Key result
Dual blockade of the renin-angiotensin system with benazepril and irbesartan improved pathological damage and functional impairments in diabetic nephropathy rats compared to monotherapy (P<0.05).
Why the study?
Does dual RAS blockade improve kidney histopathology and inflammatory markers in a rat model of diet-induced diabetic nephropathy?
RCT (n=50)
Randomly divided
Does dual RAS blockade improve kidney histopathology and inflammatory markers in a rat model of diet-induced diabetic nephropathy?
p-value: p=<0.05
Dual RAS blockade provides enhanced renoprotection in a rat model of diabetic nephropathy, potentially through increased tubular kallikrein expression and reduced interstitial inflammation.
Dual RAS blockade may add renoprotection via kallikrein upregulation in diabetic rats; leaves open clinical relevance and safety.
PURPOSE: The objective of this study is to investigate the effect of dual blockage of renin-angiotensin system (RAS) on renal kallikrein expression and inflammatory response in diabetic nephropathy (DN). METHODS: Rats were randomly divided into 5 groups with 10 rats in each group: normal control; DN model induced by high fat and high sucrose diets; and DN treated with either benazepril 10 mg/kg/d, irbesartan 30 mg/kg/d, or both. After 8-week treatment, we examined changes in the kidney histopathology, function and immunohistochemical stain of kallikrein, macrophage marker CD68, and profibrotic markers transforming growth factor- (TGF-) β and α-smooth muscle action (SMA). RESULTS: DN rats showed enlarged kidneys with glomerulosclerosis, interstitial chronic inflammation and fibrosis, and proteinuria. All the pathological damage and functional impairments were improved after the RAS blockades (all P < 0.05). Compared with monotherapy, combined treatment further alleviated the kidney impairments in parallel to increased tubular immunoreactivity for kallikrein and decreased immunopositive cells for CD68, TGF-β, and α-SMA. CONCLUSION: The renoprotective effects of the dual RAS blockade in diabetic nephropathy may be attributed to improved tubular kallikrein expression and interstitial inflammatory response.
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Zou et al. (2015) conducted an RCT in Diabetic nephropathy (n=50). Dual blockade of renin-angiotensin system (benazepril and irbesartan) vs. Normal control, untreated DN model, or monotherapy (benazepril or irbesartan) was evaluated on Kidney histopathology, function, and immunohistochemical stain of kallikrein, CD68, TGF-β, and α-SMA (p=<0.05). Dual blockade of the renin-angiotensin system with benazepril and irbesartan improved pathological damage and functional impairments in diabetic nephropathy rats compared to monotherapy (P<0.05).
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