eGFR in Athletes: Why Your Kidney Function Test Might Be Lying to You
Table of Contents
Introduction: eGFR in Athletes
eGFR (estimated glomerular filtration rate) is the standard marker of kidney filtration capacity, calculated from serum creatinine using one of several mathematical formulas. Most modern eGFR calculators adjust for age, sex, and serum creatinine, but they do not directly account for clinically important individual factors such as body weight, muscle mass, training status, recent exercise, or hydration. This is where athletes can be misclassified.
Creatinine is released from skeletal muscle, so a trained athlete — or any patient with unusually high muscle mass or larger body size — may generate more creatinine than the formula expects. The calculator then interprets that higher creatinine as reduced filtration, even when kidney function may be normal. In practice, this means eGFR can appear falsely low in athletic or highly muscular individuals unless the result is interpreted in context.
In this article I will break down what eGFR in athletes actually measures, why standard reference ranges frequently mislead, which formulas hold up best in trained populations, and what to do when numbers fall outside expected limits. This is part of a broader series on athlete blood work interpretation at drantti.com, where each biomarker is examined in the specific context of training physiology rather than general population norms.
Why eGFR in Athletes Is Frequently Misinterpreted: The Creatinine Problem
Before you can understand eGFR in athletes, you need to understand what it is actually estimating. Glomerular filtration rate is the volume of plasma filtered by the kidneys per unit time — the gold-standard measure of renal function. True GFR measurement requires inulin clearance or radioisotope-based techniques that are invasive, expensive, and impractical outside of research settings. In clinical practice, eGFR is calculated instead from serum creatinine — a waste product of muscle metabolism — combined with age, sex, and body size variables.
This is where athletes immediately run into trouble. Creatinine is produced in proportion to skeletal muscle mass. A larger, more muscular athlete generates more creatinine per unit time than a sedentary individual of the same age and sex. When a standard formula receives that higher creatinine input, it outputs a lower eGFR — not because the kidneys are filtering less, but because the creatinine input is disproportionately large relative to what the formula expects.
Research has quantified this effect directly. In a study evaluating 137 kidney transplant recipients using isotopic measured GFR (mGFR) as the reference standard, eGFR based on the CKD-EPI formula was falsely reduced by −5.9 ± 1.4 mL/min per 10 kg lean mass [2]. Although this population was not athletes, the result supports the broader concern that higher lean mass can bias creatinine-based eGFR downward. Creatinine-based equations assume equal muscle mass across individuals of the same demographic — an assumption that systematically fails when applied to athletes. This same principle explains why HbA1c in athletes and other metabolically sensitive markers require sport-specific interpretation frameworks rather than standard lab cutoffs.
In clinical practice, this issue is not limited to competitive athletes. I see the same pattern in many otherwise healthy patients who are simply large-framed, muscular, or recently physically active. Modern eGFR calculators usually adjust for age, sex, and serum creatinine, but they often do not directly account for body size, muscle mass, recent exercise, or hydration. As a result, a mildly elevated creatinine can push the eGFR below the reference range even when the explanation is physiological rather than pathological.
Another common situation is that serum creatinine itself remains within the laboratory reference range, yet the calculated eGFR is still flagged as low. This can be confusing for patients. The reason is that eGFR is not the same thing as creatinine; it is an algorithmic estimate that reinterprets creatinine through variables such as age and sex. Therefore, a creatinine value that looks acceptable on its own may still generate a borderline eGFR once the formula is applied.
Another important confounder is hydration. Many blood panels are taken fasting in the morning, and patients often arrive mildly dehydrated after not drinking normally overnight. Even a small degree of dehydration can concentrate serum creatinine and make eGFR appear lower than it would under well-hydrated baseline conditions. This is why I usually interpret borderline eGFR results together with the sampling context: Was the patient fasting? Had they trained recently? Were they dehydrated? Was creatinine only minimally elevated? Without that context, a mildly low eGFR can look more alarming than it really is.
When I explain this to patients, I emphasize that a mildly low eGFR does not automatically mean kidney disease, especially if creatinine is normal or only slightly elevated and there is a clear contextual explanation such as muscle mass, body size, recent training, fasting-related dehydration, or hydration status. In many mild borderline cases, the most appropriate next step is not panic, but follow-up under standardized conditions. For a stable, mildly abnormal result, annual monitoring may be sufficient. If the abnormality is more marked, progressive, associated with urine abnormalities, or clinically unexplained, then earlier re-testing and further evaluation are needed.
How Common Is the Problem? eGFR in Athletes: Data from 490 Olympians
A 2025 study evaluated 490 Olympic athletes using four different eGFR formulas and classified them against KDIGO (Kidney Disease Improving Global Outcomes) GFR categories [1]. The sample included athletes preparing for the Rio 2016, PyeongChang 2018, and Tokyo 2020 Olympic Games, divided into endurance disciplines (308 athletes: cycling, rowing, canoeing, triathlon, long-distance running, swimming, cross-country skiing) and skills disciplines (182 athletes: archery, equestrian, sailing, golf) serving as a low-training-load comparator.
The finding that matters most: using the Cockcroft-Gault (CG) formula — still widely used in many clinical labs — 18.5% of endurance athletes were classified into KDIGO category G2 (“mildly decreased” kidney function) despite having normal serum creatinine values and no history of kidney disease [1]. Among female endurance athletes specifically, the figure reached 43.3% in G2 when CG was applied [1]. These classifications should not be interpreted as evidence of kidney disease: all athletes had normal creatinine at baseline and no kidney disease history, and the study’s conclusions attribute the G2 classifications to the formula’s behaviour in lean athletic populations rather than genuine filtration impairment [1].
The same study found that endurance athletes showed higher serum creatinine values than skills athletes (0.91 ± 0.14 mg/dL vs. 0.88 ± 0.13 mg/dL, p = 0.014) — consistent with higher training volumes characteristic of endurance disciplines — despite showing no significant difference in eGFR when calculated with CKD-EPI or MCQE [1].
Among clinicians, it is also widely recognized that creatinine and creatinine-based eGFR require caution in athletic or highly muscular patients. The result should not be read in isolation, because the formula may be reacting to muscle mass, recent training, or hydration rather than true kidney filtration.
However, this does not mean kidney disease should be dismissed in athletes. If there is a genuine clinical concern about reduced kidney function — for example a clearly abnormal or progressive eGFR, abnormal urine findings, hypertension, systemic illness, or symptoms suggesting renal disease — cystatin C can be a useful additional test. In my experience, it is often not included in standard first-line laboratory panels, because serum creatinine is usually the routine screening test. But when creatinine-based eGFR is difficult to interpret, cystatin C can help clarify whether the low eGFR is likely to be a muscle-mass artefact or a true filtration problem.
This pattern of training-induced elevation affecting a metabolic marker is not unique to creatinine. LDH in athletes and uric acid in athletes follow a similar logic: values that look pathological in a sedentary patient often reflect normal athletic physiology when interpreted in context.
Which eGFR Formula Should Be Used in Athletes?
Not all eGFR formulas perform equally when applied to athletic populations. Understanding which formula your lab used — and whether it is appropriate — is the first step in interpreting eGFR in athletes correctly.
The Di Gioia et al. (2025) study compared four formulas head to head in the same 490 Olympic athletes [1]:
Cockcroft-Gault (CG): Incorporates total body weight, which can behave poorly as an indirect body-size adjustment in lean athletic populations. With the CG formula, a significant percentage of athletes fell into KDIGO G2 (13.2% of skills athletes and 18.5% of endurance athletes), and among female athletes, 38.9% were classified in G2 [1].
MDRD (Modification of Diet in Renal Disease): Developed in people with CKD — a population metabolically very different from competitive athletes. It produced significantly higher eGFR values for endurance athletes compared to skills athletes (129.3 ± 25.8 vs. 122.6 ± 24 mL/min/1.73 m², p = 0.004), suggesting it is influenced by exercise training load and intensity in ways that do not reflect true GFR differences [1].
CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration): Showed no significant difference in eGFR between endurance and skills athletes (121.7 ± 7.9 vs. 121 ± 7.1 mL/min/1.73 m², p = 0.321) and classified 100% of athletes — both groups — into KDIGO G1 (normal) [1].
MCQE (Mayo Clinic Quadratic Equation): Also showed no significant difference between groups and classified 99–99.5% of athletes in G1 [1].
The conclusion from this large-sample study is stated explicitly by the authors: CKD-EPI and MCQE showed better stability and reliability, making them the most suitable for kidney function evaluation in athletes [1]. CG should be interpreted with particular caution in athletic populations, and recalculation using CKD-EPI is warranted before drawing clinical conclusions. MDRD is sensitive to training effects and should be interpreted with caution in heavily trained individuals.
The direct practical implication: if your athlete receives a lab report calculated with Cockcroft-Gault — and many automated lab systems still default to CG — a borderline or low eGFR result warrants re-calculation using CKD-EPI before any clinical action is taken.
It is also worth remembering why this problem exists in routine care. Most standard laboratory panels report a creatinine-based eGFR automatically, but the calculation is usually based on serum creatinine, age, and sex — not direct measurement of body composition or skeletal muscle mass. From a practical perspective, this is understandable. Routine laboratories cannot realistically require accurate muscle-mass assessment for every patient before reporting kidney function. For the average sedentary patient, this approach often works well enough as a screening tool.
The limitation becomes visible at the edges of the population: athletes, highly muscular individuals, very large-framed patients, and people who have recently trained hard or arrived mildly dehydrated for fasting blood work. In these cases, creatinine may be higher because of muscle mass or recent physiology, and the eGFR may look lower than the patient’s true filtration capacity.
This is where clinical judgment matters. The number should never be ignored, but it should also never be interpreted without context. The physician has to ask whether the creatinine and eGFR fit the whole clinical picture: body size, training background, hydration, urine findings, blood pressure, medication use, previous results, and the direction of change over time. In the end, eGFR is a useful estimate — not an absolute diagnosis.
eGFR in Athletes and Exercise Timing: When You Draw Blood Changes Everything
Even when the right formula is used, eGFR in athletes depends critically on when the blood sample was taken relative to training. The kidneys are not passive bystanders during intense exercise — they are actively deprioritised in the cardiovascular hierarchy.
Exercise-induced sympathetic activity induces vasoconstriction of afferent arterioles, reducing renal blood flow [3]. At maximal exercise intensities, the kidney’s share of cardiac output can be drastically reduced to approximately 3% during maximal exercise [4]. A direct ultrasound measurement study found that renal blood flow after maximum exercise decreased by 51%, with a significant decrease of 31% already occurring at 100% of the lactate acid breaking point [5]. The kidneys tolerate reduced perfusion during exercise in order to redirect cardiac output to active muscle — a physiological trade-off that is well-compensated in healthy trained athletes.
The functional consequence is a measurable, transient fall in eGFR immediately post-exercise. In 17 trained, middle-aged males assessed before and after a 21-km half-marathon, the mean EGFR at baseline was 76 mL/min/1.73 m²; it decreased at the end of the run to 62 mL/min/1.73 m² (mean decrease 16%, p < 0.01), and for the following 3 hours (68 mL/min/1.73 m²) and 6 hours (70 mL/min/1.73 m²), though statistical significance was only achieved immediately after the run [6]. A systematic review of 30 studies (n = 1,724 participants) covering marathons, ultramarathons, half-marathons, Ironman, and cycling events found that across 21 studies, mean serum creatinine increase was 25.7 (± 11.6) µmol/L — and that in the 13 studies reporting recovery data, all had returned to baseline or were improving within 48 hours [7].
This 48-hour recovery window is important context for any blood work panel. Just as aldosterone in athletes fluctuates acutely with hydration and exercise load, eGFR and serum creatinine reflect the immediate physiological state at the time of sampling, not a stable measure of kidney health. The same timing logic applies to other post-exercise-sensitive markers including free testosterone in athletes and fasting glucose in athletes.
For athletes, a practical first step is to take kidney-related blood tests under standardized conditions: rested, well hydrated, and with enough time since the last hard training session. This reduces the risk that the result simply reflects acute exercise physiology.
However, even a rested athlete may have a higher creatinine level because of greater skeletal muscle mass. That is why creatinine-based eGFR can remain difficult to interpret even when the blood draw is timed correctly. In cases where the clinical question is important — for example, repeated borderline eGFR values, uncertainty about true renal function, or concern before medication decisions — cystatin C is often the more useful additional test. It provides a way to assess filtration without relying as heavily on muscle-derived creatinine.
In practice, I do not treat creatinine-based eGFR in athletes as a final answer. I treat it as a screening estimate that has to be interpreted in context. If the result does not fit the athlete’s body composition, history, urine findings, or clinical picture, cystatin C can give a clearer estimate of whether there is a true kidney function issue or mainly a creatinine-related artefact.
When Low eGFR in Athletes Is Actually Concerning: Exercise-Induced AKI
The above sections describe physiological, reversible decreases in eGFR. But there is a clinically meaningful scenario in which athletes do develop true acute kidney injury (AKI) — and this must not be dismissed as routine exercise physiology.
A narrative review of ultra-endurance events found wide variation in AKI prevalence ranging from 0% to 85%, driven largely by differences in event type, duration, hydration status, and — critically — NSAID use [8]. In a multi-stage 150-mile ultramarathon (BIERS study), there were significant declines in GFR after each stage compared with the pre-race baseline (p < 0.001), with the majority of participants (55–80%) incurring AKI [9]. By contrast, in a properly hydrated 120 km ultramarathon study with strict exclusion of NSAID users, the prevalence of AKI was observed from 0 to 4.2% depending on methodology used [10].
The mechanisms by which extreme endurance exercise can cause genuine AKI include:
1. Haemodynamic stress. Sustained reductions in renal blood flow combined with dehydration and activation of the renin-angiotensin-aldosterone system — a hormonal axis also covered in the aldosterone in athletes article — can reduce glomerular perfusion pressure beyond the kidney’s autoregulatory capacity.
2. Exertional rhabdomyolysis. In ultra-endurance events, myoglobin released from damaged muscle cells can cause toxicity to renal tubular cells, obstruction of tubular flow by myoglobin casts, and vasoconstriction of intrarenal blood vessels [8]. The narrative review found 43 cases of exertional rhabdomyolysis in ultra-endurance events, of which 30 occurred alongside AKI diagnosis [8]. This muscle damage connection is also relevant to LDH in athletes, where elevated lactate dehydrogenase often appears alongside significant muscle breakdown events.
3. NSAID use. NSAIDs have been linked to increased AKI risk and severity in ultra-endurance athletes, plausibly through impaired renal prostaglandin-mediated protection during renal hypoperfusion [8]. The narrative review identified NSAID use as a major risk factor for AKI severity and progression in ultra-endurance athletes [8].
Red flags warranting clinical investigation rather than “exercise effect” attribution:
- Serum creatinine remaining elevated beyond 48–72 hours of rest
- Oliguria (urine output below 0.5 mL/kg/h) or macroscopic haematuria (tea-coloured urine)
- Creatinine rise of ≥ 0.3 mg/dL within 48 hours, or ≥ 1.5× baseline within 7 days, in the context of a clinical event
In clinical practice, exertional rhabdomyolysis becomes a concern when an athlete develops unusual or disproportionate muscle pain, marked swelling, weakness, or dark urine after training. Patients often describe the urine as cola-coloured, coffee-coloured, or tea-coloured. This is a red flag that should never be dismissed as normal post-workout soreness.
Rhabdomyolysis can also disturb electrolytes, especially potassium. Significant hyperkalaemia can increase the risk of dangerous cardiac arrhythmias, which is one reason severe rhabdomyolysis is treated as a medical emergency. These patients need urgent assessment in hospital care, and severe cases may require intensive monitoring, aggressive intravenous fluids, and sometimes intensive care support. In the worst cases, rhabdomyolysis can become life-threatening.
I have also seen rhabdomyolysis present with surprisingly modest symptoms. One example was a patient who developed pectoral muscle rhabdomyolysis after a CrossFit-style workout and ultimately required hospital treatment. A useful clinical clue is that the urine dipstick may be positive for “blood” even when the problem is not true haematuria. In this situation, the test is often reacting to myoglobin released from damaged muscle rather than haemoglobin from red blood cells. This is exactly why dark urine after intense exercise should be taken seriously.
Cystatin C: The Better Solution for eGFR Assessment in Athletes
For athletes in whom creatinine-based eGFR is consistently borderline or low despite clinical plausibility of normal renal function, cystatin C offers a more reliable alternative.
Cystatin C is a small protein produced at a constant rate by all nucleated cells and filtered exclusively by the glomeruli. Unlike creatinine, its serum concentration is less affected by skeletal muscle mass or dietary protein intake — the same two variables that make standard eGFR in athletes so unreliable. A 2024 retrospective analysis of 227 male elite athletes with testosterone-induced muscle hypertrophy — all characterized as competitive or recreational athletes — found that cystatin C measurements display less variance compared with creatinine across different BMI categories [11]. The authors concluded that cystatin C may have a future role as the primary or sole renal filtration biomarker in elite athletes, while noting that creatinine generation is primarily determined by muscle mass and dietary intake, creating high variability that makes it a misleading marker that is not universally generalizable [11].
The 2024 analysis cites KDIGO guidance supporting supplementary tests such as cystatin C or clearance measurement when creatinine-based eGFR is expected to be less accurate [11]. In clinical practice, an athlete with a consistently low CKD-EPI eGFR (e.g., 60–75 mL/min/1.73 m²) but no symptoms, no proteinuria, no haematuria, and plausible muscularity is a reasonable candidate foIn many athletic patients, cystatin C ultimately becomes more clinically useful than creatinine alone when the goal is to estimate true kidney filtration. Unlike creatinine, cystatin C is not primarily generated from skeletal muscle metabolism, which means it is generally less influenced by muscle mass, body size, or the muscular adaptations seen in trained athletes. Because of this, cystatin C often provides a clearer estimate of renal function in situations where creatinine-based eGFR appears borderline or difficult to interpret.
In my own clinical practice, I find cystatin C more useful when evaluating athletes with unexpectedly low eGFR values, particularly when the creatinine result does not seem to match the overall clinical picture. It is often more informative in highly trained or muscular individuals, where creatinine alone can easily overestimate the degree of renal impairment.r cystatin C measurement to help distinguish a creatinine-muscle mass artefact from genuine reduced filtration.
Conclusion: eGFR in Athletes Requires Context, Not Panic
eGFR in athletes is one of the clearest examples of why laboratory medicine cannot be separated from clinical context. Creatinine-based formulas work reasonably well for the average sedentary population, but athletes, highly muscular individuals, and physically active patients exist outside the assumptions those equations were originally built on. Muscle mass, recent training, hydration status, fasting blood work, and body size can all shift creatinine upward and push eGFR downward without reflecting true kidney disease.
That does not mean abnormal kidney markers should be ignored. The important question is whether the laboratory result fits the overall clinical picture. A mildly low eGFR in a healthy, asymptomatic athlete with normal urine findings and stable long-term values is very different from a progressive decline in kidney function, dark urine, hypertension, proteinuria, or signs of systemic illness. In practice, the interpretation matters more than the isolated number itself.
For this reason, creatinine-based eGFR should often be treated as a screening estimate rather than a definitive answer in athletic populations. When uncertainty remains, cystatin C frequently provides a more clinically useful assessment because it is less influenced by skeletal muscle mass and training-related physiology. In many athletic patients, it offers a clearer picture of whether there is true renal dysfunction or simply a creatinine-related artefact.
Ultimately, the key message is simple: athletes should not panic over a borderline eGFR value without proper interpretation, but clinicians should not dismiss abnormal kidney markers blindly either. The goal is not to ignore the number — it is to understand what the number actually means in the context of the individual athlete standing in front of you.
References
[1] https://pmc.ncbi.nlm.nih.gov/articles/PMC12072620/
[2] https://pmc.ncbi.nlm.nih.gov/articles/PMC7788434/
[3] https://pmc.ncbi.nlm.nih.gov/articles/PMC9535345/
[4] https://journals.physiology.org/doi/full/10.1152/japplphysiol.00392.2022
[5] https://pubmed.ncbi.nlm.nih.gov/29525855/
[6] https://pubmed.ncbi.nlm.nih.gov/18600608/
[7] https://pmc.ncbi.nlm.nih.gov/articles/PMC5731225/
[8] https://pmc.ncbi.nlm.nih.gov/articles/PMC9779673/
[9] https://pubmed.ncbi.nlm.nih.gov/24650338/
