SGLT2 INHIBITORS PROTECT THE KIDNEY
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The above is a picture of how a glomerulus looks. The glomerulus is one of a million filtering units that elegantly filter urine. When the tiny afferent arteriole that leads into the filter is dilated, it allows a larger amount of blood to flow into the glomerulus. Over time this damages the delicate membranes that separate the blood and protein from the fluids and minerals that will ultimately make up urine. The process of hyperfiltration occurs in kidney disease, particularly in diabetes and hypertension. Although the kidney has a regulatory mechanism to block the damaging effects of hyperfiltration, this mechanism becomes damaged over time, leading to an acceleration in kidney disease.
Sodium-glucose transporter 2 (SGLT2) inhibition allows more glucose to be trapped in the tubules and eliminated into the urine, helping reduce excess blood sugar and better controlling diabetes. It also allows sodium to be trapped, inducing the regulatory feedback mechanism that controls hyperfiltration to become more effective in reducing the blood flowing through the afferent arteriole. The decreased hyperfiltration helps protect the kidneys.
Clinical trials have now shown that the SGLT2 inhibitors do protect the kidneys. On March 16, 2022, Boehringer Ingelheim and Eli Lilly announced that an Independent Data Monitoring Committee recommended that the EMPA-KIDNEY trial of their drug empagliflozin (Jardiance) be stopped because patients with mild to severe CKD with and without diabetes were demonstrated to have slower disease progression.
The protective effect of SGLT2 inhibitors has previously been demonstrated using dapagliflozin (Farxiga), another SGLT2 inhibitor, in patients with and without kidney disease [1].
1. Heerspink HJL, Stefánsson BV, Correa-Rotter R, Chertow GM, Greene T, Hou FF, et al. Dapagliflozin in Patients with Chronic Kidney Disease. N Engl J Med. 2020;383(15):1436-46. doi: 10.1056/NEJMoa2024816.
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