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      Renal Functional Reserve and Renal Recovery after Acute Kidney Injury

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          Abstract

          Renal functional reserve (RFR) represents the capacity of the kidney to increase glomerular filtration rate (GFR) in response to certain physiological or pathological stimuli or conditions. Once baseline GFR is determined, RFR can be assessed clinically after an oral protein load or intravenous amino acid infusion. In clinical practice, baseline GFR displays variable levels due to diet or other factors. RFR is the difference between peak ‘stress' GFR induced by the test (p.o. or i.v.) and the baseline GFR. In clinical scenarios where hyperfiltration is present (high baseline GFR due to pregnancy, hypertension or diabetic nephropathy, in solitary kidney or kidney donors), RFR may be fully or partially used to achieve normal or supranormal renal function. Since commonly used renal function markers, such as GFR, may remain within normal ranges until 50% of nephrons are lost or in patients with a single remnant kidney, the RFR test may represent a sensitive and early way to assess the functional decline in the kidney. RFR assessment may become an important tool to evaluate the ability of the kidney to recover completely or partially after a kidney attack. In case of healing with a defect and progressive fibrosis, recovery may appear complete clinically, but a reduced RFR may be a sign of a maladaptive repair or subclinical loss of renal mass. Thus, a reduction in RFR may represent the equivalent of renal frailty or susceptibility to insults. The main aim of this article is to review the concept of RFR, its utility in different clinical scenarios, and future perspective for its use.

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          Most cited references 15

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          Age changes in glomerular filtration rate, effective renal plasma flow, and tubular excretory capacity in adult males.

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            Predicting progression to chronic kidney disease after recovery from acute kidney injury.

            This review examines the association between acute kidney injury (AKI) and subsequent risk for chronic kidney disease (CKD) development. The discussion focuses on patients who fully recover from an episode of AKI, the majority of whom do not receive follow-up care with nephrology services. Several studies have demonstrated a strong association between AKI and later CKD risk. Animal models provide evidence for a causal link between AKI and CKD while also elucidating some of the potential mechanisms for this progression. Large observational studies have quantified the risk of CKD following AKI recovery, and clinical and emerging biomarker risk factors have been identified. The association between AKI with incomplete recovery or nonrecovery and CKD is evident. Recent studies demonstrate that even AKI with apparent full recovery confers an increased risk for subsequent CKD development. Risk prediction models have been developed and require further refinement and validation. The ability to identify patients with AKI recovery who are at high risk for later CKD development is an important clinical and research goal, as there exists a significant opportunity to improve care in this population.
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              Renal repair and recovery.

              To review the cellular and molecular mechanisms of renal repair and recovery after acute kidney injury (AKI). The data were summarized from published research articles. In AKI, there is an acute inflammatory response, epithelial cell necrosis and apoptosis, and shedding of epithelial cells into the tubular lumen. Recent work demonstrates that repopulation of damaged renal tubules occurs primarily from proliferation of tubular epithelial cells and resident renal-specific stem cells, with some contribution of paracrine factors from bone marrow-derived mesenchymal stem cells. In addition, growth factors seem to play a critical role in the repair process in animal models of renal injury. However, attempts to use growth factors in the clinical setting to attenuate human AKI or accelerate renal repair have not yet been successful. The endothelium also plays a critical role in the pathogenesis of AKI. Lastly, in human studies, the effect of dialysis on renal recovery remains poorly understood. Experimental animal models of AKI demonstrate that renal recovery and repair involves proliferation of tubular epithelial cells and stem cell populations and the coordinated contribution of multiple growth factors. Future efforts to improve recovery from AKI and improve patient outcomes may include novel therapies based on manipulation of populations of stem cells and augmenting repopulation of renal tubules.
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                Author and article information

                Journal
                NEC
                Nephron Clin Pract
                10.1159/issn.1660-2110
                Nephron Clinical Practice
                S. Karger AG
                1660-2110
                2014
                September 2014
                24 September 2014
                : 127
                : 1-4
                : 94-100
                Affiliations
                aInternational Renal Research Institute of Vicenza (IRRIV), and bDepartment of Nephrology, Dialysis and Transplantation, San Bortolo Hospital, Vicenza, Italy; cDepartment of Nephrology, Indraprastha Apollo Hospitals, New Delhi, India; dIntensive Care Unit, Médica Sur Clinic and Foundation, Mexico City, Mexico
                Author notes
                *Prof. Claudio Ronco, Department of Nephrology and IRRIV, San Bortolo Hospital, IT-36100 Vicenza (Italy), E-Mail cronco@goldnet.it
                Article
                363721 Nephron Clin Pract 2014;127:94-100
                10.1159/000363721
                25343829
                © 2014 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 5, Tables: 2, Pages: 7
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