Causal Safety: Does an NSAID Cause Kidney Injury?

Association isn't causation. Using a new-user active-comparator design with propensity-score matching and a self-controlled case series — on data with a sealed true effect — I show how a naive comparison understates a real harm by nearly half, and how two independent causal methods recover it.

Switch between the crude, propensity-matched, and self-controlled estimates to see each odds ratio move toward the sealed true effect of 2.20.

RWE · CAUSAL ESTIMATE

Adjust, and the harm appears.

The crude comparison says these two drugs barely differ. But sicker patients were steered toward one of them — confounding. Switch on each method and watch the estimate climb toward the sealed truth.

ODDS RATIO
GAP TO TRUTH
true effect · OR 2.20
true · 2.20
OR 1.02.6

The question

Do NSAIDs cause acute kidney injury (AKI) compared with acetaminophen? Every project before this one asked is there a signal? This one asks the harder question — does the drug actually cause the harm? — which means confronting confounding head-on.

What I did

  • Design. A new-user, active-comparator emulation (NSAID vs acetaminophen), the standard pharmacoepidemiology guard against confounding by indication.
  • Propensity-score matching with a covariate-balance Love plot — the standard-mean-differences fell from ~0.14–0.27 to ~0.01, so the two groups became genuinely comparable.
  • A self-controlled case series (SCCS) as an independent cross-check — each patient is their own control, so it has different blind spots to the matched cohort.
  • Robustness: bootstrap confidence intervals, a window-sensitivity check, and a negative-control outcome (which correctly came back null).

Key finding

The estimates are in the interactive above. The naive, crude comparison gave an odds ratio of 1.19 — it understated a real harm by 46%, because channeling (sicker patients steered toward acetaminophen) hid it. Propensity-score matching moved that to 2.05, and the self-controlled series independently landed at 2.14. Both causal methods converged on roughly a doubling of AKI risk.

Why a sealed truth — and what this is not

This is a simulation study, and I want to be plain about that. The patient data is synthetic: I generated it with a known true odds ratio of 2.20 and kept that number sealed until the analysis was finished. So the finding here is not “NSAIDs cause AKI at OR 2.14” — that claim would need real claims or EHR data.

What it does demonstrate is the thing real data can never show you: whether your estimator recovers an effect you already know is there. Checking an estimator against a known answer is the standard way methods are validated, and it’s the point of the exercise — the crude estimate missed by nearly half, and both causal designs recovered the truth to within a few percent. The next step is the same protocol on real data (MIMIC-IV, credentialing in progress).