Successful treatment of severe renal failure caused by malignant hypertension using a combination of renin-angiotensin-aldosterone system inhibitors: a case report.
Direct renin inhibitor
Malignant hypertension
Mineralocorticoid receptor antagonist
Renin–angiotensin–aldosterone system
Journal
CEN case reports
ISSN: 2192-4449
Titre abrégé: CEN Case Rep
Pays: Japan
ID NLM: 101636244
Informations de publication
Date de publication:
30 Sep 2024
30 Sep 2024
Historique:
received:
10
06
2024
accepted:
20
09
2024
medline:
1
10
2024
pubmed:
1
10
2024
entrez:
30
9
2024
Statut:
aheadofprint
Résumé
Marked activation of the renin-angiotensin-aldosterone system (RAAS) plays an important role in malignant hypertension (MHT) by worsening hypertension and renal function. The rates of readmission for severe hypertension and cardiovascular disease in such emergencies are high, suggesting that suppression of the RAAS may be inadequate during the acute phase in some cases. This report presents a case of MHT complicated with renal insufficiency (creatinine 3.93 mg/dL) and massive proteinuria, in which antihypertensive therapy, including an angiotensin receptor blocker, aliskiren, and spironolactone, normalized blood pressure (BP) and preserved renal function. Plasma renin activity was extremely high (131.9 ng/mL/h) on admission but normalized within almost 2 weeks. Although aliskiren and spironolactone were discontinued before discharge, BP was well controlled and renal function was further improved (creatinine 1.14 mg/dL) at follow-up 24 months later. This case of renal failure induced by MHT was successfully treated with a combination of RAAS inhibitors during the acute phase. The controlled BP and improved renal function in this patient suggest that adequate suppression of the RAAS cascade during the acute phase is potentially effective in terms of breaking the vicious cycle of MHT with hyperreninemia.
Identifiants
pubmed: 39349898
doi: 10.1007/s13730-024-00934-7
pii: 10.1007/s13730-024-00934-7
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Japan Society for the Promotion of Science
ID : 23K19566
Organisme : Japan Society for the Promotion of Science
ID : 24K19148
Informations de copyright
© 2024. The Author(s).
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