The clinical diagnosis and recovery of acute kidney injury (AKI) are mainly based on the rapid decline of glomerular filtration rate (GFR) and its subsequent recovery. The factors that determine kidney recovery and reduce the risk of subsequent progression to chronic kidney disease (CKD), however, are poorly understood. Thus, there is a need to better define the magnitude and time pattern of changes in kidney function during AKI and its recovery that go beyond GFR. Tubular transport regulates body homeostasis and the associated transport work is a primary determinant of the kidneys' energy needs. The tubular system is at the center of the pathophysiology of AKI and its recovery. In particular, proximal tubules and thick ascending limbs have been proposed to act as sensors, effectors and injury recipients of AKI stimuli. Surprisingly little attention has been given to aspects of tubular transport function in AKI and the relevance for kidney recovery. This review aims to outline changes in tubular transport function in AKI, discusses their potential consequences and relevance for the diagnosis and prognosis of AKI and its recovery, including changes in GFR, and poses the question whethertubulartransport provides an opportunity for intervention to rest the tubular system, which may have consequences for the progression to CKD.
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