The drug is lisinopril, and millions of Americans swallow it every morning without a second thought. A landmark 2024 study from the University of Virginia School of Medicine revealed that ACE inhibitors and ARBs — the two most common classes of blood pressure medication — can cause structural kidney damage by forcing kidney cells to revert to an embryonic, invasive state. With over 76 million prescriptions for lisinopril alone written in 2023, making it the fourth most prescribed drug in America, the number of people potentially affected is staggering. Before anyone flushes their pills down the toilet, the picture is more complicated than a single headline suggests.
The researchers themselves do not recommend stopping these medications, which remain potentially life-saving for people with hypertension and heart failure. High blood pressure was a primary or contributing cause of 664,470 deaths in the United States in 2023, according to the CDC. The real question is not whether to take blood pressure drugs, but whether patients and their doctors understand the full scope of what these drugs do inside the body — and whether better alternatives are finally on the horizon. This article breaks down the new research, the mechanism of kidney damage, what the National Kidney Foundation says, how ARBs compare to ACE inhibitors, and a promising new drug called baxdrostat that may change the treatment landscape entirely.
Table of Contents
- How Does the Most Common Blood Pressure Drug Damage Kidneys Without Patients Knowing?
- What Happens Inside the Kidney — And Why Doctors Did Not Catch It Sooner
- ARBs Versus ACE Inhibitors — Which Carries Greater Kidney Risk?
- Should You Stop Taking Your Blood Pressure Medication?
- Why Kidney Damage From Blood Pressure Drugs Matters for Dementia Risk
- Baxdrostat — A New Drug That May Protect Kidneys Instead of Harming Them
- Where the Research Goes From Here
- Conclusion
- Frequently Asked Questions
How Does the Most Common Blood Pressure Drug Damage Kidneys Without Patients Knowing?
Nearly 120 million U.S. adults have high blood pressure, according to CDC data from 2021 to 2023. That is 48.1 percent of the adult population. Over half of those with hypertension — 51.2 percent — take medication to manage it, and ACE inhibitors as a drug class account for roughly 162.8 million prescriptions per year. These are not obscure specialty drugs. They sit in medicine cabinets in nearly every neighborhood in America. The University of Virginia study, published as the cover article of Circulation Research in November 2024, finally explained why long-term use of these medications can quietly erode kidney function.
The research team, led by Maria Luisa S. Sequeira-Lopez, discovered that renin-angiotensin system inhibitors cause renin-producing cells in the kidney to revert to an invasive, embryonic state. These transformed cells line the tiny arteries of the kidney and begin growing abnormally large, secreting renin and other substances that trigger a cascade of damage. The kidney, in effect, shifts its priority from filtering blood to producing renin — the very hormone the drug was designed to regulate. Consider a patient who has taken lisinopril for fifteen years with stable blood pressure readings and no obvious symptoms. Routine bloodwork might show a slight dip in kidney filtration, which a doctor might dismiss as normal aging. But underneath that modest lab change, structural damage may be accumulating: scarring around the tiny blood vessels, abnormal nerve growth, buildup of immature smooth muscle cells, and infiltration of inflammatory cells. The damage is silent, gradual, and until this research, poorly understood.
What Happens Inside the Kidney — And Why Doctors Did Not Catch It Sooner
The mechanism the UVA team uncovered is not a simple side effect like a cough or dizziness. It is a fundamental reprogramming of kidney cells. When ACE inhibitors or ARBs block the renin-angiotensin system over long periods, the renin-producing cells do not simply stop making renin. they transform. They revert to an earlier developmental state and become invasive, behaving more like fetal cells than adult kidney tissue. New nerves grow abnormally around the affected arterioles. Immature smooth muscle cells accumulate. Scars form around the tiniest blood vessels. Inflammatory cells move in.
The kidney’s architecture slowly warps. This matters for brain health in a way that is often overlooked. The kidneys and the brain share a dependence on healthy small blood vessels. When kidney function declines, waste products build up in the blood, inflammation increases throughout the body, and cerebral blood flow can suffer. Chronic kidney disease is an established risk factor for cognitive decline and dementia. A drug that quietly damages the kidneys over years may, by extension, be contributing to brain vulnerability in aging adults. However, this does not mean every patient on an ACE inhibitor is headed for kidney failure. The National Kidney Foundation notes that ACE inhibitors and ARBs are known to slightly lower eGFR — a standard measure of kidney function — when first started, but this initial dip is not necessarily a sign of worsening kidney disease. In many patients, particularly those with early-stage chronic kidney disease, these drugs have actually been associated with slower progression of CKD compared to patients not taking them. The damage mechanism the UVA team identified appears to be a long-term, cumulative effect, and the clinical picture depends heavily on the individual patient, their kidney health at baseline, and how long they remain on the medication.
ARBs Versus ACE Inhibitors — Which Carries Greater Kidney Risk?
Patients often assume that ARBs like losartan or valsartan are gentler alternatives to ACE inhibitors like lisinopril. ARBs were originally marketed partly on the basis of fewer side effects — they do not cause the persistent dry cough that drives many patients away from ACE inhibitors. But a 2025 study published in The American Journal of Medicine found that in patients with heart failure, ARBs are actually associated with a higher risk of kidney failure compared to ACE inhibitors. This finding complicates a common clinical assumption.
For years, doctors have switched patients from ACE inhibitors to ARBs when side effects became bothersome, treating the two classes as roughly interchangeable in terms of kidney safety. The 2025 data suggests that trade-off may not be as clean as it seemed. A patient who switches from lisinopril to losartan to escape a nagging cough might be trading one problem for a more serious one — at least in the context of heart failure. The practical takeaway is not that ARBs should be avoided entirely, but that patients with heart failure or existing kidney disease should have a frank conversation with their doctor about which class of drug makes more sense for their specific situation. Blanket assumptions about safety profiles do not hold up when the research gets granular.
Should You Stop Taking Your Blood Pressure Medication?
No. That is the clear, direct answer from the UVA researchers themselves, and it deserves emphasis because alarming headlines can push people toward dangerous decisions. Uncontrolled high blood pressure kills. It damages the heart, the brain, the eyes, and yes, the kidneys — often far more aggressively than the medications designed to treat it. Stopping blood pressure drugs without medical supervision can lead to stroke, heart attack, or kidney crisis. The STOP ACEi trial, published in the New England Journal of Medicine, studied patients with advanced chronic kidney disease who were already on RAS inhibitors.
Researchers found no evidence of harm from continuing the medications and noted that patients who stayed on them possibly experienced a reduced need for dialysis. In other words, even in patients whose kidneys were already significantly compromised, the drugs appeared to do more good than harm on balance. The tension here is real, though. A medication that is broadly protective at the population level can still cause harm in specific individuals over specific time frames. The UVA research does not invalidate the use of ACE inhibitors and ARBs. It sharpens the case for closer monitoring, more frequent kidney function testing, and a more honest conversation between doctors and patients about what long-term use actually does at the cellular level.
Why Kidney Damage From Blood Pressure Drugs Matters for Dementia Risk
The connection between kidney health and brain health is stronger than most people realize, and it is a connection that rarely comes up in a routine cardiology appointment. When the kidneys lose filtering capacity, toxins accumulate in the bloodstream. Uremic toxins, inflammatory markers, and metabolic waste products that healthy kidneys would clear begin circulating through the brain’s delicate vascular system. Over time, this contributes to small vessel disease in the brain, white matter damage, and accelerated cognitive decline. For older adults already managing multiple risk factors for dementia — age, genetics, cardiovascular disease, diabetes — the addition of silent, drug-induced kidney damage is not trivial.
It represents one more avenue through which the brain’s support system is quietly undermined. This is especially concerning because the population most likely to be on long-term ACE inhibitors or ARBs is the same population most vulnerable to dementia: adults over 65 with decades of hypertension behind them. The limitation worth noting is that no study has yet drawn a direct causal line from ACE inhibitor-induced kidney damage specifically to dementia. The link between chronic kidney disease and cognitive decline is well established, but attributing a given patient’s cognitive changes to their blood pressure medication rather than to the hypertension itself, or to aging, or to other factors, remains difficult. What the UVA research does is add a plausible biological pathway that warrants further investigation.
Baxdrostat — A New Drug That May Protect Kidneys Instead of Harming Them
A drug called baxdrostat, which works by inhibiting aldosterone production rather than blocking the renin-angiotensin system, showed striking results in a study highlighted by the University of Utah Health and the American Heart Association in September 2025. In people with treatment-resistant hypertension and chronic kidney disease, baxdrostat lowered systolic blood pressure and reduced urine albumin loss by 55 percent compared to placebo.
Albumin in the urine is a marker of kidney damage, so a 55 percent reduction suggests the drug may actually help delay kidney disease progression rather than contribute to it. This is significant because treatment-resistant hypertension — blood pressure that remains high despite three or more medications — affects a substantial number of patients, and those patients are often the ones most exposed to the cumulative effects of long-term RAS inhibitor use. If baxdrostat proves safe and effective in larger trials, it could offer a fundamentally different approach: lowering blood pressure without triggering the cellular reprogramming in the kidneys that the UVA team documented.
Where the Research Goes From Here
Sequeira-Lopez and her team at UVA stated that their next goal is to map the full picture of interactions between renin cells, smooth muscle cells, nerves, and inflammatory cells under RAS inhibition. That work could lead to strategies for mitigating kidney damage in patients who need to stay on ACE inhibitors or ARBs — perhaps through combination therapies, periodic drug holidays, or targeted interventions that prevent the cellular reversion without undermining blood pressure control. For patients and caregivers navigating dementia risk, the broader lesson is that no medication exists in isolation.
A drug that controls one risk factor can quietly amplify another. The best defense is not fear of medication but informed engagement: regular kidney function monitoring, honest conversations with prescribers about long-term risks, and attention to emerging research that may open doors to safer alternatives. The science is moving. Patients should make sure their treatment plans move with it.
Conclusion
ACE inhibitors and ARBs have saved countless lives by controlling blood pressure in a population where hypertension contributes to more than 660,000 deaths annually. But the 2024 University of Virginia research makes clear that these drugs carry a hidden cost — a slow, structural transformation of kidney cells that can lead to scarring, inflammation, and diminished filtration over years of use. For the tens of millions of Americans taking these medications daily, this is not a reason to panic, but it is a reason to pay closer attention.
Going forward, patients should ask their doctors about regular eGFR and albumin testing, discuss whether their current medication class is the best fit for their individual risk profile, and stay informed about emerging alternatives like baxdrostat. For those concerned about dementia, protecting kidney health is an underappreciated but meaningful part of protecting brain health. The goal is not to avoid treatment but to pursue it with full knowledge of what the treatment does — both the good and the quietly damaging.
Frequently Asked Questions
Should I stop taking lisinopril or losartan after reading about this research?
No. The UVA researchers explicitly do not recommend stopping these medications. Uncontrolled high blood pressure poses far greater immediate risks than the gradual kidney effects described in the study. Any changes to your medication should be discussed with your doctor.
How can I tell if my blood pressure medication is affecting my kidneys?
Ask your doctor to check your eGFR and urine albumin levels regularly. A slight drop in eGFR when first starting an ACE inhibitor or ARB is expected and not necessarily harmful. Persistent or significant declines over time warrant a closer look.
Are ARBs safer for the kidneys than ACE inhibitors?
Not necessarily. A 2025 study in The American Journal of Medicine found that ARBs were associated with a higher risk of kidney failure than ACE inhibitors in patients with heart failure. The relative safety depends on the patient’s specific health conditions.
Does kidney damage from blood pressure drugs increase dementia risk?
Chronic kidney disease is an established risk factor for cognitive decline and dementia, but no study has yet proven a direct causal link between ACE inhibitor-induced kidney changes specifically and dementia onset. The biological plausibility is there, but more research is needed.
When will baxdrostat be available?
Baxdrostat showed promising results in 2025 trials, but it has not yet received FDA approval for widespread use. Patients with treatment-resistant hypertension should ask their doctors about clinical trial eligibility and watch for updates from the American Heart Association.
How does kidney damage from these drugs happen without symptoms?
The kidneys have significant reserve capacity. Damage can accumulate at the cellular level — scarring, abnormal cell growth, inflammation — long before it shows up in lab results or produces noticeable symptoms like fatigue or swelling. This is why routine monitoring matters.
