The answer to this is same as in most cases and as I always say: bullshit studies.
In a euvolemic or hydrated state, renal blood flow is maintained by multiple redundant vasodilatory pathways. Prostaglandins are present but not critical; inhibiting them with aspirin has negligible hemodynamic impact.
In a hypovolemic or dehydrated state, the kidney loses all redundant vasodilatory capacity and becomes 100% dependent on prostaglandins to keep the afferent arteriole open. Here, aspirin removes the only remaining mechanism for blood flow, causing immediate vasoconstriction and ischemia.
The primary flaw here is, essentially ALL these studies have this confounder. And the other subsequent flaw - most likely also intentional mind you - is they put out in the public eye an average of these two distinct physiological states. So they can report a "small average risk" which obscures the binary reality: zero risk in hydration vs. high risk in depletion.
Aspirin is not inherently nephrotoxic in a metabolically competent, hydrated host. The "detrimental" label is largely an artifact of studying compromised systems: dehydrated, elderly, poly-medicated, and then of course projecting those risks onto the general population.
