Silent Risks: How Kidney Disease Fuels Heart Disease If you’re a baby boomer or moving through middle age… this may be about you.

September 10, 2025•13 min read

Silent Risks: How Kidney Disease Fuels Heart Disease

If you’re a baby boomer or moving through middle age… this may be about you.

When we talk about chronic kidney disease (CKD), we are not talking about a rare condition. We are talking about millions of baby boomers and adults entering the later decades of life, whose kidney function — measured by a glomerular filtration rate (GFR) below 60 — already places them in stage 3 CKD. By age 65, about one-third of people will have a GFR under 60, and by age 70, the percentage is even higher¹. That is tens of millions of Americans who may not realize they carry the diagnosis, or the prognosis, nor understand its grim implications.

It’s not like a hidden time bomb. It’s more like walking around with your pants ripped in the back and your shoelaces untied — plain as day, yet everyone stays silent instead of warning you. And in this case, that silence can be deadly.

Too often, a low GFR is brushed off as nothing more than “normal aging,” and the conversation ends there. But CKD is not just a kidney problem — it is one of the most powerful accelerators of cardiovascular disease (CVD) that we know². The tragedy is that many patients with CKD will never progress to dialysis or transplant. Instead, they will die first of a heart attack, stroke, or sudden cardiac death³. The kidneys may decline slowly, but the heart often fails suddenly. That is why CKD should never be dismissed as benign or inevitable. It is a red flag for aggressive cardiovascular prevention.

Understanding GFR and CKD

The kidneys filter waste and toxins out of the bloodstream, a process measured by the glomerular filtration rate (GFR). Normal kidney function corresponds to a GFR of about 90 mL/min/1.73m² or higher. As kidney function declines, so does GFR:

Stage 1–2 CKD: GFR ≥60 (mild changes, often silent)
Stage 3 CKD: GFR 30–59 (moderate decline)
Stage 4 CKD: GFR 15–29 (severe decline)
Stage 5 CKD (ESRD): GFR <15 (kidney failure, dialysis or transplant usually required)

By the time a patient is in stage 3 CKD — a GFR under 60 — their risk of cardiovascular disease is already doubled. With stage 4 CKD, that risk triples. And with stage 5, the risk is more than 17 times higher than the general population, with a 20-fold increase in mortality⁴.

Think about it this way: almost everyone knows their cholesterol level, but how many know their GFR? Cholesterol is taught as the “silent risk,” but kidney function is even more potent as a predictor of cardiovascular events. If cholesterol is the smoke detector, GFR is the house on fire. Ignoring it because “it comes with age” is like ignoring smoke in the kitchen because the flames haven’t reached the living room yet.

The Heart–Kidney Connection: Siamese Twins of Survival

The heart and kidneys are so interconnected that physicians often describe them as “Siamese twins” of human physiology. They share the same blood supply, respond to the same hormones, and deteriorate under the same toxic metabolic environment. When kidney function drops, the heart is forced to work harder against increased vascular stiffness, inflammation, and fluid overload. When the heart weakens, reduced cardiac output further impairs kidney perfusion. One organ cannot suffer in isolation without dragging the other down with it⁵.

This inseparable relationship explains why CKD is more than just a kidney problem — it is a cardiovascular emergency in disguise. Treating one without the other is like caring for only half of the same patient.

Why “Normal Aging” is a Dangerous Excuse

A common mistake is assuming that CKD in older adults is simply a byproduct of aging. After all, kidney function does tend to decline with time. But the presence of a reduced GFR is far more than a laboratory curiosity. It signals systemic vascular strain, inflammation, and metabolic dysfunction⁶.

Imagine being told your cholesterol was twice the normal level but not to worry because “it comes with age.” Absurd, right? Yet this is precisely how low GFR is treated in millions of older adults. The reality is that a reduced GFR rivals high cholesterol in its predictive power for heart disease, yet it remains outside the standard conversation of cardiovascular prevention.

The Vicious Cycle: Cardiac Risk Factors and CKD

What often goes unrecognized is that the same risk factors that drive heart disease also drive kidney disease. Diabetes, high blood pressure, and dyslipidemia account for the vast majority of CKD cases worldwide⁷. Each of these conditions damages blood vessels — both large and small — leading to scarring in the kidneys and progressive decline in filtration.

Diabetes is the single most common cause of CKD, and CKD itself worsens insulin resistance, making blood sugar control harder over time⁸. Hypertension stiffens arteries and accelerates vascular calcification, raising pressure within delicate kidney capillaries until they scar and fail. Dyslipidemia, especially the combination of high triglycerides and low HDL cholesterol, worsens endothelial injury and vascular inflammation. In fact, the triglyceride-to-HDL ratio is one of the strongest markers of insulin resistance and cardiometabolic risk⁹.

The result is a vicious cycle: cardiac risk factors damage the kidneys, kidney disease magnifies those same risk factors, and the cardiovascular system collapses under the combined burden. CKD and CVD do not simply coexist; they accelerate one another.

Diffuse Coronary Disease in CKD

In otherwise healthy adults, coronary artery disease often presents as a discrete blockage — one artery narrowed 80 or 90 percent, which can be treated with a stent. In CKD, the disease pattern is different. The coronary arteries are diffusely involved, with widespread calcification and microvascular dysfunction¹⁰. In most people, coronary disease looks like a single blockage — like a speedbump in the road, one obstacle that can be treated directly. In CKD, it is not a speedbump, it is a cobblestone street — the entire vascular bed is uneven, hardened, and dysfunctional. There isn’t one simple fix because the problem is everywhere.

This has profound clinical implications. A discrete blockage can cause chest pain with exertion, prompting evaluation and treatment. Diffuse disease may cause no symptoms until it triggers sudden cardiac arrest. This explains why CKD patients are far more likely to present with their first event as a heart attack or sudden death¹¹.

The Failure of Functional Stress Testing

Despite this, the standard cardiac evaluation for CKD patients continues to rely heavily on functional stress testing: treadmill exercise, nuclear SPECT, stress echocardiograms, or stress MRIs. These tests are designed to detect reduced blood flow to the heart muscle — but only when the narrowing is severe, usually greater than 70 percent.

The main purpose of cardiac testing is threefold: to find out if someone has coronary artery disease, to figure out how serious their risk really is, and to help guide future treatment decisions. Functional stress testing falls short on all three counts. It does not reliably show the presence of hidden plaque, it fails to capture the true danger in people with widespread disease, and it gives little information to guide long-term prevention. Instead, it only shows areas of the heart that struggle when blood flow is severely reduced. By the time a stress test turns “positive,” the disease process is already advanced — and the chance for early, life-saving prevention has been lost.

Here’s the problem: most heart attacks do not occur at those severely narrowed sites. Pathology studies show that 65–70 percent of heart attacks occur in arteries that were less than 50 percent narrowed beforehand¹². Only 15–20 percent occur in vessels that were already critically narrowed. The plaques most likely to rupture are those with thin fibrous caps and high inflammatory activity — plaques that do not block flow and therefore never show up on a stress test¹³.

The limitations of stress testing are even more dangerous in CKD. With diffuse, multivessel disease, patients often develop “balanced” low blood flow across all arteries. Because there is no relative difference, the stress test may appear normal — even in the setting of severe disease¹⁴. Studies estimate that as many as one in six patients with triple-vessel disease are falsely reassured by a “normal” stress test. Left main disease can also be missed entirely.

Relying on functional stress testing in CKD patients is like inspecting only the roof of a house for leaks while ignoring the crumbling foundation. It gives a false sense of security when the danger lies elsewhere.

Cultural Barriers and the Definition of “Fine”

There’s also a cultural barrier. Cardiologists are trained and financially incentivized to perform functional stress testing and invasive catheterization. These tests are their domain, both professionally and economically. Meanwhile, advanced anatomical testing like coronary CT angiography (CCTA) with FFRct is performed by radiologists. Referring patients away means giving up both control and prestige, so cardiologists often hesitate to recommend it — even though it provides clearer answers and better outcomes¹².

For CKD patients, the safest and most logical pathway begins with a CT coronary calcium score (CAC). If the score is zero, no further testing is needed — the absence of calcium is a strong short-term protective marker¹³. If plaque is present and the patient is not on dialysis, functional stress testing can still play a supplemental role, given the risks of contrast dye. But in end-stage renal disease (ESRD) patients on dialysis, where contrast can do no further harm, CCTA with FFRct is the superior choice, combining nearly 99% negative predictive value with actionable information for risk reduction¹⁴.

Unfortunately, many cardiologists will reassure patients that their hearts are “fine” simply because they do not need a stent or bypass. But not needing revascularization is not the same thing as having a healthy heart. If coronary artery disease is present, the heart is not fine — it is at risk, and it demands aggressive therapy and prevention. The only true definition of “fine” is the absence of coronary disease altogether. Patients should feel empowered to ask their cardiologist: When you say my heart is fine, do you mean I have no coronary disease, or just that I don’t need a stent today? The difference is life-changing.

The Role of Coronary Calcium Scoring

Because contrast-based CT angiography carries risks in patients not yet on dialysis, a safer first-line test is the coronary calcium score. This quick, non-contrast CT scan measures calcified plaque in the coronary arteries.

0: No detectable plaque (very low short-term risk)
1–99: Mild plaque burden
100–399: Moderate plaque burden
≥400: High plaque burden, very high risk

A calcium score of zero provides some reassurance. A score over 400 confirms extensive atherosclerosis and demands urgent attention¹⁵. For CKD patients, it is one of the most powerful tools we have, because it makes the invisible visible.

CCTA and FFR: Precision in Select Patients

In patients already on dialysis — where the kidneys are essentially gone and contrast dye can no longer cause harm — coronary CT angiography (CCTA) with fractional flow reserve (FFRct) offers unmatched precision. It not only shows plaque burden and vessel narrowing but also determines whether those lesions actually limit blood flow.

The accuracy is remarkable: FFRct has a negative predictive value of ~99 percent. If it says your heart is fine — it’s fine. Believe it. Radiation exposure is lower than nuclear stress testing (1–3 mSv vs. 9–12 mSv), and diagnostic precision is far higher.

Studies have also shown that this approach translates into real survival benefits — with a 41% reduction in death and heart attacks compared with functional testing, and a 25% overall reduction in major cardiovascular events, including a 62% reduction in diabetics within just 42 months.

The Metabolic Burden of CKD

CKD is not just about filtration; it is about metabolism. Patients often develop atherogenic lipid patterns: elevated triglycerides, low HDL, and abnormal triglyceride-to-HDL ratios. Even when LDL cholesterol appears “normal,” risk remains high²⁰. Low HDL alone is a universal risk factor for heart disease.

Inflammation is another overlooked driver. High-sensitivity C-reactive protein (hsCRP) is normally <3 mg/L, but many CKD patients measure 20–40 mg/L, signaling active vascular injury²¹.

Microalbuminuria — even at 30 mg/dL — predicts cardiovascular events. In CKD, values often exceed hundreds of mg/dL²².

Finally, HbA1c is unreliable in dialysis patients. Shortened red blood cell lifespan and dialysis-related blood loss falsely lower readings²³. The gold standard in this population is a 2-hour oral glucose tolerance test (OGTT) with insulin response, which uncovers insulin resistance early, before diabetes develops.

Transplant Considerations

For those who reach transplant, cardiovascular disease remains the leading cause of death²⁴.

Early (1–2 years): perioperative stress and undiagnosed coronary disease missed by stress testing.
Late (5–10 years): the metabolic toxicity of immunosuppressive medications.

Calcineurin inhibitors raise blood pressure and cholesterol²⁵. Corticosteroids induce insulin resistance and central weight gain²⁶. mTOR inhibitors raise triglycerides and impair vascular repair²⁷.

The results are predictable: 20–50% of transplant recipients develop post-transplant diabetes, and 30–60% gain significant weight in the first year²⁸. Even after transplant, the Siamese twin relationship between heart and kidney remains. Unless cardiovascular risk is addressed aggressively, the gift of a new kidney is too often overshadowed by the loss of the heart.

Conclusion: From Silence to Advocacy

Chronic kidney disease is not simply about kidney failure. It is a cardiovascular disease in disguise. For CKD patients, functional testing fails to protect, inflammation accelerates damage, and metabolic dysfunction fuels vascular collapse. Many never live to see dialysis or transplant; they die first of the heart.

Testing strategies must change. For those with residual kidney function, start with a coronary calcium score. For those on dialysis, where contrast is no longer a risk, proceed with CCTA + FFRct. And for every CKD patient without diabetes, insist on a 2-hour OGTT with insulin response.

Too often, these warnings are ignored — like ripped pants or untied shoelaces that everyone sees but no one points out. That silence has deadly consequences.

At CardioCore Metabolic Wellness, we don’t wait for disease to announce itself. We get to the core drivers of risk — insulin resistance, inflammation, and metabolic dysfunction — and modify them upstream, before they manifest downstream as heart attacks, strokes, or kidney failure. This is the proactive path. Because being Healthy is not an Accident.

Author: Dr John Sciales

Director, CardioCore Metabolic Wellness Center

"Getting to the Core- where being Healthy is Not an Accident"

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