More than half of people with chronic kidney disease die from heart problems. New research reveals a toxic signal from the kidney to the heart — and a path toward earlier diagnosis and targeted treatment.
For years, doctors have known that chronic kidney disease and heart failure often go hand in hand. Now, scientists say they have uncovered a direct, toxic link between the two organs that could change how millions of patients are diagnosed and treated.
Researchers at the University of Virginia Health System and Mount Sinai report that diseased kidneys release tiny particles into the bloodstream that can poison the heart. The discovery helps explain why more than half of people with chronic kidney disease ultimately die from cardiovascular problems and opens the door to new blood tests and therapies aimed at stopping that damage.
Chronic kidney disease, or CKD, affects more than 1 in 7 Americans, according to the National Institutes of Health. It is especially common among people with diabetes and high blood pressure. Yet both kidney and heart disease often progress quietly for years.
“Kidney and heart disease can develop silently, so they are often discovered only after damage has already been done,” co-author Uta Erdbrügger, an internal medicine physician-scientist in the University of Virginia School of Medicine’s Division of Nephrology, said in a news release. “Our findings can help to identify patients at risk for heart failure earlier, enabling earlier treatment and improved outcomes.”
Doctors have long seen that the worse a person’s kidney function becomes, the more likely they are to develop serious heart problems. But it has been hard to tease out why, because kidney disease and heart disease share many of the same risk factors, including obesity and high blood pressure. That overlap has made it difficult to prove that the kidney itself was sending a harmful signal to the heart.
The new study, published in the journal Circulation, points to that signal: microscopic particles called “circulating extracellular vesicles” that are produced in diseased kidneys.
Extracellular vesicles are tiny, bubble-like packages released by almost all cells. Under normal conditions, they act as messengers, carrying proteins and bits of genetic material from one cell to another to help coordinate how tissues work together.
In chronic kidney disease, however, the vesicles released by the kidney appear to carry a dangerous cargo. The team found that these vesicles are loaded with small, noncoding RNA molecules known as microRNA, or miRNA, that are toxic to heart tissue.
In laboratory mice, the researchers blocked these vesicles from circulating in the bloodstream. When they did, the animals’ heart function improved significantly, and signs of heart failure eased. That experiment suggested that the vesicles are not just bystanders but active drivers of heart damage.
To see if the same process might be happening in people, the scientists analyzed blood plasma from patients with chronic kidney disease and from healthy volunteers. They found harmful extracellular vesicles circulating in the blood of CKD patients but not in the healthy group.
“Doctors always wondered how organs such as the kidney and heart communicate with each other. We show that EVs from the kidney can travel to the heart and be toxic,” Erdbrügger added. “We are just at the beginning to understand this communication.”
If further studies confirm these findings in larger groups of patients, the work could have several practical payoffs.
First, the toxic vesicles or their miRNA cargo could serve as biomarkers — measurable signals in the blood that flag which kidney patients are at highest risk for heart failure. That could allow doctors to monitor those patients more closely, adjust medications sooner and intervene before the heart is badly damaged.
Second, the vesicles themselves could become targets for new treatments. Therapies that block their release from the kidney, neutralize their harmful contents, or prevent them from reaching the heart might help protect cardiac function in people with CKD.
That is the team’s long-term goal.
“Our hope is to develop novel biomarkers and treatment options for our kidney patients at risk for heart disease,” added Erdbrügger. “Potentially our work will improve precision medicine for CKD and Heart failure patients, so that each patient gets the exact treatment they need.”
To accelerate progress, Erdbrügger is organizing a five-day, hands-on workshop at UVA focused on extracellular vesicle research. By training more scientists to study these particles, she aims to build a broader effort to understand and eventually control organ-to-organ communication in disease.
The project also reflects the mission of UVA’s new Paul and Diane Manning Institute of Biotechnology, which is designed to speed the path from lab discoveries to real-world treatments. By uncovering a specific, testable mechanism linking kidney disease to heart failure, the study gives researchers a concrete target to pursue.
For patients and families living with chronic kidney disease, the work does not change standard care overnight. But it offers a clearer picture of why the heart so often fails when the kidneys do — and a hopeful glimpse of future tools to detect and disarm that hidden threat before it is too late.