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Abstract: PO1844

RAAS vs. COVID: Case of an 18-Year-Old with New-Onset Hypertension

Session Information

Category: Hypertension and CVD

  • 1403 Hypertension and CVD: Mechanisms

Authors

  • Thiruvarudsothy, Srikanth, Virtua Health, Marlton, New Jersey, United States
  • Jeyarajasingam, Arsitha, National Hospital of Sri Lanka, Colombo, Western , Sri Lanka
  • Srikanth, Theesitha, Sichuan University West China Hospital, Chengdu, Sichuan, China
Introduction

It has been increasingly known that SARS-CoV-2 causes an imbalance in the Renin-Angiotensin-Aldosterone System (RAAS). Here we present an interesting case of a young man, who presented with new onset of HTN and elevated renin and aldosterone levels with a h/o COVID-19.

Case Description

An 18-year-old Caucasian man with a remote history of asthma initially presented to his primary care physician with new onset of headaches. He was noted to have an elevated blood pressure, but otherwise a benign physical examination. A workup for secondary HTN revealed an elevated renin (8.7 ng/mL/hr), aldosterone levels (42 ng/dL) and otherwise unremarkable. He was started on Enalapril 5mg daily. A workup including CT and MRI of the brain, were unremarkable. He was referred to nephrology for the new diagnosis of HTN and abnormal renin and aldosterone levels. During the initial renal evaluation, patient was asymptomatic and his BP was well controlled on the Enalapril. Renin and aldosterone levels were repeated, about 8 weeks after the cessation of Enalapril. Patient’s blood pressure remained well controlled and didn’t require any medications. Since the diagnosis of HTN, the patient maintained a strict low salt diet. He always had good fluid intake. At a follow up visit, patient continued to remain asymptomatic and with good blood pressure control without needing medications. Repeat renin (1.9 ng/mL/hr) and aldosterone (16.8 ng/dL), as well as aldosterone/renin levels were resulted within normal limits. Later patient admitted that he was diagnosed with COVID-19 a month prior to his onset of headaches.

Discussion

SARS-CoV-2, which causes COVID-19, is known to hijack the RAAS cascade and use ACE2 enzyme to make human cell entry. Studies have demonstrated the possible correlation between COVID severity and comorbidities such as HTN (potentially involving the RAAS). Current recommendations are to continue the use of ACE Inhibitors (ACEI) and Angiotensin Receptor Blockers (ARB) in COVID-19 patients. Our case, not only supports the above findings, but also demonstrates how RAAS is vulnerable to SARS-CoV-2, can manifest with new onset HTN and other complications. It is also interesting to see, how ACEIs and ARBs should be utilized as first line agents for BP control and to improve outcomes. To much relief, the effect on RAAS by the SARS-CoV-2 seems to be transient and short lived.