration (268 vs 185 minutes, P < .001), and time to OR from ultrasound read (187 vs 123 minutes, P = .03). Older patients also had lower rates of testicular salvage approaching significance (orchiectomy rate 48.8% vs 31.5%, P = .057)., Conclusion: While no significant delays in testicular torsion management were detected between management by on-call vs day team nor pediatric vs adult attending, increased age of patient was associated with delays in definitive surgical management. Greater index of suspicion for testicular torsion diagnosis in adult patients may improve the rate of testicular salvage., Competing Interests: Declaration of Competing Interest The authors have no conflict of interest to declare., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Purpose: We performed a retrospective analysis of a sarcoidosis cohort who had sACE obtained at their initial clinic visit, but the treating physician was blinded to the results. We examined the relationship between sACE and the treating physician's decision to escalate sarcoidosis treatment., Methods: Treatment was considered escalated if the prednisone dose was increased or if the prednisone dose was not changed but an additional anti-sarcoidosis drug was added or the dose was increased., Results: 561 sarcoidosis patients were analyzed. The most common target organ was the lung (84%). Using a cut-off of > 82 units/L for an elevated sACE, 31/82 (38%) with an elevated sACE had treatment escalation whereas 91/497 (18%) had treatment escalation with a normal sACE (p < 0.0001). For the need of treatment escalation, a sACE (cut-off of > 82) had sensitivity 0.25, specificity 0.89, positive predictive value 0.38, negative predictive value 0.81. These results were not appreciably different using other sACE cut-off values such as 70, 80, 90, or 100. A multivariable logistic regression model that included demographics, the target organ, spirometry results estimated that sACE level and lower FVC were significantly associated with the likelihood of treatment escalation. These findings held when sACE > 82 replaced sACE level in the multivariable logistic regression model., Conclusions: Although there was a strong correlation between sACE at the initial sarcoidosis clinic visit and subsequent treatment escalation of sarcoidosis, the predictive power was such that sACE is not adequately reliable to be used in isolation to make this determination., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Background: The impact of the right ventricular (RV) structure and function on the in-hospital outcomes in patients with COVID-19 infection has not been rigorously investigated., Objectives: The main aim of our study was to investigate in-hospital outcomes including mortality, ICU admission, mechanical ventilation, pressor support, associated with RV dilatation, and RV systolic dysfunction in COVID-19 patients without a history of pulmonary hypertension., Methods: It was a single academic tertiary center, retrospective cohort study of 997 PCR-confirmed COVID-19 patients. One hundred ninty-four of those patients did not have a history of pulmonary hypertension and underwent transthoracic echocardiography at the request of the treating physicians for clinical indications. Clinical endpoints which included mortality, ICU admission, need for mechanical ventilation or pressor support were abstracted from the electronic charts., Results: Patients' mean age was 68+/-16 years old and 42% of the study population were females. COPD was reported in 13% of the study population, whereas asthma was 10%, and CAD was 25%. The mean BMI was 29.8+/-9.5 kg/m2. Overall mortality was 27%, 46% in ICU patients, and 9% in the rest of the cohort. There were no significant differences in co-morbidities between expired patients and the survivors. A total of 19% of patients had evidence of RV dilatation and 17% manifested decreased RV systolic function. RV dilatation or decreased RV systolic function were noted in 24% of the total study population. RV dilatation was significantly more common in expired patients (15% vs 29%, p = 0.026) and was associated with increased mortality in patients treated in the ICU (HR 2.966, 95%CI 1.067-8.243, p = 0.037), who did not need require positive pressure ventilation, IV pressor support or acute hemodialysis., Conclusions: In hospitalized COVID-19 patients without a history of pulmonary hypertension, RV dilatation is associated with a 2-fold increase in inpatient mortality and a 3-fold increase in ICU mortality., Competing Interests: Declaration of Competing Interest None., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Idiopathic pulmonary hemosiderosis (IPH) is a rare disease without a known incidence or prevalence in adults. Our knowledge of this entity is limited as there is no prospective or retrospective study with a reasonable number of patients. The objective is to describe the demographics, clinical manifestations, diagnosis, treatment, and prognosis of adult patients with IPH. The Medline and Embase databases were searched from inception to 2021 with appropriate search formulas to identify relevant articles following strict inclusion and exclusion criteria. Statistical analyses were performed for the entire cohort and prespecified subgroups. A total of 84 patients were identified. The majority of patients were males 54/84 (64.3%). The median age was 27 years. The manifesting symptoms were present in the following frequencies: anemia 76/83 (91.6%), dyspnea 71/83 (85.5%), hemoptysis 70/84 (83.3%), cough 22/84 (26.2%), and chest pain 9/84 (10.7%). The classic triad was present in 61/84 (79%) patients. The mean hemoglobin during the initial presentation was 8.4 gm/dL. A total of 16/57 (19.5%) tested positive for autoantibodies. The median delay in the diagnosis of IPH was 1.02 years. Immunosuppressive therapy was prescribed in 49/79 (62%) patients, and recurrence occurred in more than half of the patients 36/66 (54.5%). A total of 63/79 (79.7%) patients were alive during the final follow-up. IPH is more common in young adults with a male predominance. A high index of suspicion is necessary to attain an early diagnosis and possibly reduce the short-term mortality of nearly 20% and long-term complications., (© 2022. International League of Associations for Rheumatology (ILAR).)

Human pulmonary dirofilariasis (HPD) is a rare zoonotic disease caused by Dirofilaria immitis, the nematode responsible for canine cardiopulmonary dirofilariasis (dog heartworm). The incidence of HPD is on the rise throughout the world due to increased awareness and factors affecting the vector (mosquito). Humans are accidental hosts for D. immitis. Most patients are asymptomatic and present with an incidental pulmonary nodule that mimics primary or metastatic pulmonary malignancy. Some patients suffer from pulmonary and systemic symptoms in the acute phase of pneumonitis caused by pulmonary arterial occlusion by the preadult worms resulting in pulmonary infarction and intense inflammation. These patients may have ill-defined pulmonary infiltrate on chest radiology. Pulmonary nodules represent the end result of initial pneumonitis. There are no specific clinical, laboratory, or radiologic findings that differentiate HPD from other causes of a pulmonary nodule. Although serologic tests exist, they are usually not commercially available. The majority of patients are diagnosed by histopathologic identification of the decomposing worm following surgical resection of the lesion., Competing Interests: Declaration of Competing Interest The authors have no conflict of interest., (Copyright © 2021 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.)

Hodgkin Lymphoma (HL) typically presents similarly to an infectious etiology, thus awareness of its atypical presentations is essential. We present a case of an adult woman who was found to have HL after presenting with a dry, non-productive cough and showing cavitary lesions on chest computed tomography (CT). We also describe the clinical, laboratory, and radiological workup done leading to the diagnosis and management of HL in a critical care setting., Learning Points: Cavitary lung lesions, particularly multiloculated, are often caused by mycobacterium tuberculosis (TB), aspergillosis, granulomatosis with polyangiitis, sarcoidosis, and rheumatic nodules.Pulmonary infiltration is a rare disorder of an extra-nodal site in Hodgkin's Lymphoma. The mediastinum and head and neck regions remain the most common sites affected by HL.Radiologically, primary pulmonary HL may mimic pneumonia, carcinoma making the diagnosis unclear., Competing Interests: Conflicts of Interests: The authors declare there are no competing interests., (© EFIM 2021.)

Rhabdomyosarcoma is an uncommon soft tissue sarcoma that rarely presents in adults. Clinical presentation is dependent on site and size. We present the case of a woman who presented with acute-onset dyspnoea and whose pathology report confirmed embryonal rhabdomyosarcoma (ERMS) seen as an incidental finding on chest computed tomography. We also describe the clinical, laboratory and radiological work-up conducted to diagnose and manage ERMS in the critical care setting., Learning Points: Rhabdomyosarcoma is a rare malignancy with a poor prognosis in adults compared with children, especially if it presents in an unfavourable primary site and has an unfavourable histological diagnosis.Immunohistochemical diagnosis remains the gold standard for embryonal rhabdomyosarcoma diagnosis and differentiation from similar malignancies on initial imaging studies.Management of adult rhabdomyosarcoma is usually multimodal with surgical resection and a combination of chemo and radiotherapy., Competing Interests: Conflicts of Interests: The authors declare there are no competing interests., (© EFIM 2021.)

Background: The clinical features and outcomes of mechanically ventilated patients with COVID-19 infection who develop a pneumothorax has not been rigorously described or compared to those who do not develop a pneumothorax., Purpose: To determine the incidence, clinical characteristics, and outcomes of critically ill patients with COVID-19 infection who developed pneumothorax. In addition, we compared the clinical characteristics and outcomes of mechanically ventilated patients who developed a pneumothorax with those who did not develop a pneumothorax., Methods: This study was a multicenter retrospective analysis of all adult critically ill patients with COVID-19 infection who were admitted to intensive care units in 4 tertiary care centers in the United States., Results: A total of 842 critically ill patients with COVID-19 infection were analyzed, out of which 594 (71%) were mechanically ventilated. The overall incidence of pneumothorax was 85/842 (10%), and 80/594 (13%) in those who were mechanically ventilated. As compared to mechanically ventilated patients in the non-pneumothorax group, mechanically ventilated patients in the pneumothorax group had worse respiratory parameters at the time of intubation (mean PaO 2 :FiO 2 ratio 105 vs 150, P<0.001 and static respiratory system compliance: 30ml/cmH 2 O vs 39ml/cmH 2 O, P = 0.01) and significantly higher in-hospital mortality (63% vs 49%, P = 0.04)., Conclusion: The overall incidence of pneumothorax in mechanically ventilated patients with COVID-19 infection was 13%. Mechanically ventilated patients with COVID-19 infection who developed pneumothorax had worse gas exchange and respiratory mechanics at the time of intubation and had a higher mortality compared to those who did not develop pneumothorax., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Objective: This narrative review aims to provide a detailed overview of pleural abnormalities in patients with coronavirus disease 19 or COVID-19., Background: Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) is a novel beta coronavirus responsible for COVID-19. Although pulmonary parenchymal and vascular changes associated with COVID-19 are well established, pleural space abnormalities have not been the primary focus of investigations., Methods: Narrative overview of the medical literature regarding pleural space abnormalities in COVID-19. The appropriate manuscripts were identified by searching electronic medical databases and by hand searching the bibliography of the identified papers. Pleural abnormalities on transverse and ultrasound imaging are discussed. The incidence, clinical features, pathophysiology, and fluid characteristics of pleural effusion are reviewed. Studies reporting pneumothorax and pneumomediastinum are examined to evaluate for pathogenesis and prognosis. A brief comparative analysis of pleural abnormalities among patients with COVID-19, severe acute respiratory syndrome (SARS), and Middle Eastern respiratory syndrome (MERS) has been provided., Conclusions: Radiologic pleural abnormalities are common in COVID-19, but the incidence of pleural effusion appears to be low. Pneumothorax is rare and does not independently predispose the patient to worse outcomes. SARS-CoV-2 infects the pleural space; however, whether the pleural fluid can propagate the infection is unclear., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://dx.doi.org/10.21037/jtd-21-542). The authors have no conflicts of interest to declare., (2021 Journal of Thoracic Disease. All rights reserved.)

Case Presentation: A 74-year-old man was referred to a pulmonologist for evaluation of a 1-year history of nonproductive cough and progressive exertional dyspnea. He was initially evaluated by his primary care physician, where he had spirometry that was negative for any obstructive or restrictive lung disease. An echocardiogram showed a normal left ventricular ejection fraction, with no wall motion abnormality or valvular heart disease. He had an outpatient chest radiograph performed (Fig 1), and he was subsequently treated empirically for a COPD exacerbation with 5 days of oral prednisone and azithromycin. He was eventually referred to a pulmonologist because of a lack of clinical improvement. On seeing his pulmonary physician, he described the same exertional dyspnea and a nonproductive cough. A review of systems was negative for fever, chills, wheezing, angina, arthralgia, myalgia, rash, or leg swelling. He denied any medical illness and was not taking any medications. He was currently retired and had worked as a cashier his entire adult life. He had no occupational exposure to asbestos, coal dust, beryllium, silica dust, or dust from hard metal objects, such as cobalt. However, he had smoked approximately 1 to 2 packs of cigarettes per day and had done so for the past 50 years. His vital signs were unremarkable, aside from an oxygen saturation of 94% on room air. His physical examination revealed bibasilar "velcro-like" inspiratory crackles on lung examination. There was no digital clubbing, nor was there peripheral edema in his lower extremities. He had no muscle tenderness and demonstrated normal muscle strength against resistance., (Copyright © 2020 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.)

Competing Interests: Competing interests: None declared.

Background: There are limited data examining the diagnostic accuracy of thoracic ultrasonography (TUS) in distinguishing transudative from exudative pleural effusions., Research Question: What is the diagnostic accuracy of TUS in distinguishing transudative from exudative effusions in consecutive patients with pleural effusion?, Study Design and Methods: Consecutive patients who underwent TUS and subsequently a diagnostic thoracentesis with a pleural fluid analysis were identified. TUS images of the pleural effusions were interpreted by previously published criteria. We evaluated the diagnostic performance of TUS findings in predicting a transudative vs exudative pleural effusions and specific pleural diagnoses., Results: We evaluated 300 consecutive pleural effusions in 285 patients. The pleural effusions were classified as exudative in 229 of 300 cases (76%). TUS showed anechoic effusions in 122 of 300 cases (40%) and complex effusions in 178 of 300 cases (60%). An anechoic appearance on TUS was associated with exudative effusions (68/122; 56%) as compared with transudative effusions (54/122; 44%). The presence of a complex-appearing effusion on TUS was highly predictive of an exudative effusion (positive predictive value of 90%). However, none of the four TUS characteristics were highly specific of a pleural diagnosis., Interpretation: Thoracic ultrasonography is inadequate to diagnose a transudative pleural effusion reliably. Although the TUS findings of a complex effusion may suggest an exudative pleural effusion, specific pleural diagnoses cannot be predicted confidently., (Copyright © 2020 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.)

Objectives: To compare the clinical outcome of mechanically ventilated patients with severe acute respiratory syndrome coronavirus 2-related acute respiratory distress syndrome, who received corticosteroid with those who did not., Design: Retrospective analysis., Setting: Intensive care setting., Patients: All adult mechanically ventilated patients, who were admitted to the ICU between March 20, 2020, and May 10, 2020, for severe acute respiratory syndrome coronavirus 2-related acute respiratory distress syndrome., Interventions: None., Measurements and Main Results: Cohort was divided into two groups based on corticosteroid administration. The primary outcome variable was ventilator-free days at day 28. Secondary outcome variable was ICU-free days at day 30, and hospital-free days at day 30. Consecutive 61 mechanically ventilated patients with severe acute respiratory syndrome coronavirus 2-related acute respiratory distress syndrome were analyzed. Patient in corticosteroid group as compared with noncorticosteroid group have higher 28-day ventilator-free days (mean, 10.2; median, 7 [interquartile range, 0-22.3] vs mean, 4.7; median, 0 [interquartile range, 0-11]; p = 0.01).There was no significant difference noted in secondary outcomes (ICU-free days at day 30 and hospital-free days at day 30)., Conclusions: Among mechanically ventilated severe acute respiratory syndrome coronavirus 2-related acute respiratory distress syndrome patients, corticosteroids use was associated with significant improvement in 28-day ventilator-free days at day 28, but no significant improvement in ICU-free days at day 30, and hospital-free days at day 30., Competing Interests: Dr. Feustel received funding as a statistical consultant forTransonic Systems, Scientific advisor with shares in Penrose TherapeuTx, LLC. Dr. Jaitovich received funding from National Institutes of Health under the award number K01-HL130704 and by the Collins Family Foundation Endowment. The remaining authors have disclosed that they do not have any potential conflicts of interest., (Copyright © 2020 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of the Society of Critical Care Medicine.)

Rationale: 20-Hydroxyeicosatetraenoic acid (20-HETE), one of the principle cytochrome P450 eicosanoids, is a potent vasoactive lipid whose vascular effects include stimulation of smooth muscle contractility, migration, and proliferation, as well as endothelial cell dysfunction and inflammation. Increased levels of 20-HETE in experimental animals and in humans are associated with hypertension, stroke, myocardial infarction, and vascular diseases., Objective: To date, a receptor/binding site for 20-HETE has been implicated based on the use of specific agonists and antagonists. The present study was undertaken to identify a receptor to which 20-HETE binds and through which it activates a signaling cascade that culminates in many of the functional outcomes attributed to 20-HETE in vitro and in vivo., Methods and Results: Using crosslinking analogs, click chemistry, binding assays, and functional assays, we identified G-protein receptor 75 (GPR75), currently an orphan G-protein-coupled receptor (GPCR), as a specific target of 20-HETE. In cultured human endothelial cells, 20-HETE binding to GPR75 stimulated Gα q/11 protein dissociation and increased inositol phosphate accumulation and GPCR-kinase interacting protein-1-GPR75 binding, which further facilitated the c-Src-mediated transactivation of epidermal growth factor receptor. This results in downstream signaling pathways that induce angiotensin-converting enzyme expression and endothelial dysfunction. Knockdown of GPR75 or GPCR-kinase interacting protein-1 prevented 20-HETE-mediated endothelial growth factor receptor phosphorylation and angiotensin-converting enzyme induction. In vascular smooth muscle cells, GPR75-20-HETE pairing is associated with Gα q/11 - and GPCR-kinase interacting protein-1-mediated protein kinase C-stimulated phosphorylation of MaxiKβ, linking GPR75 activation to 20-HETE-mediated vasoconstriction. GPR75 knockdown in a mouse model of 20-HETE-dependent hypertension prevented blood pressure elevation and 20-HETE-mediated increases in angiotensin-converting enzyme expression, endothelial dysfunction, smooth muscle contractility, and vascular remodeling., Conclusions: This is the first report to identify a GPCR target for an eicosanoid of this class. The discovery of 20-HETE-GPR75 pairing presented here provides the molecular basis for the signaling and pathophysiological functions mediated by 20-HETE in hypertension and cardiovascular diseases., (© 2017 American Heart Association, Inc.)

Increased vascular 20-hydroxyeicosatetraenoic acid (20-HETE), a cytochrome P450 arachidonic acid metabolite, promotes vascular dysfunction, injury, and hypertension that is dependent, in part, on the renin angiotensin system (RAS). We have shown that, in human microvascular endothelial cells, 20-HETE increases angiotensin-converting enzyme (ACE) mRNA, protein, and ACE activity via an epidermal growth factor receptor (EGFR)/tyrosine kinase/mitogen-activated protein kinase (MAPK)/inhibitor of κB kinase (IKK)β-mediated signaling pathway. In this work, we show that, similar to epidermal growth factor (EGF), 20-HETE (10 nM) activates EGFR by stimulating tyrosine phosphorylation; however, unlike 20-HETE, EGF does not induce ACE expression, and pretreatment with a neutralizing antibody against EGF does not prevent the 20-HETE-mediated ACE induction. Inhibition of nuclear factor κB (NF-κB) activation prevented the 4.58-fold (±0.78; P < 0.05) 20-HETE-mediated induction of ACE. The 20-HETE increased NF-κB-binding activity in nuclear extracts and the activity of both the somatic and germinal ACE promoters by 4.37-fold (±0.18; P < 0.05) and 2.53-fold (± 0.24; P < 0.05), respectively. The 20-HETE-stimulated ACE promoter activity was abrogated by the 20-HETE antagonist 20-hydroxy-6,15-eicosadienoic acid and by inhibitors of EGFR, MAPK, IKKβ, and NF-κB activation. Sequence analysis demonstrated the presence of two and one putative NF-κB binding sites on the human somatic and germinal ACE promoters, respectively. Chromatin immunoprecipitation assay indicated that 20-HETE stimulates the translocation and subsequent binding of NF-κB to each of the putative binding sites (S1, 3.43 ± 0.3-fold enrichment versus vehicle; S2, 3.72 ± 0.68-fold enrichment versus vehicle; S3, 3.20 ± 0.18-fold enrichment versus vehicle; P < 0.05). This is the first study to identify NF-κB as a transcriptional factor for ACE and to implicate a distinct EGFR/MAPK/IKK/NF-κB signaling cascade underlying 20-HETE-mediated transcriptional activation of ACE mRNA and stimulation of ACE activity., (Copyright © 2016 by The American Society for Pharmacology and Experimental Therapeutics.)

Increased vascular 20-HETE is associated with hypertension and activation of the renin-angiotensin system (RAS) through induction of vascular angiotensin-converting enzyme (ACE) expression. Cyp4a12tg mice, whose Cyp4a12-20-HETE synthase expression is under the control of a tetracycline (doxycycline, DOX) promoter, were used to assess the contribution of ACE/RAS to microvascular remodeling in 20-HETE-dependent hypertension. Treatment of Cyp4a12tg mice with DOX increased systolic blood pressure (SBP; 136 ± 2 vs. 102 ± 1 mmHg; P < 0.05), and this increase was prevented by administration of 20-HEDGE, lisinopril, or losartan. DOX-induced hypertension was associated with microvascular dysfunction and remodeling of preglomerular microvessels, which was prevented by 20-HEDGE, a 20-HETE antagonist, yet only lessened, but not prevented, by lisinopril or losartan. In ACE 3/3 mice, which lack vascular endothelial ACE, administration of 5α-dihydrotestosterone (DHT), a known inducer of 20-HETE production, increased SBP; however, the increase was about 50% of that in wild-type (WT) mice (151 ± 1 vs. 126 ± 1 mmHg). Losartan and 20-HEDGE prevented the DHT-induced increase in SBP in WT and ACE 3/3 mice. DHT treatment increased 20-HETE production and microvascular remodeling in WT and ACE 3/3 mice; however, remodeling was attenuated in the ACE 3/3 mice as opposed to WT mice (15.83 ± 1.11 vs. 22.17 ± 0.92 μm; P < 0.05). 20-HEDGE prevented microvascular remodeling in WT and ACE 3/3 mice, while losartan had no effect on microvascular remodeling in ACE 3/3. Taken together, these results suggest that RAS contributes to 20-HETE-mediated microvascular remodeling in hypertension and that 20-HETE-driven microvascular remodeling independent of blood pressure elevation does not fully rely on ACE activity in the vascular endothelium., (Copyright © 2015 the American Physiological Society.)