This is a groundbreaking article I believe and one of the doyens of Australian intensive care research is an author- Rinaldo Bellomo.
It demonstrates that urine output and renal blood flow can be inversely related (and I would argue- often are in our population of patients), and that renal dysfunction can evolve with increasing/normal renal blood flow in septic patients.
It’s all about the filtration pressure generated as a result of the pressure gradient which exists (or not) between the afferent and efferent arteriole in the glomerulus.
Hence I prefer the terminology “renal dysfunction” over “acute kidney injury”. We are safer asserting there is renal dysfunction when creatinine rises than we are in asserting that the kidneys are damaged.
Also- understanding the physiology behind the renal dysfunction described in this paper may help us avoid using the wrong therapies- if your patient is adequately volume loaded and has a reasonable cardiac output but is septic and oliguric, then giving them more fluid is unlikely to help.
Also, many will claim these patients have ATN…But anuria due to ATN often takes weeks to resolve, whereas many of our anuric septic patients improve within days of them coming off their noradrenaline- as the vasoplegia in the kidney settles and the gradient between the afferent and efferent arterioles returns.