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      Are There Modifiable Risk Factors to Improve AKI?

      review-article
      , , , * , *
      BioMed Research International
      Hindawi

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          Abstract

          Acute kidney injury (AKI) is a common critical syndrome, with high morbidity and mortality. Patients with AKI typically have an adverse prognosis, from incident chronic kidney disease (CKD), progression to end-stage renal disease (ESRD), subsequent cardiovascular disease, and ultimately death. However, there is currently no effective therapy for AKI. Early detection of risk factors for AKI may offer a good approach to prevention or early intervention. Traditional risk factors include extreme age, many common comorbid diseases, such as preexisting CKD, some specific exposures, such as sepsis, and exposure to some nephrotoxic agents. Recently, several novel risk factors for AKI, such as hyperuricemia, hypoalbuminemia, obesity, anemia, and hyperglycemia, have been identified. The underlying mechanisms between these nontraditional risk factors and AKI and whether their correction can reduce AKI occurrence remain to be clarified. This review describes the current epidemiology of AKI, summarizes its outcome, outlines the traditional risk profile, and finally highlights some recently identified novel risk factors.

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          Chronic hypoxia and tubulointerstitial injury: a final common pathway to end-stage renal failure.

          Recent studies emphasize the role of chronic hypoxia in the tubulointerstitium as a final common pathway to end-stage renal failure. When advanced, tubulointerstitial damage is associated with the loss of peritubular capillaries. Associated interstitial fibrosis impairs oxygen diffusion and supply to tubular and interstitial cells. Hypoxia of tubular cells leads to apoptosis or epithelial-mesenchymal transdifferentiation. This in turn exacerbates fibrosis of the kidney and subsequent chronic hypoxia, setting in train a vicious cycle whose end point is ESRD. A number of mechanisms that induce tubulointerstitial hypoxia at an early stage have been identified. Glomerular injury and vasoconstriction of efferent arterioles as a result of imbalances in vasoactive substances decrease postglomerular peritubular capillary blood flow. Angiotensin II not only constricts efferent arterioles but, via its induction of oxidative stress, also hampers the efficient utilization of oxygen in tubular cells. Relative hypoxia in the kidney also results from increased metabolic demand in tubular cells. Furthermore, renal anemia hinders oxygen delivery. These factors can affect the kidney before the appearance of significant pathologic changes in the vasculature and predispose the kidney to tubulointerstitial injury. Therapeutic approaches that target the chronic hypoxia should prove effective against a broad range of renal diseases. Current modalities include the improvement of anemia with erythropoietin, the preservation of peritubular capillary blood flow by blockade of the renin-angiotensin system, and the use of antioxidants. Recent studies have elucidated the mechanism of hypoxia-induced transcription, namely that prolyl hydroxylase regulates hypoxia-inducible factor. This has given hope for the development of novel therapeutic approaches against this final common pathway.
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            Acute kidney injury and chronic kidney disease: an integrated clinical syndrome.

            The previous conventional wisdom that survivors of acute kidney injury (AKI) tend to do well and fully recover renal function appears to be flawed. AKI can cause end-stage renal disease (ESRD) directly, and increase the risk of developing incident chronic kidney disease (CKD) and worsening of underlying CKD. In addition, severity, duration, and frequency of AKI appear to be important predictors of poor patient outcomes. CKD is an important risk factor for the development and ascertainment of AKI. Experimental data support the clinical observations and the bidirectional nature of the relationships between AKI and CKD. Reductions in renal mass and nephron number, vascular insufficiency, cell cycle disruption, and maladaptive repair mechanisms appear to be important modulators of progression in patients with and without coexistent CKD. Distinction between AKI and CKD may be artificial. Consideration should be given to the integrated clinical syndrome of diminished GFR, with acute and chronic stages, where spectrum of disease state and outcome is determined by host factors, including the balance of adaptive and maladaptive repair mechanisms over time. Physicians must provide long-term follow-up to patients with first episodes of AKI, even if they presented with normal renal function.
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              Albumin: biochemical properties and therapeutic potential.

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                Author and article information

                Journal
                Biomed Res Int
                Biomed Res Int
                BMRI
                BioMed Research International
                Hindawi
                2314-6133
                2314-6141
                2017
                4 July 2017
                : 2017
                : 5605634
                Affiliations
                Department of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Diseases, Beijing 100853, China
                Author notes

                Academic Editor: Jean Claude Dussaule

                Author information
                http://orcid.org/0000-0003-3178-1228
                http://orcid.org/0000-0002-7851-8999
                http://orcid.org/0000-0001-8774-6021
                Article
                10.1155/2017/5605634
                5514336
                28744467
                7dfb5827-111a-41de-8c1a-5bde96727544
                Copyright © 2017 Sasa Nie et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 7 January 2017
                : 26 April 2017
                : 23 May 2017
                Funding
                Funded by: Beijing Municipal Science and Technology Commission
                Award ID: Z131107002213011
                Funded by: Chinese PLA 12th Five-Year Plan for Medical Sciences
                Award ID: BWS14J040
                Award ID: BWS11J027
                Funded by: National Natural Science Foundation of China
                Award ID: 81670694
                Categories
                Review Article

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