Key result
Sacubitril/valsartan lowers systolic blood pressure more than valsartan but provides less renoprotection in CKD rats.
Why the study?
Studies suggested sacubitril/valsartan has better renal protective effects than valsartan, but evidence remained inconsistent.
Does sacubitril/valsartan improve renal function and reduce blood pressure compared to valsartan in a rat model of adenine-induced chronic kidney disease?
RCT (n=24)
Open-label (not explicitly stated as blinded, typical for animal studies)
Random allocation into four groups
No
Does sacubitril/valsartan improve renal function and reduce blood pressure compared to valsartan in a rat model of adenine-induced chronic kidney disease?
Effect estimate: Significant reduction in systolic blood pressure with sacubitril/valsartan vs. valsartan (p < 0.001); valsartan showed greater improvements in renal function markers and histopathology
Absolute Event Rate: 144.3% vs 174.2%
p-value: p=<0.001
In a rat model of adenine-induced chronic kidney disease, sacubitril/valsartan provided superior blood pressure reduction, while valsartan alone offered more pronounced renoprotective and histopathological benefits.
Valsartan may be preferable for renoprotection in CKD despite lesser BP reduction; hypothesis-generating in adenine-CKD rats only.
Sacubitril/valsartan is a combined neprilysin inhibitor/angiotensin II receptor blocker which simultaneously potentiates the beneficial effects of natriuretic peptides while blocking angiotensin II accumulation. Numerous studies suggest that sacubitril/valsartan has better renal protective effects compared to valsartan but the evidence remains inconsistent. This study compared renal and blood pressure (BP)-lowering effects of sacubitril/valsartan versus valsartan in rats with adenine-induced chronic kidney disease (CKD). This model replicates slow progression and structural and functional characteristics of human CKD. Male Wistar rats (n = 24) were divided into four groups and treated for 35 days as follows: group 1 served as control; group 2 received 0.25% adenine; group 3 received adenine plus sacubitril/valsartan; group 4 received adenine plus valsartan. Adenine significantly increased systolic BP. It also significantly increased the urinary albumin/creatinine ratio, N-acetyl-β-D-glucosaminidase (NAG), plasma urea, creatinine, uric acid, and neutrophil gelatinase-associated lipocalin (NGAL) while reducing creatinine clearance. Additionally, adenine significantly increased inflammatory markers, decreased antioxidant activity, and induced tubular necrosis, dilatation, and interstitial inflammation. Sacubitril/valsartan significantly reduced systolic BP, with greater effects than valsartan. Both treatments reversed adenine-induced alterations in urinary albumin/creatinine ratio, NAG, plasma urea, creatinine, NGAL, and creatinine clearance, with more pronounced improvements in urea, NAG, and creatinine clearance observed with valsartan. Furthermore, both treatments ameliorated inflammatory and antioxidant changes to a comparable extent. Both treatments showed histopathological improvements, but these were more marked with valsartan. To conclude, both sacubitril/valsartan and valsartan effectively mitigated adenine-induced CKD changes, with sacubitril/valsartan producing greater systolic BP reduction and valsartan showing more pronounced renoprotective effects.
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Maskari et al. (2026) conducted an RCT in Male Wistar rats with adenine-induced chronic kidney disease (CKD) model replicating slow progression and structural and functional human CKD (n=24). Sacubitril/valsartan vs. Valsartan 30 mg/kg daily by gavage was evaluated on Systolic blood pressure and renal function markers (urea, creatinine clearance, urinary albumin/creatinine ratio, NAG, NGAL), and histopathological kidney damage in adenine-induced CKD (Significant reduction in systolic blood pressure with sacubitril/valsartan vs. valsartan (p < 0.001); valsartan showed greater improvements in renal function markers and histopathology, p=<0.001). Sacubitril/valsartan reduced systolic blood pressure more than valsartan (p < 0.001), but valsartan produced more pronounced renoprotective effects in adenine-induced CKD rats.
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