Fructosamine

Fructosamine denotes glycated serum proteins — chiefly albumin — formed via non-enzymatic glucose binding and Amadori rearrangement to a stable ketoamine. Albumin's ~14–21-day turnover yields a 2–3-week glucose window versus HbA1c's 8–12 weeks. Reference values: 200–285 µmol/L. Its primary role is substituting for HbA1c when red-blood-cell turnover is abnormal: haemolytic anaemia, sickle-cell disease, iron- or B12-deficiency anaemia, erythropoietin-treated CKD, and pregnancy all distort HbA1c. Results are unreliable below serum albumin 3.0 g/dL (cirrhosis, nephrotic syndrome, protein-losing enteropathy); separately assayed glycated albumin is then preferred. In ARIC (Selvin et al., 2014; n ≈ 12,300; up to 20 years), elevated fructosamine predicted incident diabetes and microvascular complications comparably to HbA1c; associations with retinopathy and CKD persisted after HbA1c adjustment. AMORIS (Malmström et al., 2015; n = 338,443; median 19 years) found MI and all-cause mortality risk rising at ≥2.30 mmol/L; the highest tier (≥2.70 mmol/L) yielded HR 2.88 for MI and 2.31 for all-cause mortality after adjustment for cardiovascular risk factors and fasting glucose. In octogenarians without diabetes, albumin-corrected fructosamine predicted all-cause mortality (HR 1.27 per 1-µmol/g; Zhou et al., 2022, Healthy Ageing and Biomarkers Cohort Study). Fructosamine assays lack cross-laboratory standardisation, and an independent causal contribution to cardiometabolic risk beyond the hyperglycaemia they reflect has not been established in intervention trials.