Key result
Dual NEP-ACE inhibition provides no additional renoprotection over standard ACE inhibition alone.
Why the study?
Myocardial infarction aggravates preexistent mild renal damage likely involving the renin-angiotensin-aldosterone-system and vasoactive peptides metabolized by neutral endopeptidase, but the renoprotective effects of ACE inhibition and combined ACE/NEP inhibition were unclear.
Does ACEi or VPI prevent renal damage in a rat model of cardiorenal interaction?
Does ACEi or VPI prevent renal damage in a rat model of cardiorenal interaction?
In a rat model of cardiorenal interaction, both ACE inhibition and vasopeptidase inhibition similarly prevented renal damage, with no added benefit from VPI.
No takes yet. Share an insight, caveat, or question.
Similar renoprotection by ACEi and VPI in this rat model without VPI superiority; leaves open clinical translation and human applicability.
Windt et al. (2006) studied Renal damage after myocardial infarction (n=42). Lisinopril (ACEi) and AVE7688 (VPI) vs. Vehicle was evaluated on Renal damage assessed by proteinuria, interstitial alpha-smooth muscle actin (alpha-SMA) staining, and focal glomerulosclerosis (FGS). In a rat model, both ACEi and VPI similarly reduced proteinuria (76±6% vs 77±4%) and prevented renal damage compared with vehicle, with VPI providing no additional renoprotection.
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