Chronic kidney disease (CKD) makes HbA1c readings less reliable, and the distortion generally pushes results lower than your true average blood sugar. This becomes especially problematic when your estimated glomerular filtration rate (eGFR) drops below 30 mL/min/1.73 m², the threshold where multiple overlapping factors combine to make HbA1c an unreliable standalone marker. If you have both diabetes and advanced kidney disease, a “good” HbA1c number on paper may be masking blood sugar levels that are actually much higher.
Why Red Blood Cell Lifespan Matters
HbA1c measures the percentage of hemoglobin (the oxygen-carrying protein in red blood cells) that has been coated with sugar. Because this coating builds up gradually over a red blood cell’s life, HbA1c reflects your average blood sugar over roughly two to three months, which is the normal lifespan of a red blood cell.
CKD shortens that lifespan. Toxins that accumulate when kidneys aren’t filtering properly damage red blood cells, causing them to die sooner. When red blood cells live for a shorter period, hemoglobin spends less total time exposed to glucose, so less sugar attaches to it. The result: your HbA1c reads lower than it should for your actual average glucose. Research confirms that between-patient differences in red blood cell age explain virtually all the glucose-independent variation in HbA1c. In other words, two people with identical average blood sugar can have meaningfully different HbA1c values if their red blood cells have different lifespans.
How Anemia Pulls HbA1c in Both Directions
CKD causes anemia through several mechanisms, and each one distorts HbA1c differently.
Damaged kidneys produce less erythropoietin, the hormone that signals your bone marrow to make new red blood cells. Fewer new cells means fewer young cells in circulation. Since older red blood cells have had more time to accumulate sugar on their hemoglobin, a population skewed toward older cells can push HbA1c slightly upward relative to your actual glucose levels.
Iron deficiency, which is extremely common in CKD, has an even clearer effect. When your body is low on iron, red blood cell production slows, and the average age of circulating cells increases. Studies in both diabetic and non-diabetic individuals show that iron deficiency significantly elevates HbA1c, creating false-high readings that can make glucose control appear worse than it is. In CKD patients with diabetes, iron deficiency has been shown to make it impossible to accurately determine glycemic status from HbA1c alone.
This creates a confusing situation: some CKD-related factors push HbA1c down while others push it up, and the net effect depends on your specific combination of anemia type, iron status, and kidney function.
How Treatment for Anemia Adds More Distortion
Many people with advanced CKD receive erythropoietin-stimulating agents (ESAs) to treat their anemia. These medications ramp up red blood cell production, flooding the bloodstream with young cells that haven’t had time to accumulate much sugar on their hemoglobin. This dilutes the HbA1c measurement.
The effect is dose-dependent and substantial. For every 10,000 IU per week increase in ESA dose, HbA1c drops by an estimated 0.6 percentage points, a decrease that has nothing to do with actual blood sugar control. If your doctor adjusts your diabetes treatment based on this artificially lowered number, you could end up undertreated.
Chemical Interference From Uremia
When kidneys fail to clear waste products, urea builds up in the blood. Urea reacts with hemoglobin to form a modified version called carbamylated hemoglobin. In uremic patients, carbamylated hemoglobin levels are roughly 83% higher than in people with normal kidney function.
Carbamylated hemoglobin can interfere with the laboratory methods used to measure HbA1c. Different assay techniques are affected to different degrees. Some older chromatography-based methods are more susceptible, while immunoassay methods tend to be less affected. Regardless of the method, guidelines recommend interpreting HbA1c with caution in uremic patients because the chemical noise from carbamylation can shift results in unpredictable ways.
What Continuous Glucose Monitoring Reveals
Continuous glucose monitors (CGMs) measure actual glucose levels in real time, bypassing all the red blood cell variables that distort HbA1c. Studies in hemodialysis patients show just how large the gap between HbA1c and reality can be.
In a study of 59 hemodialysis patients with type 2 diabetes, the average HbA1c was 7.1% while the glucose management indicator (GMI, the CGM-derived equivalent of HbA1c) was 7.8%, a difference of 0.74 percentage points. Nearly half the participants, 49%, had a discordance greater than 1 full percentage point between their HbA1c and GMI. The correlation between HbA1c and GMI was only moderate, while GMI correlated almost perfectly with time-in-range. For patients on dialysis, CGM-based metrics like mean glucose, GMI, and time-in-range give a far more accurate picture of glucose control than HbA1c.
Alternative Blood Tests
Glycated albumin (GA) measures sugar attached to albumin, a blood protein, rather than hemoglobin. Because albumin turns over every two to three weeks rather than two to three months, GA reflects a shorter window of glucose control and responds faster to changes in blood sugar management. More importantly for CKD patients, GA is not affected by red blood cell lifespan or erythropoietin treatment.
In advanced CKD, GA correlates more strongly with average glucose than HbA1c does. A pooled analysis found a correlation of 0.57 between GA and average glucose in advanced CKD, compared to 0.49 for HbA1c. GA also appears to predict cardiovascular complications in people with diabetes and kidney disease, giving it potential value beyond simple glucose tracking. However, GA has its own limitations: it can be influenced by age, BMI, iron levels, and the presence of protein in the urine.
Fructosamine is another alternative marker that reflects glycated serum proteins over a two-to-three-week window. Like GA, it avoids the red blood cell lifespan problem. But research from the American Diabetes Association found that fructosamine was not less variable than HbA1c at a given glucose level and was biased by several of the same confounders as GA. For patients with an eGFR below 60, the ADA’s data actually supports continuing to use HbA1c to monitor trends in blood sugar, while recognizing its limitations rather than relying solely on alternative markers.
What This Means in Practice
If you have CKD with an eGFR below 30, your HbA1c most likely underestimates your true average blood sugar. The degree of underestimation depends on how severe your anemia is, whether you’re receiving ESA therapy, and your iron status. A “normal” or “well-controlled” HbA1c in this range should not be taken at face value.
If your eGFR is between 30 and 60, HbA1c is still useful for tracking trends over time, but single readings should be interpreted cautiously, especially if your hemoglobin levels are unstable or you’ve recently started iron or ESA therapy. The best approach for people with advanced CKD and diabetes typically combines HbA1c with at least one other method: CGM data when available, glycated albumin, or frequent fingerstick monitoring. No single test tells the whole story when kidney disease is in the picture.