Key result
SGLT2 inhibitors protect renal tubules in type 2 CRS via natriuresis, reduced fibrosis and oxidative stress.
Why the study?
In type 2 cardiorenal syndrome, renal tubules are the first to be damaged during progression from chronic heart failure to chronic renal insufficiency, but this damage may be reversible by SGLT2 inhibitors.
SGLT2 inhibitors offer a promising therapeutic approach for type 2 cardiorenal syndrome by specifically targeting and reversing renal tubular damage.
May support SGLT2 inhibitor use in type 2 cardiorenal syndrome; extends mechanistic insights but leaves open need for clinical trials.
The pathogenesis of type 2 cardiorenal syndrome (CRS) is mostly associated with reduced cardiac output, increased central venous pressure (CVP), activation of the renin-angiotensin-aldosterone system (RAAS), inflammation, and oxidative stress. As a drug to treat diabetes, sodium-glucose transporter 2 inhibitor (SGLT2i) has been gradually found to have a protective effect on the heart and kidney and has a certain therapeutic effect on CRS. In the process of chronic heart failure (CHF) leading to chronic renal insufficiency, the renal tubular system, as the main functional part of the kidney, is the first to be damaged, but this damage can be reversed. In this review, we focus on the protective mechanisms of SGLT2i targeting renal tubular in the treatment of CRS, including natriuresis and diuresis to relieve renal congestion, attenuate renal tubular fibrosis, improve energy metabolism of renal tubular, and slow tubular inflammation and oxidative stress. This may have beneficial effects on the treatment of CRS and is a direction for future research.
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Wang et al. (2023) conducted a review in Type 2 cardiorenal syndrome. SGLT2 inhibitors was evaluated. SGLT2 inhibitors protect renal tubules in type 2 cardiorenal syndrome through mechanisms including natriuresis, reduced tubular fibrosis, improved energy metabolism, and decreased oxidative stress.
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