Background: Marked activation of the renin-angiotensin-aldosterone system (RAAS) plays an important role in hypertensive emergencies, in particular malignant hypertension, 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 not adequate during the acute phase in some cases. Although treatment with a combination of RAAS inhibitors decreases blood pressure (BP) to a greater extent than monotherapy, its specific impact on malignant hypertension has not been reported.
Case presentation: A 41-year-old woman presented with malignant hypertension complicated with renal insufficiency (creatinine 3.93 mg/dL) and massive proteinuria (4.0 g/day). Renal biopsy confirmed malignant nephrosclerosis and thrombotic microangiopathy. Antihypertensive therapy was administered, including an angiotensin receptor blocker (ARB), aliskiren (a direct renin inhibitor), and spironolactone, a nonselective mineralocorticoid receptor antagonist, which preserved renal function effectively and normalized BP. Plasma renin activity was extremely high (131.9 ng/mL/h) on admission but normalized within almost 2 weeks after initiation of antihypertensive treatment. 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 after discharge.
Discussion: This case of renal failure induced by malignant hypertension was successfully treated with a combination of RAAS inhibitors (i.e., a direct renin inhibitor, an angiotensin receptor blocker, and a nonselective mineralocorticoid receptor antagonist). The controlled BP and improved renal function during both the short term and long term in this patient suggest that adequate suppression of the RAAS cascade during the acute phase of malignant hypertension is potentially effective in terms of breaking the vicious circle of malignant hypertension and hyperreninemia.