University of Virginia School of Medicine researchers have discovered how long-term treatment of high blood pressure with commonly prescribed drugs can destroy the kidney’s ability to filter and purify blood.
The finding could open the door to better ways to manage high blood pressure and other vascular diseases.
The class of drugs, known as renin-angiotensin system (RAS) inhibitors, block the effects of the renin enzyme, relaxing blood vessels and allowing blood to flow more easily.
They are widely used as first-line medications for hypertension (high blood pressure).
But long-term use can take a toll on the kidney, causing scarring and dramatic physical changes that shift the organ’s role from blood filtration to renin production.
Unable to clean blood properly, the kidney becomes a pathological neuro-immune endocrine organ, according to the UVA researchers.
This transformation can lead to serious health consequences, but the findings set the stage for discovering protective strategies and new treatments.
“The most commonly used and believed-to-be safe blood pressure medications may be damaging the kidneys,” said researcher Dr. R. Ariel Gomez. “We need to accurately understand the effects of long-term use of RAS inhibitors on the kidneys.”
High blood pressure affects over 1.3 billion people globally, increasing the risk of stroke, heart attack, kidney damage, and vision loss.
The renin-angiotensin system (RAS) is critical in blood pressure regulation, where renin is produced when blood pressure drops.
RAS inhibitors are effective and generally safe under medical supervision. However, patients are advised to report signs of kidney damage, including decreased urination and swelling.
UVA’s research found that long-term RAS inhibition excessively stimulates renin-producing cells, causing them to revert to an embryonic-like state.
These cells grow excessively and secrete more renin and other substances that drive pathological changes: nerve overgrowth, muscle cell buildup, scarring, and inflammation. This leads to vascular disease and impaired kidney filtration.
“Our 3D imaging clearly revealed that long-term RAS inhibition leads to hyperinnervation of renal arteries, together with arteriolar hypertrophy and immune inflammatory cell infiltration,” said researcher Dr. Manako Yamaguchi. “This synergistic interaction boosts renin production to maintain blood pressure, but also impairs kidney function.”
Researchers aim to map out interactions among renin cells, nerves, and immune cells under RAS inhibition. According to Dr. Maria Luisa S. Sequeira-Lopez, this could lead to new methods to prevent or treat the harmful effects of hypertension drugs on the kidneys.
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