A new treatment that can prevent acute kidney injury from worsening into chronic kidney failure has been proposed for the first time in the world by a Korea-based research team.
Gwangju Institute of Science and Technology (GIST) said on the 28th that a joint team led by Lee Jae-young of the department of materials science and engineering and Kim Su-wan of Chonnam National University College of Medicine developed an intelligent nanomedicine technology that blocks the pathological process in which acute kidney failure progresses to a chronic condition.
Acute kidney injury (AKI) is a condition in which kidney function suddenly declines due to surgery, contrast agents, or sepsis. Even when most cases recover, many worsen over time into chronic kidney disease (CKD). One of the main causes of this worsening is excessive production of reactive oxygen species (ROS) in the kidney. Reactive oxygen species damage cells and cause inflammation and fibrosis, ultimately impairing kidney function.
Until now, there has been no therapy that can precisely control reactive oxygen species and deliver drugs only to damaged sites. To solve this problem, the team designed a graphene-based nanodrug platform that responds only to reactive oxygen species at injured sites to release the drug.
The newly developed drug uses a vitamin D derivative antifibrotic (paricalcitol) as the main component, encapsulated with hyaluronic acid (HA) and reduced graphene (rGO). Hyaluronic acid selectively binds to the "CD44 receptor" on the surface of damaged kidney cells, helping the drug accumulate only at injury sites. In environments rich in reactive oxygen species, the drug is self-released, treating only diseased cells while leaving healthy tissue untouched.
In experiments, this nanocomposite released 2.7 times more drug at injury sites, and in cell studies, it maintained kidney cell viability above 70% even in strongly oxidative conditions such as with hydrogen peroxide. In animal studies, the drug concentrated in injured kidneys and showed marked reductions in inflammation, fibrosis, and cellular damage.
In particular, major blood markers indicating the degree of kidney function damage (NGAL, Cystatin C) also decreased significantly. This suggests it can prevent the "AKI-to-CKD transition," in which acute injury worsens into chronic disease.
Lee said, "This study presents a smart drug delivery platform that reacts to reactive oxygen species and works only at lesion sites," adding, "It has strong potential for application not only to kidney failure but also to various kidney diseases such as diabetic nephropathy."
Kim said, "This is a new therapeutic strategy that simultaneously suppresses cell damage and fibrosis caused by reactive oxygen species, and it could overcome the limitations of existing treatments."
The results were published on the 23rd in the international journal "Theranostics."
References
Theranostics (2025): https://www.thno.org/v16p0618.htm