High renin hypertension in focal renal fibromuscular dysplasia: turn off of renin system angiotensin overactivation by renal angioplasty cured high blood pressure and quickly reversed myocardial hypertrophy.


Journal

Acta bio-medica : Atenei Parmensis
ISSN: 2531-6745
Titre abrégé: Acta Biomed
Pays: Italy
ID NLM: 101295064

Informations de publication

Date de publication:
30 04 2021
Historique:
received: 01 03 2020
accepted: 03 03 2020
entrez: 4 5 2021
pubmed: 5 5 2021
medline: 29 6 2021
Statut: epublish

Résumé

Background Fibromuscolar dysplasia (FMD) is an idiopathic, non-atherosclerotic and non-inflammatory stenotic lesion of renal arteries causing renovascular hypertension up-regulating renin-angiotensin-aldosterone system. Case report: A 18-year-old man was referred to our Hypertension Center (Clinica e Terapia Medica) for the recent onset of hypertension, poorly controlled on calcium channel blockers, already associated to electrocardiographic and echocardiography signs of left ventricular hypertrophy and significant albuminuria (728 mg/24 h). An increased plasma renin activity (PRA), aldosterone level and a mild hypokalemia raised the suspicion of renovascular hypertension. Abdominal CT and MRI angiography showed mild kidneys asymmetry and a tubular stenosis of the right renal artery in its mid-distal portion close to renal hilum. Radionuclide renal scintigraphy documented a kidneys asymmetry of separated glomerular filtration rate. Renal FMD was diagnosed based on patient age and the absence of cardiovascular risk factors for atherosclerosis. Patient successfully underwent right renal angioplasty giving a rapid normalization of blood pressure levels without antihypertensive drugs. Plasma aldosterone and PRA rapidly normalized as well as serum potassium levels. Six months after angioplasty echocardiography showed a regression of left ventricular hypertrophy and the patient albumin urine excretion became normal (14 mg/24 h). Conclusions FMD can cause renovascular hypertension associated to organ damage such myocardial hypertrophy and albuminuria through mechanisms dependent but also independent from blood pressure levels. Renal angioplasty turned off renin-angiotensin-aldosterone overactivity allowing the cure the hypertension and a surprisingly rapid reverse of myocardial hypertrophy and of excess of albumin urine excretion not only dependent on blood pressure normalization.

Identifiants

pubmed: 33944843
doi: 10.23750/abm.v92iS1.9358
pmc: PMC8142778
doi:

Substances chimiques

Angiotensins 0
Renin EC 3.4.23.15

Types de publication

Case Reports Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e2021162

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Auteurs

Simona Merla (S)

Centro per lo Studio dell'Ipertensione Arteriosa e delle malattie Cardiorenali, Dipartimento di Medicina e Chirurgia, Università di Parma. simona.merla@studenti.unipr.it.

Riccardo Simoni (R)

Università di Parma. riccardo.simoni90@gmail.com.

Stefano Tedeschi (S)

Università di Parma. stefano83tede@icloud.com.

Massimiliano Ferrari (M)

Università di Parma. massi.ferro76@gmail.com.

Giovanni Passeri (G)

Università di Parma. giovanni.passeri@unipr.it.

Carla Marcato (C)

Azienda Ospedaliera-Universitaria di Parma. cmarcato@ao.pr.it.

Enrico Epifani (E)

Azienda Ospedaliera-Universitaria di Parma. eepifani@ao.pr.it.

Ignazio Semproni (I)

Università di Parma. ignazio.semproni@studenti.unipr.it.

Giulia Zini (G)

Università di Parma. mariagiulia.corradinizini@studenti.unipr.it.

Ignazio Verzicco (I)

Università di Parma. ignazio.verzicco@studenti.unipr.it.

Pietro Coghi (P)

Università di Parma. pcoghi@ao.pr.it.

Riccardo Volpi (R)

Università di Parma. riccardo.volpi@unipr.it.

Aderville Cabassi (A)

University of Parma. aderville.cabassi@unipr.it.

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Classifications MeSH