Understanding eGFR and Creatinine: What Do Your Kidney Results Actually Mean?
For many people with kidney disease, eGFR becomes the number they watch most closely. A result of 48 becomes 45 and there is immediate concern that kidney function is deteriorating. Three months later it comes back at 51 and there is relief that the kidneys are improving.
Sometimes these changes are meaningful. Often, however, they reflect the normal variability of a test that is estimating kidney filtration rather than measuring it directly.
This is important because one of the most common questions I hear from patients is whether they can improve their eGFR. The answer depends partly on why kidney function is reduced, but it also requires understanding what eGFR and creatinine actually represent and how much significance should be attached to individual results.
What is eGFR?
GFR stands for glomerular filtration rate. It describes the rate at which blood plasma is filtered through the glomeruli, the microscopic filtration units within the kidneys.
GFR can be measured more directly using specialised filtration markers such as iohexol, but this is cumbersome and unnecessary for routine monitoring. Instead, laboratories usually report an estimated glomerular filtration rate — eGFR.
In Australia, eGFR is generally calculated from serum creatinine together with factors such as age and sex (Kidney Health Australia 2024).
This means eGFR is not a direct measurement of kidney function. It is a calculated estimate based largely on another measurement: creatinine.
An eGFR of 45 is also not equivalent to having exactly 45% kidney function remaining. Although eGFR is sometimes spoken about informally in this way, it is not a percentage.
What does creatinine tell us?
Creatinine is produced mainly from the normal metabolism of creatine within skeletal muscle. It enters the bloodstream and is predominantly cleared by the kidneys (Kashani, Rosner and Ostermann 2020).
As kidney filtration falls, creatinine generally rises. This relationship allows serum creatinine to be used to estimate GFR.
Importantly, creatinine itself is not the cause of the kidney damage reflected by a high creatinine result. An elevated creatinine is primarily a marker that clearance has reduced; it is not normally the reason kidney function is deteriorating.
This distinction matters because people sometimes become focused on trying to lower their creatinine. The objective should not be to manipulate the blood test but to address the factors contributing to kidney injury and protect remaining kidney function.
Why eGFR moves up and down
A small movement in eGFR does not necessarily indicate a permanent change in kidney function.
For example:
48 → 46 → 49
is quite different from:
48 → 41 → 35
The first pattern may simply represent relatively stable kidney function fluctuating around the high 40s. The second is more concerning for genuine progression.
KDIGO advises caution when interpreting relatively small changes in eGFR. In someone with CKD, a change of more than approximately 20% on subsequent testing exceeds the expected level of biological and analytical variability and warrants investigation (KDIGO 2024).
This is why I generally find at least three sequential results more informative than one result in isolation. Rather than becoming overly concerned about whether eGFR has moved by two or three points, it is more useful to look at where kidney function appears to be hovering and whether the longer-term trend is stable, improving or deteriorating.
The same principle applies in the opposite direction. An increase from 42 to 47 is encouraging, but it does not necessarily mean that five units of kidney function have been permanently restored.
What can temporarily affect creatinine and eGFR?
Several factors can change serum creatinine or kidney filtration without necessarily representing permanent loss or improvement in kidney function.
Hydration
Reduced circulating blood volume can temporarily reduce kidney perfusion. Dehydration from inadequate fluid intake, diarrhoea, vomiting, excessive sweating or illness can therefore raise creatinine and lower eGFR.
The solution is not to deliberately drink litres of water before a blood test. Ideally, kidney function should be assessed under normal hydration conditions.
This is particularly important for people with advanced kidney disease or heart failure who have been given a fluid restriction. They should not increase fluid intake simply to try to achieve a better blood result.
Exercise
Strenuous exercise can transiently alter kidney blood-test results through increased creatinine production, dehydration and, after particularly prolonged or intense exercise, temporary changes in kidney filtration.
Research has shown that creatinine-based eGFR can fall after exercise and that prolonged exercise combined with greater dehydration can also produce changes in cystatin C-derived eGFR and kidney injury biomarkers (Bongers et al. 2018).
If you are monitoring CKD closely, it can therefore be sensible to avoid unusually strenuous resistance training, endurance exercise or a particularly demanding workout immediately before testing.
Normal day-to-day physical activity is different. The aim is simply to make serial blood tests reasonably comparable.
Cooked meat
A large cooked meat meal before testing can increase serum creatinine and consequently reduce calculated eGFR.
Cooking converts some creatine within meat into creatinine, which is subsequently absorbed. This effect has been demonstrated in people with CKD as well as people with normal kidney function.
In one study involving healthy participants and people across several stages of diabetes-related CKD, a cooked meat meal significantly increased serum creatinine and reduced calculated eGFR. The effect was no longer significant following a 12-hour overnight fast (Nair et al. 2014).
Where an accurate baseline is important, avoiding cooked meat for around 12 hours before testing can therefore improve consistency.
Testing under similar conditions each time is often more useful than trying to achieve one artificially favourable result.
Creatine supplements can make eGFR look worse
Creatine supplementation is another important consideration.
Because supplemental creatine can increase creatinine production, serum creatinine may rise and a creatinine-based eGFR may fall without a corresponding deterioration in actual kidney filtration.
A recent systematic review and meta-analysis found a modest increase in serum creatinine with creatine supplementation but no significant reduction in measured or estimated GFR overall, supporting the possibility that changes in creatinine may sometimes reflect creatine metabolism rather than kidney injury (Kabiri Naeini et al. 2025).
This means creatine is not necessarily damaging the kidneys simply because serum creatinine increases.
However, it can complicate interpretation of the test.
If we are trying to establish someone's baseline kidney function, it may be useful to temporarily stop creatine before testing, where clinically appropriate, and interpret the result in the context of recent supplementation. There is not a universally established washout period that applies to everyone.
People with established kidney disease should also discuss creatine use with their treating practitioner because safety data are considerably stronger in healthy populations than in people with significant CKD.
Muscle mass is an important limitation of eGFR
One of the major limitations of creatinine-based eGFR occurs at the extremes of muscle mass.
A very muscular person generally produces more creatinine than an average person. Their creatinine may therefore appear high and their eGFR relatively low even when kidney filtration is better than the result suggests.
The opposite problem occurs in people with very low muscle mass.
An elderly or frail person, or someone with significant sarcopenia, an amputation or another condition causing muscle loss, may produce relatively little creatinine. Their serum creatinine can look reassuringly low and their calculated eGFR correspondingly high.
In this situation, creatinine-based eGFR can overestimate actual kidney function (Kashani, Rosner and Ostermann 2020; KDIGO 2024).
This is one reason I am cautious when someone tells me their creatinine is "good" without considering their age, body composition and overall clinical picture.
When cystatin C can help
Where creatinine may be unreliable, cystatin C can provide another way of estimating kidney filtration.
Cystatin C is a small protein produced by nucleated cells throughout the body and filtered by the kidneys. Unlike creatinine, its concentration is much less dependent on skeletal muscle mass.
GFR can be estimated from cystatin C alone or, often more accurately, by combining creatinine and cystatin C.
KDIGO recommends greater use of combined creatinine–cystatin C estimates where creatinine alone may be inaccurate or where greater precision would affect clinical decision-making (KDIGO 2024).
Cystatin C is not perfect. It can also be affected by non-GFR factors, including inflammation, thyroid dysfunction, corticosteroid use and some other clinical conditions. However, its limitations are different from those affecting creatinine.
For a very muscular person with a surprisingly low creatinine-derived eGFR, or a frail person whose eGFR appears unexpectedly good, cystatin C can therefore be particularly useful.
Where an extremely accurate assessment is required, a formally measured GFR using an exogenous filtration marker such as iohexol may be considered.
Medications can affect creatinine and eGFR
Medication changes also need to be considered when interpreting kidney results.
Some medicines, including trimethoprim, can increase serum creatinine by reducing its tubular secretion without necessarily reducing true GFR.
Other medications cause an expected haemodynamic change in filtration.
ACE inhibitors, angiotensin receptor blockers and SGLT2 inhibitors, for example, can cause an initial reduction in eGFR after commencement while providing important longer-term kidney protection in appropriately selected patients (KDIGO 2024).
A lower eGFR after starting one of these medications therefore does not automatically mean the medication is damaging the kidneys.
Again, context matters.
Can you actually improve eGFR?
Sometimes.
The extent to which kidney function can improve depends largely on why it has fallen.
If eGFR is reduced because of a reversible factor such as dehydration, acute illness, urinary obstruction, medication effects or an acute kidney injury, treating the underlying cause may produce substantial recovery.
There may also be improvement when previously uncontrolled factors such as blood pressure, metabolic health or the underlying kidney disease are treated effectively.
The situation is different when CKD involves substantial permanent nephron loss and kidney scarring.
In established CKD, completely restoring eGFR to a normal young-adult range may not be realistic. This does not mean treatment is unsuccessful.
For someone whose kidney function has been progressively declining, changing the trajectory from:
45 → 39 → 33 → 27
to:
45 → 44 → 45 → 43
may represent an extremely meaningful outcome.
In many cases, the most important objective is therefore not to continually push eGFR upwards but to protect functioning nephrons and slow the rate of decline.
Maintaining relatively stable kidney function for five or ten years can be a significant therapeutic achievement even if the eGFR itself remains below the normal reference range.
eGFR is only part of the kidney picture
Another mistake is focusing exclusively on eGFR.
CKD is assessed according to the cause of kidney disease, GFR and albuminuria, and abnormalities generally need to persist for at least three months before being classified as chronic kidney disease (KDIGO 2024).
Urinary albumin-to-creatinine ratio, or uACR, is therefore another important part of assessing kidney health.
Two people can have exactly the same eGFR but very different renal risk profiles if one has minimal albuminuria and the other has substantial urinary albumin loss.
Blood pressure is equally important.
For this reason, Kidney Health Australia recommends assessing kidney health using eGFR, urinary ACR and blood pressure together, rather than relying on serum creatinine alone (Kidney Health Australia 2024).
Depending on the type of kidney disease, other factors such as haematuria, imaging findings and the rate of previous eGFR decline may also be clinically important.
How to get more meaningful kidney blood tests
When monitoring kidney disease, consistency makes serial results easier to interpret.
Where practical:
be normally hydrated rather than deliberately overhydrating or arriving significantly dehydrated
avoid unusually strenuous exercise immediately before testing
avoid cooked meat for around 12 hours beforehand where establishing a comparable creatinine baseline is important
tell your practitioner if you are using creatine supplements
consider whether medications could be affecting creatinine or eGFR
consider cystatin C where muscle mass or other factors make creatinine difficult to interpret
assess eGFR alongside urinary ACR and blood pressure
compare at least three chronological results when determining the longer-term trajectory.
Using the same laboratory can also be helpful when tracking relatively small changes over time.
Most importantly, try not to attach too much significance to every movement in the number.
An eGFR moving from 42 to 39 can understandably be concerning, but it does not automatically mean kidney disease has progressed. Likewise, an increase from 39 to 43 does not by itself establish that kidney damage has reversed.
The more useful question is:
What is happening to kidney function over time?
Looking at the longer-term trend, together with albuminuria, blood pressure, medications, underlying disease and the circumstances surrounding each test, provides a much clearer picture than any single eGFR result.
For many people with chronic kidney disease, stability rather than normalisation is the most important marker of success.
References
Bongers CCWG, Alsady M, Nijenhuis T, Tulp ADM, Eijsvogels TMH, Deen PMT and Hopman MTE (2018) ‘Impact of acute versus prolonged exercise and dehydration on kidney function and injury’, Physiological Reports, 6(11), doi:10.14814/phy2.13734.
Kabiri Naeini E, Eskandari M, Mortazavi M, Gholaminejad A and Karevan N (2025) ‘Effect of creatine supplementation on kidney function: a systematic review and meta-analysis’, BMC Nephrology, 26(1):622, doi:10.1186/s12882-025-04558-6.
Kashani K, Rosner MH and Ostermann M (2020) ‘Creatinine: From physiology to clinical application’, European Journal of Internal Medicine, 72:9–14, doi:10.1016/j.ejim.2019.10.025.
Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group (2024) ‘KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease’, Kidney International, 105(4S)–S314, doi:10.1016/j.kint.2023.10.018.
Kidney Health Australia (2024) Chronic Kidney Disease (CKD) Management in Primary Care, 5th edn, Kidney Health Australia, Melbourne.
Nair S, O'Brien SV, Hayden K, Pandya B, Lisboa PJG, Hardy KJ and Wilding JPH (2014) ‘Effect of a cooked meat meal on serum creatinine and estimated glomerular filtration rate in diabetes-related kidney disease’, Diabetes Care, 37(2):483–487, doi:10.2337/dc13-1770.