Researchers have discovered that elevated levels of a stress response protein are associated with a reduced risk of kidney damage after heart surgery in patients. Their preliminary analysis of 60 patients has implications for the development of new therapies and risk management strategies to reduce the likelihood of severe kidney complications stemming from invasive cardiac procedures.

The most common complication from open-heart surgery is acute kidney injury (or AKI), which occurs when the patient’s kidneys suddenly fail to filter waste products. AKI worsens patient outcomes and extends the length of hospital stays, resulting in significantly higher healthcare costs. 

Scientists previously found that a cell signaling molecule named macrophage migration inhibitory factor (MIF) protects the heart from damage induced by fluctuating oxygen levels, leading Christian Stoppe and colleagues to suspect that MIF could also mitigate damage to other organs such as the kidneys.

They measured the concentrations of MIF in serum and urine samples taken from patients at several time points before and after heart surgery. The authors found that patients with high levels of MIF in serum 12 hours after surgery were less likely to develop AKI compared to individuals with lower MIF levels.

Furthermore, removing the gene that encodes for MIF resulted in increased death of kidney cells in mouse models of AKI. Administering MIF both before and after blocking blood flow to the kidneys also ameliorated AKI in wild type mice.

The study does not prove a causative effect, and larger clinical studies should validate the clinical significance of circulating MIF as a potentially effective tool to identify patients at risk for AKI.