Key result
Aliskiren increases renal perfusion by ~6%, reversing after withdrawal despite sustained blood pressure lowering.
Why the study?
Renal hemodynamic effects of renin-angiotensin system inhibitors can increase acute kidney injury risk, and the reversibility of aliskiren's renal effects was unclear.
Does aliskiren withdrawal reverse renal hemodynamic effects compared to systemic blood pressure effects in subjects with arterial hypertension?
Does aliskiren withdrawal reverse renal hemodynamic effects compared to systemic blood pressure effects in subjects with arterial hypertension?
Absolute Event Rate: 287% vs 272%
p-value: p=0.03
Renal hemodynamic effects of aliskiren are more readily reversible than its systemic blood pressure-lowering effects upon withdrawal.
Aliskiren-induced renal perfusion increase reverses rapidly after withdrawal unlike sustained BP effect; leaves open differential reversibility in larger randomized studies.
BACKGROUND AND OBJECTIVES: Renal hemodynamic effects of inhibitors of the renin-angiotensin system can increase the risk of acute kidney injury under certain conditions. The BP-lowering effects of the renin inhibitor aliskiren are sustained 3-4 weeks after withdrawal. In this study, the reversibility of the renal hemodynamic effects of aliskiren was tested. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: In this open-label study, renal perfusion was measured by 1.5-T magnetic resonance imaging-arterial spin labeling in 34 subjects with arterial hypertension before aliskiren (pre-aliskiren), after 4 weeks of aliskiren treatment (300 mg), and 4-5 days (∼2.5-3.0× plasma half-life) after withdrawal (post-aliskiren). RESULTS: Aliskiren reduced systolic BP from 152 ± 14 to 139 ± 16 mmHg (P<0.0001), which was sustained post-aliskiren (136 ± 13 mmHg, P=1.00 versus aliskiren). Aliskiren significantly altered renal perfusion (P=0.005), increasing from 272 ± 25 pre-aliskiren to 287 ± 29 ml/min per 100 g during aliskiren (P=0.03). This increase in renal perfusion was completely reversed post-aliskiren (272 ± 26 ml/min per 100 g, P=0.03 versus aliskiren, P=0.63 versus pre-aliskiren). No changes were noted in urinary angiotensinogen levels. Plasma renin activity was reduced by aliskiren, which was sustained post-aliskiren. Angiotensin II and aldosterone were reduced by aliskiren but recovered post-aliskiren to pre-aliskiren levels. CONCLUSIONS: After withdrawal of aliskiren, the effects on BP were sustained, whereas increase in renal perfusion was reversed, which was associated with recovery of angiotensin II and aldosterone to pretreatment levels. Renal hemodynamic effects are more readily reversible than systemic effects of aliskiren.
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Schneider et al. (2011) studied arterial hypertension (n=34). Aliskiren vs. Pre-aliskiren baseline was evaluated on renal perfusion (ml/min per 100 g) (p=0.03). Aliskiren increased renal perfusion from 272 to 287 ml/min per 100 g (P=0.03), which completely reversed after withdrawal, whereas its blood pressure lowering effects were sustained.
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