Acute Kidney Injury Increases Risk of ESRD among Elderly

United States Renal Data System Coordinating Center and Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota 55404, USA.
Journal of the American Society of Nephrology (Impact Factor: 9.47). 11/2008; 20(1):223-8. DOI: 10.1681/ASN.2007080837
Source: PubMed

ABSTRACT 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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    • "Although renal recovery from AKI is associated with better renal outcomes and patient survival [10], no differences in long-term survival between those with kidney function recovery after AKI and those without AKI were observed in two population-based cohorts [11] [12]. However, in postoperative patients [13] [14] [15] and geriatric patients [16], temporary worsening of kidney function has been reported with a higher long-term mortality rate compared with non- AKI patients. The cohorts in previous reports have mostly focused on preexisting normal or near normal kidney function [9, 17–19] or all patients with chronic kidney disease (CKD) [8]. "
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    ABSTRACT: AKI-dialysis patients had a higher incidence of long-term ESRD and mortality than the patients without AKI. The patients who recovered from dialysis were associated with a lower incidence of long-term ESRD and mortality than in the patients who still required dialysis.
    BioMed Research International 08/2014; 2014:365186. DOI:10.1155/2014/365186 · 2.71 Impact Factor
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    • "All rights reserved. a patient with underlying CKD substantially increases the rate of transition to end-stage renal disease (ESRD), mostly because of the additional damage in the already compromised kidneys [3] [4]. "
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    ABSTRACT: Background The primary aim of the study was to investigate the cytokine/chemokine response in the kidney, lung, and liver following acute kidney injury (AKI). The secondary aim was to test whether α-melanocyte-stimulating hormone (α-MSH) could prevent a reduction in organ function, and attenuate the inflammatory cytokine/chemokine response within the kidney, lung, and liver following AKI in rats with or without preexisting chronic kidney disease (CKD). Methods A two-stage animal model, in which AKI was induced in rats with preexisting CKD, induced by 5/6 nephrectomy (Nx), was used. Six weeks later, AKI was induced by intestinal ischemia and reperfusion (IIR). Sham procedures [S(Nx) and S(IIR)] were also performed. Results Increasing levels of serum creatinine (sCr) demonstrated progressive development of CKD in response to Nx, and following IIR sCr levels increased further significantly, except in the S(Nx) group treated with α-MSH. However, no significant differences in the fractional increase in sCr were observed between any of the groups exposed to IIR. In kidney, lung, and liver tissue the levels of interleukin (IL)-1β were significantly higher in rats undergoing IIR when compared to the S(IIR) and control rats. The same pattern was observed for the chemokine MCP-1 in lung and liver tissue. Furthermore, kidney IL-1β and RANTES levels were significantly increased after IIR in the Nx rats compared to the S(Nx) rats. Conclusion Both the functional parameters and the cytokine/chemokine response are as dramatic when AKI is superimposed onto CKD as onto non-CKD. No convincing protective effect of α-MSH was detected.
    06/2014; 33(2). DOI:10.1016/j.krcp.2014.02.002
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    • "Billing codes for AKI result from the formal documentation of AKI in the medical record by treating clinicians using certain key phrases. Recognition of AKI by treating clinicians may occur in the absence of this formal documentation [9] [10], but the use of billing codes as a proxy for clinical AKI recognition is common [11] [12] [13] [14]. To our knowledge, the clinical significance of formal AKI documentation among patients with laboratory-defined AKI has yet to be studied. "
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    ABSTRACT: Aims: Modification of the mortality risk associated with acute kidney injury (AKI) necessitates recognition of AKI when it occurs. We sought to determine whether formal documentation of AKI in the medical record, assessed by billing codes for AKI, would be associated with improved clinical outcomes. Methods: Retrospective cohort study conducted at three hospitals within a single university health system. Adults without severe underlying kidney disease who suffered in-hospital AKI as defined by a doubling of baseline creatinine (n = 5,438) were included. Those whose AKI was formally documented according to discharge billing codes were compared to those without such documentation in terms of 30-day mortality. Results: Formal documentation of AKI occurred in 2,325 patients (43%). Higher baseline creatinine, higher peak creatinine, medical admission status, and higher Sequential Organ Failure Assessment (SOFA) score were strongly associated with documentation of AKI. After adjustment for severity of disease, formal AKI documentation was associated with reduced 30-day mortality - OR 0.81 (0.68 - 0.96, p = 0.02). Patients with formal documentation were more likely to receive a nephrology consultation (31% vs. 6%, p < 0.001) and fluid boluses (64% vs. 45%, p < 0.001), and had a more rapid discontinuation of angiotensin-converting enzyme inhibitor and angiotensin-receptor blocker medications (HR 2.04, CI 1.69 - 2.46, p < 0.001). Conclusions: Formal documentation of AKI is associated with improved survival after adjustment for illness severity among patients with creatinine-defined AKI.
    Clinical nephrology 09/2013; 80(12). DOI:10.5414/CN108072 · 1.23 Impact Factor
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