Scientists have long wondered why so many people with chronic kidney disease eventually develop serious heart problems. Even when blood pressure and cholesterol are treated, the risk often remains high.
A new international study offers a possible explanation. Researchers from the University Hospital Würzburg and the Experimental and Clinical Research Center (ECRC), a partnership between Charité–Universitätsmedizin Berlin and the Max Delbrück Center, report that a small natural molecule called oxalate may switch on harmful inflammation throughout the body.
Their findings were published in Cardiovascular Research.
Chronic kidney disease develops when the kidneys gradually lose their ability to remove waste products and extra fluid from the blood. As kidney function worsens, waste chemicals begin to collect inside the body.
One of these chemicals is oxalate. Most people know oxalate because it can combine with calcium to form kidney stones. The new research suggests that oxalate may also influence the immune system in unexpected ways.
To explore this idea, the researchers carried out experiments in mice. Animals given extra oxalate developed widespread inflammation. Their kidneys became damaged, their hearts showed unhealthy changes, and their ability to pump blood became weaker. This suggested that oxalate was affecting much more than the kidneys alone.
The team then looked closely at immune cells and discovered that oxalate increased production of IL-17A, an immune protein that can strongly increase inflammation. They also found that oxalate changed the way immune cells produced and used energy, making them more likely to promote inflammation.
The discovery was supported by evidence from patients with primary hyperoxaluria, a rare inherited disorder that causes the liver to make excessive amounts of oxalate. These patients also showed higher IL-17A levels.
One of the most encouraging parts of the study came when the researchers blocked IL-17A in mice. Several health problems improved at the same time. Kidney damage became less severe, inflammation fell, scar formation decreased, and heart injury was reduced. These results suggest that IL-17A could become a future treatment target.
The researchers believe they have uncovered a chain reaction. Reduced kidney function allows oxalate to accumulate. Oxalate then stimulates IL-17A and other inflammatory processes, which may damage both the kidneys and the cardiovascular system.
Earlier population studies had already shown that people with high oxalate levels were more likely to experience cardiovascular complications. The new research provides biological evidence that may explain this connection.
The scientists are now studying larger groups of patients with chronic kidney disease to determine whether measuring oxalate and IL-17A could help identify people at greatest risk. They also hope to learn whether similar inflammatory pathways occur in other kidney disorders.
The findings should not change current treatment for patients today. Instead, they provide an important direction for future research. Current CKD care still focuses on controlling blood pressure, blood sugar, cholesterol, diet, and other risk factors while slowing kidney damage.
This is a strong early-stage study because it combines laboratory experiments with observations from human patients. The work moves beyond simply identifying high oxalate levels and proposes a detailed mechanism explaining how kidney disease may increase cardiovascular risk.
However, the treatment results were demonstrated mainly in animals, not large clinical trials. Future studies in people will determine whether blocking IL-17A truly improves outcomes for patients with chronic kidney disease.
If you care about heart disease, please read studies that herbal supplements could harm your heart rhythm, and how eating eggs can help reduce heart disease risk.
For more health information, please see recent studies that apple juice could benefit your heart health, and results showing yogurt may help lower the death risks in heart disease.
Source: University Hospital Würzburg.
