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Abstract: TH-PO490

Hypertension Associated with Hyper-Reninemic Hyperaldosteronism After COVID-19 Infection in a Pediatric Patient

Session Information

  • Pediatric Nephrology - I
    November 02, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Pediatric Nephrology

  • 1900 Pediatric Nephrology


  • Sivakumar, Devyani, Brown University Warren Alpert Medical School, Providence, Rhode Island, United States
  • Shi, Vivian, Stanford Medicine, Stanford, California, United States
  • Faizan, Mohammed Khurram, Brown University Warren Alpert Medical School, Providence, Rhode Island, United States

COVID-19 was a leading cause of death among children and adolescents from Aug 2021 through Jul 2022, ranking 8th for all causes and 1st for infectious causes [Kompaniyets, 2022]1. Children and adolescents are at risk for certain post-COVID complications. [Tadeo, 2023]2 [Flaxman, 2023]3. In a prospective multicenter study in Turkey, 28% of the children ages 10-18 yrs had abnormal blood pressure 8 weeks after a mild COVID-19 infection, of whom 39.2% had stage 1 HTN [Uysal, 2022]4. The pathophysiology of SARS-CoV-2 associated hypertension (HTN) remains unclear [Kukarni, 2022]5.

Case Description

A 13-yr-old male with no significant past medical history presents to the pediatric nephrology clinic for evaluation of HTN. He had COVID infection 9 mths ago and was noted to be hypertensive since then. He was asymptomatic. Vitals notable for BP 142/87 mmHg, BMI 31 kg/m2. Exam was normal. Labs revealed normal CBC, urinalysis, lytes, creatinine, TSH, serum metanephrine levels. Renin [4.2ng/mL/h] and aldosterone [37.6 ng/dL] levels were elevated. Renal US with doppler was unremarkable. MRA abdomen was negative for renal artery stenosis. 24-hour ABPM showed a daily average 135/70 mmHg and night average 140/73 mmHg. He was started on lisinopril with improvement in BP.


Angiotensin converting enzyme 2 (ACE2), which is utilized by SARS-CoV-2 for entry into host cells, is widely expressed in the lungs, kidneys, testes, gut, adipose tissue, and brain. Infection within host cells mediates RAS overactivation. One hypothesis is that the increased activity of the ACE/AngII/AT1R axis or the decreased activity of the ACE2/Ang-(1–7)/Mas Receptor axis generates pulmonary and neurogenic HTN [3]. We were able to rule out secondary causes in our patient with hyper-renninemic hyperaldosteronism and clinical response to lisinopril further supports this proposed mechanism. In a retrospective and prospective cohort study of adult patients, 21.6% patients had uncontrolled HTN requiring treatment, 23 days post-discharge from the hospital or ER for COVID infection [Wrona, 2022]6. In a cross-sectional study in Korea, an increase in the prevalence of HTN was observed among youths during the pandemic [Song, 2019]7. There are limited studies available in pediatric patients in comparison to adults assessing prevalence and risk factors for HTN post COVID infection.