An overview of the definition of AKI and its common etiologies, including a description of the prerenal-intrarenal-postrenal paradigm. The terms uremia and azotemia are also discussed.
How exactly does AIN lead to AKI? Cause I've read that interstitial inflammation causes tubular dysfunction, but then how does the GFR decrease? Is it also from sloughing of tubule cells with obstruction like in ATN? Or compression of tubules by interstitial edema and cellular infiltrates?