Yes, AKI truly leads to CKD.

Division of Nephrology, University of California-San Francisco, San Francisco, California.
Journal of the American Society of Nephrology (Impact Factor: 9.47). 04/2012; 23(6):967-9. DOI: 10.1681/ASN.2012030222
Source: PubMed
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    ABSTRACT: Acute kidney injury (AKI) leads to worsening of chronic kidney disease (CKD), and CKD predisposes to the clinical entity of AKI. The tubules of the kidney play a central role in the fibrotic response, which ultimately leads to progressive kidney disease. The cellular mechanisms responsible for the epidemiological association between AKI and CKD are complex. In order to unravel characteristics of this direct involvement of the tubules, in particular the proximal tubules, we established a model to specifically target injury to the proximal tubule using a genetic approach to express the simian diphtheria toxin (DT) receptor in the proximal tubule. A single administration of DT to the proximal tubule resulted in inflammation, reversible injury, and adaptive repair. By contrast, thrice repeated injury led to maladaptive repair with sustained tubule injury, vascular rarefaction, proliferation of interstitial myofibroblasts, interstitial fibrosis, and glomerular sclerosis. An important feature of the maladaptive repair process after severe injury is the development of cell cycle arrest in G2/M. There is a subsequent activation of the DNA repair response with activation of a secretory phenotype whereby profibrotic factors are released. This insight introduces a number of potential new targets for therapeutic intervention to prevent and/or arrest CKD progression. © 2014 S. Karger AG, Basel.
    Nephron Clinical Practice 01/2014; 127(1-4):61-4. DOI:10.1159/000363673 · 1.65 Impact Factor
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    ABSTRACT: Background and Objectives Acute kidney injury (AKI) complicates the course of disease in critically ill patients. Efforts to change its clinical course have failed because of the fail in the early detection. This study was designed to assess whether heat shock protein (Hsp72) is an early and sensitive biomarker of acute kidney injury (AKI) compared with kidney injury molecule (Kim-1), neutrophil gelatinase-associated lipocalin (NGAL), and interleukin-18 (IL-18) biomarkers. Methods A total of 56 critically ill patients fulfilled the inclusion criteria. From these patients, 17 developed AKI and 20 were selected as controls. In AKI patients, Kim-1, IL-18, NGAL, and Hsp72 were measured from 3 days before and until 2 days after the AKI diagnosis and in no-AKI patients at 1, 5 and 10 days after admission. Biomarker sensitivity and specificity were determined. To validate the results obtained with ROC curves for Hsp72, a new set of critically ill patients was included, 10 with AKI and 12 with no-AKI patients. Results Urinary Hsp72 levels rose since 3 days before the AKI diagnosis in critically ill patients; this early increase was not seen with any other tested biomarkers. Kim-1, IL-18, NGAL, and Hsp72 significantly increased from 2 days before AKI and remained elevated during the AKI diagnosis. The best sensitivity/specificity was observed in Kim-1 and Hsp72: 83/95% and 100/90%, respectively, whereas 1 day before the AKI diagnosis, the values were 100/100% and 100/90%, respectively. The sensibility, specificity and accuracy in the validation test for Hsp72 were 100%, 83.3% and 90.9%, respectively. Conclusions The biomarker Hsp72 is enough sensitive and specific to predict AKI in critically ill patients up to 3 days before the diagnosis.
    PLoS ONE 10/2014; 9(10):e109407. DOI:10.1371/journal.pone.0109407 · 3.53 Impact Factor
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    ABSTRACT: The use of renal replacement therapy (RRT) for severe acute kidney injury (AKI) is frequently necessary in the face of life-threatening complications; however, there is wide practice variation with respect to triggers for RRT initiation. Recent evidence suggests that RRT may be independently associated with impaired recovery following AKI. There are plausible mechanistic reasons why RRT may be harmful and this concept is supported by ancillary evidence in the form of studies that have assessed the impact of different modalities of RRT for AKI as well as some of the literature pertaining to initiation of chronic hemodialysis in end-stage kidney disease patients (ESKD). As such, avoiding unnecessary RRT (URRT) is a desirable goal. There is emerging evidence of strategies that may be effective to help limit URRT. These strategies primarily involve early identification of AKI and limiting iatrogenic harm once AKI is established. Further research into defining and preventing URRT may help improve the consistently poor outcomes following severe AKI with respect to development of chronic kidney disease and ESKD.
    Seminars in Dialysis 10/2014; 28(1). DOI:10.1111/sdi.12300 · 2.07 Impact Factor