Rethinking Cardiac and Metabolic Risk in Kidney Transplant Candidates
Reevaluating Standard Cardiac Testing in Renal Transplant Candidates
Author’s Note
Although published here in my blog, this article was originally written in the style of a medical journal by Dr. John Sciales and is intended for both healthcare professionals caring for transplant patients and the patients themselves. Transplant recipients represent a unique group of people with unique responsibilities and unique illnesses. This piece is directed to those entrusted with their care, with the goal of supporting wise, evidence-based, and life-saving decisions.
Case Study
Patient: Thomas L.
Age: 64
Condition: Cystinuria, congenital solitary functioning kidney, end-stage renal disease (ESRD), on dialysis for over six months.
Transplant Plan: Scheduled for renal transplantation with his son as the donor.
Medical Background:
Athletic, BMI 28.46, nonsmoker, follows a healthy diet.
Hypertension and hyperlipidemia in the past, with a family history of myocardial infarction (father died in his 50s).
Not on any cardiometabolic medications.
Current imaging & lipid profile:
HgbA1c: 5.4
Low HDL: 40
Elevated TG: 166
TG/HDL Ratio: 4.15 (previously >7)
Imaging shows abdominal aortic atherosclerosis.
Nuclear stress test: Normal, and he was cleared for surgery.
Medical clearance: Acknowledged his cardiovascular (CV) risk factors.
Intervention:
As a cardiometabolic specialist and friend, I was concerned about the validity of the normal stress test. Given his history of chronic kidney disease (CKD), which is a strong driver of atherosclerosis, I suspected the stress test might not reflect his true CV risk. His lipid profile and TG/HDL ratio indicated insulin resistance and elevated CV risk.
To better assess his coronary status, I ordered a coronary calcium score, which came back as 538, showing heavy calcification in the proximal LAD and diffuse disease in the RCA. This raised red flags.
Symptoms:
While he denied chest pain, he reported declining exercise tolerance, fatigue, and dyspnea since starting dialysis. These symptoms, combined with his test results, prompted an urgent cardiology referral.
Further Testing & Findings:
Catheterization was Recommended, but given his Factor V Leiden deficiency and chronic anticoagulation, I advocated for a CT coronary angiography (CCTA) with FFR. FFR has a high negative predictive value and could avoid invasive testing.
CCTA results:
Calcium score: 575
Severe stenosis in the small OM-1 branch
Mild stenosis in multiple coronary vessels (left main, LAD, Circumflex, RCA)
Mild concentric left ventricular hypertrophy (LVH)
FFR was Never Sent/Requested by his Management Team
Cardiac Catheterization: Confirmed multivessel 30-40% stenosis: LM patent, Moderate proximal Circumflex(DFR0.98), mild diffuse LAD disease, mild Proximal and diffuse mild mid RCA, high moderate stenosis in small OM-1( small vessel)...
Final Diagnosis: Triple vessel, nonobstructive CAD
OGTT showed normal glucose values (fasting 81 mg/dL, 1-hour 127, 2-hour 98), but a disproportionately high insulin response (fasting 15.4 μIU/mL, 1-hour 85, 2-hour 59)
Despite initially clearing him for surgery, the physicians managing this case missed a serious cardiac and metabolic issue that was undetected by the stress test. The additional testing allowed for proper diagnosis and safe surgical clearance although the lack of FFRct analysis may have contributed to an unnecessary invasive catheterization.
Discussion
Chronic kidney disease (CKD) is not simply a renal disorder — it is one of the most potent accelerators of cardiovascular disease. From stage 3 onward, CKD creates a chronic pro-inflammatory and insulin-resistant state that drives diffuse atherosclerosis, vascular calcification, and microvascular dysfunction. (5,6) A GFR below 60 doubles the risk of cardiovascular events, a GFR between 30–44 triples it, and a GFR <15 increases cardiovascular risk more than seventeen-fold while raising mortality twenty-fold (1).
Even when patients receive a successful transplant, they do not return to “normal.” With a single kidney, GFR remains below 60 by definition, despite a normalization in the serum creatinine, and cardiovascular risk persists — magnified further by the metabolic and vascular toxicity of anti-rejection medications.(2,3,6) It is no surprise that cardiovascular disease is the leading cause of death in renal transplant recipients, responsible for 30–40% of mortality (2,3).
Cardiovascular deaths in this population occur both early and late. In the first 1–2 years after transplantation, events are often related to perioperative stress and previously unrecognized coronary disease (4). Silent ischemia, triple-vessel balanced disease, and left main lesions — commonly missed by functional stress testing — account for a substantial portion of sudden cardiac deaths in this window. The case patient above indeed as predicted had triple vessel disease. (8-10) Beyond five to ten years, the risk remains high, now fueled by the long-term metabolic consequences of immunosuppression: hypertension, diabetes, dyslipidemia, vascular calcification, and chronic inflammation (5,6). By ten years, up to one in three transplant patients will have died from cardiovascular causes, making CVD the dominant threat to survival across the entire post-transplant course (3).
In patients that are going for a kidney transplant, the vast majority are on dialysis and have been suffering from progressive renal insufficiency for many years. Renal transplant has offered many of these hope for the future and transplant greatly improves survival compared to dialysis. However, this staggering CardioMetabolic burden greatly influences life expectancy.(2,3,5,6) Pre-existing morbidities drive adverse outcomes but in addition, the immunosuppressive(anti-rejection) medications used after the transplant increase the risk of atherosclerosis and cardiometabolic disease. (12,13)
Calcineurin inhibitors (CNIs) can cause vasoconstriction, leading to increased blood pressure and affecting kidney function by decreasing renal blood flow and increasing renal vascular resistance. CNIs, particularly cyclosporine, can also raise lipid levels by increasing triglycerides and cholesterol. This combination of hypertension, dyslipidemia, and potential nephrotoxicity can accelerate vascular damage and increase cardiovascular risk.(12,13) The corticosteroids induce insulin resistance and possible weight gain, can also promote hypertension and dyslipidemia, especially the atherogenic dyslipidemia (13). Lastly, the mTOR inhibitors are associated with the atherogenic Lipid, endothelial repair and progression of vascular disease. (12,13)
Immunosuppressive drugs used in transplant patients not only prevent rejection but also increase the risk of cardiovascular disease by inducing a pro-atherogenic state characterized by metabolic syndrome, dyslipidemia, and diabetes. This, combined with pre-existing vascular damage from chronic kidney disease or end-stage renal disease, puts transplant recipients at a significantly higher risk of long-term cardiovascular complications compared to the general population.(5,6,12,13) Essentially, these therapies can add fuel to any pre-existing vascular issues, making this population extremely high-risk for cardiovascular events.
CTA Coronary Arteries: Looking under the hood, not just going for a Test Drive
Stress testing is like taking a car for a quick spin around the block — it might seem fine on the surface, but you never actually look under the hood. For renal transplant candidates, that approach is not enough. The cardiac CT angiogram (CCTA) with fractional flow reserve (FFRct) allows us to look directly under the hood, revealing the true condition of the coronary arteries. CCTA identifies the presence of coronary artery disease, quantifies plaque burden, evaluates the degree of stenosis, and determines how many vessels are involved. This information provides powerful risk stratification and guides future treatment in a proactive, meaningful way. Importantly, a normal CCTA carries a negative predictive value of nearly 99%, meaning that if no significant stenosis is found, we can be confident this is accurate (7,17,18,20).
By contrast, nuclear stress testing is well known to be faulty when it comes to balanced ischemia. In patients with triple-vessel disease — the very highest-risk group — up to 15% (1 in 6) will have a normal test (8–10). These patients are then told, “Good news, your heart is fine,” when in fact they carry the gravest risk. Left main and triple-vessel disease simply cannot be missed — and yet stress testing does exactly that. The tragic case of journalist Tim Russert, who died of an acute heart attack just six weeks after a “normal” stress test and with an LDL <70, underscores how misleading this approach can be (10,11). Transplant candidates cannot afford this margin of error.
Identifying atherosclerosis, especially in such a high-risk population, is crucial. The purpose of transplant surgery is not just to restore independence and quality of life in the short term, but to extend life in the long term. That requires the ability to identify and address cardiovascular risk proactively, not reactively. Because CCTA requires IV contrast, it is imperative that this evaluation be performed before transplantation, not after (7,16–18,20). Functional stress testing, long entrenched in cardiology, can identify myocardial ischemia, but it is not sufficient for the long-term management of patients with advanced cardiovascular risk (7,18–20).
For transplant candidates, the choice is clear: we must look under the hood, not just take a test drive.
Why Functional Testing Fails CTA Coronary Arteries
Despite these CardioMetabolic risks, the standard pre-transplant cardiac workup continues to rely on functional testing — treadmill stress, stress echo, nuclear SPECT, or stress MRI — designed only to detect ischemia from stenoses >70%. (7,10) There is a fundamental limitation. Pathology and angiographic studies confirm that ~65–70% of myocardial infarctions arise from lesions <50% stenosed, while only 15–20% arise from lesions >70% (8,9). Vulnerable plaques with high inflammatory activity and thin fibrous caps rupture silently and unpredictably. These are the very lesions that functional tests cannot detect. (8,9) And these are the very lesions found in renal patients, fueled by the proinflammatory state and insulin resistance. This is not my opinion, this is medical and scientific fact.
When looking at nuclear stress testing, 59% of the time when the test is positive, there was no coronary artery disease on angiogram , but conversely, a negative stress test still had a 28% risk of coronary artery disease. (7,10,11,18-20) When comparing the Functional testing to the findings on invasive coronary angiography for the presence of >50% stenosis based on a positive test result, SPECT=45%, Stress echo =44%, Exercise Stress Test =45% and with Cardiac MRI=45%.
With CCTA and FFR, the specificity and sensitivity of obstructive coronary disease and full limiting disease is higher, >90%, than all of the others. Regarding risk stratification long term, In the major studies, if no plaque was present, there were no CV events in a follow up of 10 years. A higher plaque burden on CCTA imaging is associated with an exponentially increased risk. Getting it right and predicting future risks should not be an afterthought.
The problem is also cultural. Cardiologists are trained, credentialed, and reimbursed to perform functional testing and invasive catheterization. Moving diagnosis to radiology, with CCTA and FFRct, challenges both prestige and financial incentives. This entrenched system perpetuates outdated testing even as evidence demonstrates the inferiority of functional testing and invasive functional testing and invasive angiography, whereas CCTA/FFRct shifts diagnosis toward anatomic/physiologic imaging with high rule‑out value (11,18–20).
Effective long-term management is crucial for renal transplant patients, who, despite improved kidney function, still have chronic kidney disease (CKD) and face increased cardiovascular risks due to anti-rejection medications' atherogenic effects. It's essential for transplant teams to assess and stratify individual cardiovascular risks, as primary care providers may not adequately address these complexities. Notably, patients with known coronary artery disease typically have cardiology follow-up, whereas those with “negative” functional tests do not.
In this case, however, there was a lack of discussion regarding cardiac risk stratification, the heightened cardiovascular risk associated with CKD, and the potential effects of anti-rejection medications. It was always someone else’s job to do that. Triple vessel CAD, considering its severity and ominous prognosis, is not an afterthought or something that can't be missed...especially by one of the most prestigious Medical Centers in New York, if not in the entire United States.(22)
Metabolic Burden of Transplantation
The September 9, 2025 Annals of Internal Medicine has a full discussion about Chronic Kidney Disease. It states very clearly:
“Although CKD is commonly attributed to diabetes or hypertension, there is growing awareness of the interplay among cardiovascular, kidney and metabolic health. Progression of CKD can result in metabolic abnormalities and end stage kidney disease, but cardiovascular events are even more common. The main goals of CKD treatment include slowing the decline in kidney function, preventing cardiovascular disease, and treating metabolic complications.” (21)
As we saw with this patient, none of this happened. In fact, he was given the reassurance that his heart was fine. Why is nobody paying attention when the stakes are so high? The data is there and it’s not new — yet leading medical institutions continue to ignore it, clinging to outdated protocols and superficial evaluations. They wait for the catastrophe to declare the diagnosis, rather than acting on the evidence staring them in the face.
Due to multiple metabolic insults, eventually 20–50% of transplant recipients without pre-existing diabetes develop post-transplant diabetes or impaired glucose tolerance, and the majority show insulin resistance (14). Within the first year, 30–60% gain significant weight due to increased appetite, steroid use, improved overall health, and reduced activity (15). Restriction of protein intake often drives increased carbohydrate consumption, which elevates insulin, promotes fat storage, and slows metabolism — worsening the cycle of metabolic dysfunction. These are not theoretical risks; they directly translate into myocardial infarction, heart failure, stroke, and sudden cardiac death.(2,3,5,6,14,15)
HbA1c is falsely lowered in CKD due to shortened red blood cell lifespan, erythropoietin use, and dialysis circuit blood loss, making it an unreliable marker of glycemia. Fasting glucose, meanwhile, often remains normal until late disease, whereas the Oral Glucose Tolerance Test (OGTT) with a fasting, 1 & 2 hour insulin response can unmask early insulin resistance and impaired glucose handling long before overt diabetes develops. Identifying diabetes/insulin resistance — even in its earliest stages — opens the door to additional, meaningful risk reduction through targeted therapy, lifestyle intervention, and closer cardiometabolic surveillance. (5,6,14,15).
In fact, in this patient’s case, the OGTT showed normal glucose values (fasting 81 mg/dL, 1-hour 127, 2-hour 98), but a disproportionately high insulin response (fasting 15.4 μIU/mL, 1-hour 85, 2-hour 59), clearly demonstrating insulin resistance despite normal glycemia. This pattern underscores why OGTT with insulin should be a mandatory pre-transplant evaluation, as it reveals hidden metabolic dysfunction that drives post-transplant diabetes, vascular injury, and cardiovascular events.
Identifying insulin resistance is not merely academic — it opens the door to actionable interventions: targeted nutrition, lifestyle strategies, and evidence-based therapies such as SGLT2 inhibitors, GLP-1 agonists, and even pioglitazone (shown to reduce mortality by ~51% in diabetic dialysis patients). By addressing insulin resistance upfront, we can meaningfully reduce cardiometabolic risk, improve transplant outcomes, and extend survival. (5,6,14,15)
Glucose values are normal at all time points.
Insulin levels are excessively elevated, indicating insulin resistance despite normal glycemia.
This hidden metabolic dysfunction would have been missed if only HbA1c or fasting glucose were measured.
Clinical Significance:
Insulin resistance drives post-transplant diabetes, vascular calcification, and accelerated atherosclerosis.
Early identification creates opportunities for targeted therapies, lifestyle intervention, and closer surveillance — interventions that may extend survival and reduce cardiovascular events.
Why the Identification of Atherosclerosis vs Ischemia is Imperative
The goal of cardiac imaging is three fold:(7,18-20)
1. Identify pre-existing coronary artery disease.
2. Risk stratification, including how many vessels are involved and degree of stenosis.
3. Guiding treatment decisions in the future.
Traditionally, patients without a diagnosis of coronary artery disease are sent for Functional testing. They are sent for either treadmill stress testing, stress echocardiogram, stress MRI, or SPECT nuclear testing. All these tests look for evidence of myocardial ischemia indicating a stenosis of 70% or more. They do not help diagnose coronary disease, they do not assist with risk stratification, and they do not help guide future treatment decisions. In fact, they can give a false sense of security and reassurance. (7,10,11,18-20) The post-transplant period is a critical time when decision making needs to be precise, individualized and guided by science, not a false sense of security . (2,3,5,6) A patient’s hopes and dreams … and lives … are literally in our hands and when most view the actual transplant as the end of a long journey, in reality it’s just the beginning.
As an internist and a CardioMetabolic Specialist, I study the root cause of disease and try to identify and modify risk in a logical and proactive manner. In that way I can prevent or modify disease progression rather than just being reactive and treating illness. Identifying atherosclerosis especially in this high risk population is crucial. This is not something that can be ignored or overlooked. Risk is risk and disease is disease… our thorough evaluations are so crucial for life and death and this is more so in these high risk populations.
Evidence for CCTA with FFRct
CCTA meets the criteria for identifying coronary disease, excels in risk stratification and is crucial for guiding future treatment decisions. (7,17,18-20)
NEJM 2018 reported a ~41% reduction in death/MI at five years with CCTA vs. standard care (18). PROMISE (N Engl J Med 2015) demonstrated superior discrimination and reclassification with an anatomic strategy in ~10,000 patients, with particularly strong signals in higher‑risk groups such as diabetes (7,19). PRECISE (JACC 2021) showed a ~70% reduction in death/MI/unnecessary catheterization at 12 months using a CCTA + selective FFRct strategy vs. functional testing (20).
Because ESRD and diabetes feature diffuse atherosclerosis and microvascular dysfunction—often with silent ischemia and higher false‑negative rates on stress testing—an anatomic/physiologic strategy is especially compelling (5,6,8–11,17–20).
Analysis showed that the majority of late adverse cardiovascular events — 57% — occurred in patients with completely normal functional testing (17–20). These were the very individuals reassured with, “Good news, Mr. Smith, your cardiac stress test is normal,” only to be left with a false sense of security. By contrast, only 5% of events occurred in those with a normal CCTA, which demonstrated superior discrimination, risk reclassification, and more robust event prediction — detectable as early as 42 months. This raises the most important question about a negative test: “Does this mean I have no heart disease, or only that I don’t currently need revascularization?”
Given the high cardiovascular risk and mortality rates in post-transplant patients, it is logical to assume that this population would derive significant benefit, even if it has not been specifically studied in renal transplant cohorts. In both diabetes and end-stage renal disease, cardiovascular disease typically manifests as diffuse atherosclerosis and microvascular dysfunction rather than isolated blockages (5,6,8–11). Patients in both groups frequently have silent ischemia and higher false-negative rates on stress testing because the disease is widespread and involves the small vessels. The fundamental driver in each condition is a chronic proinflammatory state with insulin resistance, which accelerates plaque formation, vascular calcification, and endothelial injury.
CCTA provides direct visualization of plaque burden, number of vessels involved, and stenosis severity. Adding FFRct delivers physiologic significance with near-invasively accurate precision. (7,18-20)
Together they offer:
Presence of disease — early detection of CAD.
Risk stratification — plaque burden and distribution.
Guidance for treatment — tailoring prevention and interventions.
Performance metrics are unmatched:
Negative predictive value ~99% (7).
Radiation exposure: Average exposure from sun/TV/airline travel (3mSv/yr) vs CCTA (1–3 mSv) vs. nuclear stress (9–12 mSv) vs. angiography (5–30 mSv depending on stenting) (16).
Diagnostic accuracy: FFRct at 94%, compared with ~70% for SPECT (17).
Recommendations for New Standards of Care
Based on the overwhelming evidence and the unique risk profile of this population, my recommendations are:
1. All pre‑transplant patients without known CAD should undergo CCTA with FFRct, regardless of functional testing results, unless specifically contraindicated (7,17–20).
2.All pre-transplant patients without diagnosed diabetes should undergo a 2-hour OGTT with insulin response (fasting, 1-hour, 2-hour) to detect insulin resistance and early dysglycemia — key drivers of post-transplant diabetes and cardiovascular risk (5,6,14,15). Notably, pioglitazone has been associated with ~51% lower mortality in diabetic patients on hemodialysis, according to supportive data from the broader dialysis literature, and therefore merits individualized consideration in collaboration with nephrology and cardiology (contextualized with 5,6,14). More broadly, any intervention that targets insulin resistance has the potential to improve both renal and cardiovascular outcomes.
3. Cardiometabolic evaluation should be proactive and continuous, recognizing that CKD and post‑transplant therapies accelerate atherosclerosis and metabolic disease (2,3,5,6,12–15).
Transplant surgery aims to enhance patients' quality of life in both the short and long term. Effective long-term management involves proactive risk identification and mitigation. Considering many cardiac tests require I.V. contrast dye, it's crucial to complete these assessments before transplantation. Our current decisions impact future outcomes. A strategic approach, like planning several moves ahead in chess, allows for early intervention and a more positive long-term prognosis. Establishing baseline cardiometabolic status in a meaningful, sophisticated and efficient manner– including cardiovascular and metabolic health – empowers us to make informed decisions and take control of the health trajectory.(2,3,5-7,12-15,18-20)
Conclusion
The goal of renal transplantation is not only to restore kidney function but to improve overall health and survival. A death is a death, regardless of GFR at the time, and outcomes must be measured in lives extended and lives improved. To achieve this, blinders must be removed: risk factor identification and modification — pharmacologic, nutritional, and behavioral — must be implemented in a pragmatic, individualized way.
Pre-transplant risk assessment is central to long-term success. CCTA with FFRct should be the standard of care, not an optional add-on for select patients (5,6,8–11). Seeing plaque on a screen changes behavior in ways numbers cannot. Confusing “no ischemia” on a stress test with “no disease” is unacceptable. A normal stress test is not a normal heart, and in transplant candidates this false reassurance endangers both immediate surgical safety and long-term prognosis. Ischemia may determine perioperative risk, but undiscovered disease dictates long-term survival.
Metabolic assessment must also be mandatory in all non-diabetic transplant candidates. This case illustrates the danger of relying on static glucose or HbA1c, which in ESRD is both misleading and unpredictable. Although glucose values on the OGTT appeared normal, the insulin response revealed clear resistance — elevated fasting levels, an exaggerated one-hour peak, and incomplete recovery at two hours. This hidden dysfunction fuels atherogenic dyslipidemia, systemic inflammation, vascular calcification, and progression of CKD and CVD. We have been focusing on the wrong target for too long — glucose alone — while ignoring insulin resistance, the true driver of post-transplant diabetes and cardiovascular risk.
Insulin resistance in the transplant setting magnifies the toxicity of immunosuppressive drugs, accelerating atherosclerosis and driving morbidity and mortality. Early identification opens the door to meaningful interventions: nutrition, lifestyle modification, targeted supplementation such as high-dose omega-3 EPA, and pharmacologic agents like pioglitazone when appropriate. These strategies extend not only renal graft survival but overall survival.
Renal transplantation is meant to extend life, not shorten it. Yet when one in three transplant recipients ultimately dies of cardiovascular disease, it is clear that current practices are failing. Functional stress testing reassures when it should alarm. A normal stress test does not mean a normal heart; it means an incomplete evaluation. By contrast, a normal CCTA with FFRct carries the weight of true prognostic reassurance. Continuing to rely on functional stress testing in this population is both medically inadequate and ethically indefensible (2,3,5,6,18–20). Equally unacceptable is the absence of dynamic metabolic testing — an omission unsupported by modern standards of care. The myopic focus must widen: transplant teams must evolve from protecting kidneys to preserving life, adopting cardiometabolic principles that have been established for years but remain underutilized.
The very centers that pride themselves on performing miracles of transplantation fail to recognize a simple truth: cardiovascular disease remains the leading cause of death after kidney transplantation. Without proactive cardiometabolic care, transplantation simply exchanges one form of failure for another.
And beyond this, transplant teams often fail to use available tools that could prevent long-term adverse outcomes, staying narrowly focused on short-term accomplishments. This systemic passivity echoes the moral failure of the Tuskegee Syphilis Study. Then, physicians observed the predictable, devastating consequences of untreated disease. Today, we see the same inertia in transplant medicine — documenting risk but refusing to act, observing decline but not intervening. The disease is different; the ethical breach is the same. To know the outcome and still choose to “watch and see” is not practicing medicine — it is abandoning it.
As Arthur Schopenhauer, the German philosopher, observed:
“All truth passes through three stages.
First, it is ridiculed;
second, it is violently opposed; and
third, it is accepted as being self-evident.”
The truth here is already self-evident: in renal transplant candidates, functional testing is obsolete. CCTA with FFRct along with metabolic assessmentmust become the standard of care. Anything less is failure. Let us not forget our mission, for in this population the stakes are nothing less than life and death.
Author: Dr John Sciales
Director, CardioCore Metabolic Wellness Center
"Getting to the Core- where being Healthy is Not an Accident"
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Acknowledgment
I would like to extend a special thank you to Dr. Matthew Budoff, a true champion of cardiac imaging and preventive care. I have had the privilege of meeting him, and much of his groundbreaking work has guided my own. He is not only an exceptional physician and an extraordinary intellect, but also a man of deep humanity — his dedication to caring for others is an example to us all.
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U.S. News & World Report, 2025 NYU Medical Center ranked #1 nationally Best Hospital's Honor Roll in cardiology, heart.
