This analysis covered 287 patients, mean age 73.2, after successful endovascular thrombectomy, comparing intensive with conventional blood pressure management. Acute kidney injury within seven days occurred in 20 of 147 (13.6%) intensively managed patients and 9 of 140 (6.4%) conventionally managed, an adjusted odds ratio of 2.54 with an interval from 1.10 to 6.35. Early AKI within two days was also more common. Sixty-nine per cent of events were stage 1.
The outcomes associated with AKI are severe out of proportion to its severity. Functional independence at three months occurred in 4 of 29 patients with AKI (13.8%) against 126 of 257 without (49.0%), adjusted odds ratio 0.19. Stroke-related mortality was 11 of 29 (37.9%) against 8 of 257 (3.1%), adjusted odds ratio 13.8 with an interval from 4.14 to 49.64.
Read the causal direction carefully. Stage 1 AKI does not plausibly cause a twelve-fold increase in stroke mortality. The authors' reading — that AKI marks systemic haemodynamic vulnerability in patients whose pressure was driven down aggressively — fits better. The practical implication is not to treat the creatinine but to treat its appearance as a signal that this particular patient is not tolerating the strategy.
- After successful thrombectomy specifically, not stroke generally
- Most AKI was stage 1 — the grade usually recorded and ignored
- AKI is far more likely a marker of haemodynamic vulnerability than a cause
- A rising creatinine is a reason to reconsider the blood pressure target
- Mean age 73 — a population with limited renal reserve to begin with
The statistics, in plain English
The sensitivity analysis is the most important number here. When creatinine ascertainment was equalised between groups, the 48-hour association fell to an odds ratio of 4.20 with an interval from 0.83 to 32.6 — no longer significant. Patients managed intensively were monitored more closely, so some of the apparent excess AKI is detection bias. The direction survived; the certainty did not.
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