Chronic Kidney Disease: What eGFR and Creatinine Actually Tell You
Chronic kidney disease is largely silent until it is advanced, which is why it is usually found on a blood test done for something else. Understanding the two numbers on that report changes it from an alarming word into a manageable condition.
What the kidneys do
Beyond filtering waste, the kidneys regulate fluid balance, blood pressure, electrolytes, acid-base balance, red blood cell production through erythropoietin, and vitamin D activation. This is why kidney disease produces anaemia, bone problems and hypertension, not just a build-up of waste.
Creatinine
Creatinine is a waste product of muscle metabolism, cleared almost entirely by the kidneys. When filtration falls, creatinine rises.
Its weakness is that it depends on muscle mass. A muscular young man can have a creatinine at the top of the range with perfect kidney function, while a frail elderly woman can have a normal-looking creatinine with substantially reduced function. Creatinine also only begins to rise once roughly half of kidney function is already lost, which makes it a late signal.
eGFR
Estimated glomerular filtration rate converts creatinine into an estimate of filtration, adjusting for age and sex, reported in mL/min per 1.73 m². It is a better single number than creatinine, though it remains an estimate and is unreliable in extremes of muscle mass, in pregnancy, in acute illness and in people on certain supplements.
Current equations no longer apply a race coefficient. Cystatin C is an alternative marker used when the creatinine-based estimate is doubted.
The stages
- Stage 1: eGFR 90 or above, with evidence of kidney damage such as protein in the urine
- Stage 2: eGFR 60 to 89 with kidney damage
- Stage 3a: eGFR 45 to 59
- Stage 3b: eGFR 30 to 44
- Stage 4: eGFR 15 to 29
- Stage 5: eGFR below 15, kidney failure
CKD requires abnormality present for at least three months. A single low eGFR during dehydration, infection or after a contrast scan may be acute kidney injury, which behaves and is treated differently.
The other half of the diagnosis: protein in the urine
Staging by eGFR alone is incomplete. The urine albumin-to-creatinine ratio, ACR, is equally important, because protein leak predicts progression and cardiovascular risk independently.
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- Below 30 mg/g: normal
- 30 to 300 mg/g: moderately increased, formerly microalbuminuria
- Above 300 mg/g: severely increased
A person with stage 3a CKD and no proteinuria has a very different outlook from one with stage 3a and heavy proteinuria. Ask for the ACR, not only the eGFR.
Symptoms, and their absence
Early CKD has none. Later features include fatigue, poor appetite, nausea, itching, swelling of the ankles and around the eyes, frothy urine, night-time urination, muscle cramps, difficulty concentrating, breathlessness and a metallic taste. By the time these appear, considerable function has been lost.
Main causes
- Diabetes, the leading cause worldwide
- Hypertension
- Glomerulonephritis
- Polycystic kidney disease and other inherited conditions
- Recurrent kidney infection or obstruction, including stones and prostate enlargement
- Long-term NSAID use
- Certain unregulated herbal and heavy-metal-contaminated preparations
- Repeated episodes of acute kidney injury
- CKD of unknown aetiology, seen in agricultural communities in hot climates, likely linked to heat stress and dehydration
What slows progression
Blood pressure control, usually to below 130/80, is the most important single measure.
ACE inhibitors or ARBs reduce proteinuria and protect the kidney, particularly when ACR is raised. Creatinine may rise slightly when they are started, which is expected and not a reason to stop unless the rise is large.
SGLT2 inhibitors have changed the field. They slow progression in CKD both with and without diabetes and are now recommended widely.
Glycaemic control in diabetes.
Dietary sodium reduction, usually below 5 g of salt daily.
Moderate protein intake. Extreme restriction is not routinely advised and risks malnutrition; discuss targets with a dietitian rather than guessing.
Avoiding nephrotoxins. Regular NSAIDs including ibuprofen and diclofenac, unprescribed aminoglycoside antibiotics, contrast scans without precaution, and unverified herbal or ayurvedic preparations, some of which contain aristolochic acid or heavy metals.
Stopping tobacco, treating obesity, staying hydrated, and avoiding repeated dehydration in heat.
Statins for cardiovascular risk, which in CKD is higher than the risk of reaching dialysis.
Monitoring and complications
Expect periodic checks of eGFR, ACR, haemoglobin, potassium, calcium, phosphate, parathyroid hormone, bicarbonate and vitamin D. Anaemia, bone mineral disorder, acidosis and high potassium are managed as they appear.
When referral to a nephrologist is appropriate
eGFR below 30, rapidly falling eGFR, ACR above 300, persistent blood in the urine, uncontrolled blood pressure on multiple drugs, suspected inherited disease, or recurrent stones.
This is general information. Do not start, stop or adjust any medication based on it; kidney drug dosing in particular must be supervised.