C-Peptide Unit Converter
C-Peptide Unit Converter
Convert C-peptide between ng/mL, µg/L, nmol/L and pmol/L, and read it the way it has to be read — against a simultaneous glucose and the patient's renal function.
C-Peptide converter
Mass ⇄ molarC-peptide 1.8 ng/mL, fasting
Formula and conversion factors
pmol/L = ng/mL × 331.1
ng/mL = µg/L (numerically identical)
- 0.331
- derived from the molecular mass of human C-peptide, 3020.29; one ng/mL is 1 µg/L, and 1 µg ÷ 3020.29 g/mol gives 0.331 nmol
- µg/L
- numerically identical to ng/mL; no conversion is needed between them
- equimolar with insulin
- proinsulin is cleaved into one molecule of insulin and one of C-peptide, so molar units make the pair directly comparable
- renal clearance
- C-peptide is cleared by the kidney rather than extracted by the liver, giving it a half-life of about 30 minutes against insulin's 4 to 6
Worked example
C-peptide 1.8 ng/mL, fasting
1.8 × 0.331094 = 0.60 nmol/L
1.8 × 331.094 = 596 pmol/L
= 1.80 µg/L
Within the fasting adult reference interval of 0.8–3.9 ng/mL
Reference interval and thresholds across the units
| ng/mL | nmol/L | pmol/L | |
|---|---|---|---|
| Fasting adult reference interval | 0.8 – 3.9 | 0.26 – 1.29 | 265 – 1291 |
| Suppressed — insulin deficiency | < 0.6 | < 0.20 | < 200 |
| Suppressed during hypoglycaemia — exogenous insulin | < 0.6 | < 0.20 | < 200 |
| Not suppressed during hypoglycaemia — endogenous | ≥ 0.6 | ≥ 0.20 | ≥ 200 |
Insulin against C-peptide during hypoglycaemia
| Insulin | C-peptide | Interpretation |
|---|---|---|
| High | High | Endogenous hyperinsulinism — insulinoma, sulfonylurea or meglitinide, or post-bariatric hypoglycaemia; screen for sulfonylureas before imaging |
| High | Suppressed | Exogenous insulin administration |
| Low | Low | Hypoglycaemia not mediated by insulin — consider adrenal insufficiency, liver failure, sepsis, or IGF-2-secreting tumour |
Distinguishing the patient's own insulin from the injected kind
C-peptide is reported in ng/mL, which is numerically identical to µg/L, and in nmol/L or pmol/L. The factor of 0.331 nmol/L per ng/mL comes from its molecular mass of 3020.29. The molar units are worth preferring where a laboratory offers them, because proinsulin is cleaved into one molecule of insulin and one of C-peptide, so the two are secreted in equimolar amounts and a molar comparison of the pair is directly meaningful.
The two peptides then diverge sharply in how they are cleared, and this is the basis of the test. Insulin is extracted on its first pass through the liver, with a half-life of four to six minutes. C-peptide undergoes almost no hepatic extraction and is cleared by the kidney, with a half-life of about 30 minutes. Peripheral C-peptide therefore reflects total pancreatic secretion far better than peripheral insulin does, and it is present at higher and steadier concentrations.
Renal clearance is also the main trap. In chronic kidney disease C-peptide accumulates, and a raised result in that setting says more about glomerular filtration than about the pancreas. Renal function should be accounted for before any conclusion about secretion is drawn, and the effect is large enough that C-peptide-based classification of diabetes becomes unreliable at advanced stages of kidney disease.
The clinical uses follow from one property: C-peptide is not present in insulin preparations, so it measures endogenous secretion even in a treated patient. In hypoglycaemia, a high insulin with a suppressed C-peptide means insulin was administered, while a high insulin with a high C-peptide means the pancreas produced it — insulinoma, a sulfonylurea, or post-bariatric hypoglycaemia. It is also used to classify diabetes years after diagnosis, where a preserved C-peptide argues against type 1. In every case it must be interpreted against a glucose drawn at the same moment: a mid-range C-peptide during hypoglycaemia is inappropriately high, not normal.
Frequently asked questions
How do I convert C-peptide from ng/mL to nmol/L?
Multiply by 0.331, a factor derived from its molecular mass of 3020.29. A C-peptide of 1.8 ng/mL is 0.60 nmol/L, or 596 pmol/L. ng/mL and µg/L are numerically identical.
Why measure C-peptide instead of insulin?
C-peptide is co-secreted with insulin in equimolar amounts but is absent from insulin preparations, so it measures the patient’s own secretion even during insulin treatment. It also escapes first-pass hepatic extraction, so peripheral levels reflect total pancreatic output more faithfully than insulin does.
Does kidney disease affect C-peptide?
Yes, substantially. C-peptide is cleared by the kidney, so it accumulates as glomerular filtration falls. A raised result in chronic kidney disease does not indicate high secretion, and renal function must be accounted for before the result is interpreted.
How does C-peptide distinguish insulinoma from injected insulin?
During documented hypoglycaemia, a raised insulin with a suppressed C-peptide indicates exogenous insulin, because injected preparations contain no C-peptide. A raised insulin with a raised C-peptide indicates endogenous secretion, which then requires a sulfonylurea screen before imaging for an insulinoma.
Why does the glucose have to be measured at the same time?
C-peptide is interpreted as a response to the prevailing glucose, not as an absolute quantity. A value in the middle of the reference interval is entirely appropriate at a normal glucose and inappropriately high during hypoglycaemia, where secretion should be suppressed.
Related calculators
References
- Jones AG, Hattersley AT. The clinical utility of C-peptide measurement in the care of patients with diabetes. Diabet Med. 2013;30(7):803–817.
- Cryer PE, Axelrod L, Grossman AB, et al. Evaluation and management of adult hypoglycemic disorders: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2009;94(3):709–728.
- Leighton E, Sainsbury CA, Jones GC. A practical review of C-peptide testing in diabetes. Diabetes Ther. 2017;8(3):475–487.
Medical Disclaimer: The tools and content provided here are for educational and reference purposes only. They are not intended to substitute for professional medical advice, diagnosis, or treatment. Clinical decisions should always be based on the comprehensive assessment of a qualified healthcare professional.