Sodium Correction for Hyperglycaemia
Sodium Correction for Hyperglycaemia
Correct measured sodium for the diluting effect of hyperglycaemia, using either the Katz or Hillier factor.
Sodium Correction for Hyperglycaemia
Osmotic correctionMeasured sodium 128 mmol/L, glucose 600 mg/dL, Katz factor 1.6
Formula
- f
- 1.6 (Katz) or 2.4 (Hillier) mmol/L per 100 mg/dL of glucose above 100 mg/dL
- glucose
- mg/dL — subtract 100, the assumed normal value, before applying the factor
- result
- the sodium expected once glucose normalises; compare this, not the measured value, against the reference range
Worked example
Measured sodium 128 mmol/L, glucose 600 mg/dL, Katz factor 1.6
600 − 100 = 500 mg/dL of glucose above normal
1.6 × 500 ÷ 100 = 8.0 mmol/L of dilution to correct for
128 + 8.0 = 136.0 mmol/L corrected
Katz versus Hillier
| Factor | Value | Basis |
|---|---|---|
| Katz (1973) | 1.6 mmol/L per 100 mg/dL | Theoretical, derived from the osmotic gradient glucose creates |
| Hillier (1999) | 2.4 mmol/L per 100 mg/dL | Empirically derived from paired measurements; fits better above about 400 mg/dL |
Translocational, not true, hyponatraemia
Hyperglycaemia draws water osmotically out of cells and into the extracellular space, diluting the measured sodium. This is translocational, not true, hyponatraemia — the patient has too much glucose relative to sodium, not too little sodium relative to total body water, and the measured value understates what sodium will read once glucose returns to normal.
Katz’s factor of 1.6 mmol/L per 100 mg/dL is the original, theoretically derived linear correction, calculated from the osmotic gradient that glucose creates across the cell membrane. Hillier’s 2.4 was derived empirically from paired measurements in real patients and tracks the true relationship more closely once glucose rises above roughly 400 mg/dL, where the linear Katz model increasingly under-corrects.
The clinical point is what the corrected value tells you to do next. A patient in diabetic ketoacidosis or hyperosmolar hyperglycaemic state with a low measured sodium but a high corrected sodium has a genuine, sizeable free water deficit that is currently masked by the glucose — that deficit will be unmasked as insulin and fluid therapy bring glucose down. A rising measured sodium during treatment of DKA is therefore the expected, reassuring trajectory, not evidence that treatment is causing hypernatraemia, provided the rate of rise stays within safe correction limits.
To convert glucose from mg/dL to mmol/L, divide by 18.016.
Frequently asked questions
Why does glucose lower measured sodium?
High glucose draws water out of cells into the extracellular space, diluting sodium without any actual loss of sodium or gain of free water. It is a translocational effect, not true hyponatraemia.
Should I use the Katz or Hillier factor?
Both agree at modest glucose elevations. Hillier’s 2.4 was derived empirically and fits better once glucose is well above about 400 mg/dL, where Katz’s simpler 1.6 tends to under-correct.
Why does corrected sodium matter in DKA?
A low measured sodium with a high corrected sodium indicates a real free water deficit that is currently masked by glucose. That deficit becomes apparent as measured sodium rises while glucose falls with treatment — an expected, not alarming, change.
How do I convert glucose from mg/dL to mmol/L?
Divide the mg/dL value by 18.016. A glucose of 600 mg/dL is approximately 33.3 mmol/L.
Related calculators
References
- Katz MA. Hyperglycemia-induced hyponatremia — calculation of expected serum sodium depression. N Engl J Med. 1973;289(16):843–844.
- Hillier TA, Abbott RD, Barrett EJ. Hyponatremia: evaluating the correction factor for hyperglycemia. Am J Med. 1999;106(4):399–403.