The following is a summary of “Basigin is released in extracellular vesicles derived from the renal tubular epithelium in response to albuminuria,” published in the August 2023 issue of Nephrology by Watanabe et al.
Albuminuria, a sign of kidney damage, can lead to further injury and worsen kidney disease. Researchers started a retrospective study to investigate the morphology and origin of urinary basigin/CD147 (Bsg) in chronic kidney disease (CKD) patients to assess its role in tubular injury.
They treated 50 patients with Diabetic Kidney Disease (DKD) using either spironolactone at a dose of 25 mg for 4 weeks or conservative treatment. Urinary Bsg values correlated with clinical markers. Additionally, primary-cultured proximal tubular epithelial cells (PTECs) from adult human kidneys were subjected to high glucose or bovine serum albumin (BSA).
The results showed that in early-phase DKD patients, urinary Bsg levels strongly correlated with proteinuria but not HbA1c. The study primarily examined full-length Bsg on extracellular vesicles (EVs) in urine from DKD patients, revealing the presence of Bsg and SGLT2 proteins in these EVs. Significantly, spironolactone treatment concurrently reduced the release of Bsg-containing EVs, which correlated with reduced albuminuria. Exposing proximal tubular epithelial cells (PTECs) to BSA (but not high glucose) increased the storage of supernatant Bsg in EVs without any exposure-specific changes in Bsg transcription.
Investigators concluded that proteinuria causes the release of basin-containing vesicles from kidney cells into the urine.