UC San Diego

Acute kidney injury (AKI) is a frequent event in hospitalized patients, with an incidence that continues to rise, reaching as high as 70-80% in intensive care settings. The need for dialysis and progression to end-stage kidney disease (ESKD) after an episode of AKI is relatively low, from 5 to 20%. However, it is now recognized that patients with AKI may have very different kidney outcomes, varying from complete recovery, incipient chronic kidney disease (CKD), to progression to ESKD. Recent studies have shown that even mild AKI episodes can be associated with a 90% increased risk of developing CKD during long-term follow-up. There is a significant need to focus our efforts on factors that could mitigate the progression of kidney dysfunction and ultimately improve outcomes from AKI. The first step toward this goal encompasses a better understanding of tubular and glomerular alterations during and following an AKI episode. Our current approach, based solely on glomerular filtration rate (GFR), is flawed, since the loss of kidney function does not correspond to the degree of decline in estimated GFR (eGFR), and eGFR does not reflect tubular function. Changes in tubular concentration, reabsorptive and secretory capacity are recognized in AKI; however, they have not been incorporated in clinical assessments of overall kidney function. Here we review a few candidates to assess glomerular filtration/permeability, tubular dysfunction, and injury and how we expect these markers to alter during the development and recovery phase of AKI.