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      Acute Kidney Injury: Gateway to Chronic Kidney Disease

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      Nephron Clinical Practice
      S. Karger AG

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          Abstract

          This review examines the evidence linking acute kidney injury (AKI) with the risk of subsequently developing chronic kidney disease (CKD). The discussion focuses on subjects that recover from an episode of AKI, most of whom do not receive follow-up nephrology care. Many recent studies have shown a strong association between AKI and the risk of developing CKD. Preclinical models provide evidence for a causal link between AKI and CKD while also proposing some of the potential mechanisms for this progression. Large observational studies have begun to quantify the risk for CKD following AKI recovery and identify risk factors for the development of CKD. In summary, there is an association between AKI with incomplete recovery or lack of recovery and CKD. Multiple studies now suggest that even AKI with apparent full recovery confers an independent risk for later development of CKD. Severity of AKI, baseline CKD, and multiple episodes of AKI remain consistent risk factors for CKD after AKI. The proposed risk prediction models that have been developed require further refinement and validation. The identification of patients with AKI recovery who are at high risk for later CKD development remains an important clinical and research goal.

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          Most cited references14

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          Acute kidney injury increases risk of ESRD among elderly.

          Risk for ESRD among elderly patients with acute kidney injury (AKI) has not been studied in a large, representative sample. This study aimed to determine incidence rates and hazard ratios for developing ESRD in elderly individuals, with and without chronic kidney disease (CKD), who had AKI. In the 2000 5% random sample of Medicare beneficiaries, clinical conditions were identified using Medicare claims; ESRD treatment information was obtained from ESRD registration during 2 yr of follow-up. Our cohort of 233,803 patients were hospitalized in 2000, were aged > or = 67 yr on discharge, did not have previous ESRD or AKI, and were Medicare-entitled for > or = 2 yr before discharge. In this cohort, 3.1% survived to discharge with a diagnosis of AKI, and 5.3 per 1000 developed ESRD. Among patients who received treatment for ESRD, 25.2% had a previous history of AKI. After adjustment for age, gender, race, diabetes, and hypertension, the hazard ratio for developing ESRD was 41.2 (95% confidence interval [CI] 34.6 to 49.1) for patients with AKI and CKD relative to those without kidney disease, 13.0 (95% CI 10.6 to 16.0) for patients with AKI and without previous CKD, and 8.4 (95% CI 7.4 to 9.6) for patients with CKD and without AKI. In summary, elderly individuals with AKI, particularly those with previously diagnosed CKD, are at significantly increased risk for ESRD, suggesting that episodes of AKI may accelerate progression of renal disease.
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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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              Increased risk of death and de novo chronic kidney disease following reversible acute kidney injury.

              Acute kidney injury increases mortality risk among those with established chronic kidney disease. In this study we used a propensity score-matched cohort method to retrospectively evaluate the risks of death and de novo chronic kidney disease after reversible, hospital-associated acute kidney injury among patients with normal pre-hospitalization kidney function. Of 30,207 discharged patients alive at 90 days, 1610 with reversible acute kidney injury that resolved within the 90 days were successfully matched across multiple parameters with 3652 control patients who had not experienced acute kidney injury. Median follow-up was 3.3 and 3.4 years (injured and control groups, respectively). In Cox proportional hazard models, the risk of death associated with reversible acute kidney injury was significant (hazard ratio 1.50); however, adjustment for the development of chronic kidney injury during follow-up attenuated this risk (hazard ratio 1.18). Reversible acute kidney injury was associated with a significant risk of de novo chronic kidney disease (hazard ratio 1.91). Thus, a resolved episode of hospital-associated acute kidney injury has important implications for the longitudinal surveillance of patients without preexisting, clinically evident kidney disease.
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                Author and article information

                Journal
                Nephron Clinical Practice
                Nephron Clin Pract
                S. Karger AG
                1660-2110
                October 21 2014
                September 1 2014
                September 24 2014
                : 127
                : 1-4
                : 30-34
                Article
                10.1159/000363675
                ef198a9f-139a-404a-9c3b-51a54e3a18a3
                © 2014
                History

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