Trends in the Incidence of Acute Kidney Injury in Patients Hospitalized With Acute Myocardial Infarction

Department of Cardiovascular Medicine, University of Missouri, Kansas City, MO 64111, USA.
Archives of internal medicine (Impact Factor: 17.33). 02/2012; 172(3):246-53. DOI: 10.1001/archinternmed.2011.1202
Source: PubMed


Acute kidney injury (AKI) is common in patients with acute myocardial infarction (AMI) and is associated with permanent renal impairment and death. Although guidelines increasingly emphasize AKI prevention, whether increased awareness has translated into reduced AKI rates is unclear.
Among 33,249 consecutive hospitalizations in 31,532 unselected patients with AMI across 56 US centers from Cerner Corporation's Health Facts database, we examined the temporal trends in AKI incidence from 2000 to 2008. Acute kidney injury was defined as an absolute increase in creatinine level of at least 0.3 mg/dL or a relative increase of at least 50% during hospitalization.
From 2000 to 2008, the mean age of patients increased (from 66.5 to 68.6 years), as did the known AKI risk factors, including chronic kidney disease, cardiogenic shock, diabetes mellitus, heart failure, coronary angiography, and percutaneous coronary intervention. Despite this, AKI incidence declined from 26.6% in 2000 to 19.7% in 2008 (P < .001). After multivariate adjustment, the trend of decreasing AKI rates persisted (4.4% decline per year; P < .001). In addition, in-hospital mortality also declined over time among patients developing AKI, from 19.9% in 2000 to 13.8% in 2008 (P = .003).
In a large national study, AKI incidence in patients hospitalized with AMI declined significantly from 2000 to 2008 despite the aging population and rising prevalence of AKI risk factors. These findings may reflect increased clinician awareness, better risk stratification, or greater use of AKI prevention efforts during this time period.

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    • "Furthermore, cardio-renal syndromes type 1 and type 3, where acute dysfunction in the heart induces decreased kidney function and vice versa, are increasingly recognised but poorly understood [26, 27]. Acute kidney injury (AKI) is common in patients hospitalised with AMI and occurs in approximately one in five patients [28, 29]. Even the development of relatively mild renal impairment in AMI is associated with increased mortality [30–32] and morbidity including development of permanent renal impairment, progression to end-stage renal failure (ESRF) [30], increased length of hospital stay and cost [33]. "
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    ABSTRACT: Rationale and objective: Acute myocardial infarction (AMI) results in the recruitment of leukocytes to injured myocardium. Additionally, myocardium remote to the infarct zone also becomes inflamed and is associated with adverse left ventricular remodelling. Renal ischaemic syndromes have been associated with remote organ inflammation and impaired function. Here, we tested the hypothesis that AMI results in remote organ (renal) inflammation. Methods: Mice were subjected to either AMI, sham procedure or no procedure and the inflammatory response in peripheral blood, injured and remote myocardium, and kidneys was studied at 24 h. Results: AMI resulted in increased circulating neutrophils (P < 0.001) and monocytes (P < 0.001). mRNA for inflammatory mediators significantly increased in infarcted myocardium and in remote myocardium. VCAM-1 mRNA was increased in both infarcted and remote myocardium. VCAM-1 protein was also increased in the kidneys of AMI mice (P < 0.05) and immunofluorescence revealed localisation of VCAM-1 to glomeruli, associated with leukocyte infiltration and increased local inflammatory mRNA expression. Conclusions: We conclude that in addition to local inflammation, AMI results in remote organ inflammation evidenced by (1) increased expression of mRNA for inflammatory cytokines, (2) marked upregulation of VCAM-1 in renal glomeruli, and (3) the recruitment and infiltration of leukocytes in the kidney.
    Agents and Actions 03/2013; 62(5). DOI:10.1007/s00011-013-0605-4 · 2.35 Impact Factor
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    • "Nearly 13% of the US population is diagnosed with chronic kidney disease and its prevalence increases as the population ages [1] [2]. Even modest reductions in GFR in patients with acute myocardial infarction (AMI) are associated with a higher mortality rate [3], and the progression from chronic kidney disease to end-stage renal disease is more rapid following an AMI [4] [5]. While the relationship between GFR and mortality is unidirectional, with a stepwise increase in mortality with worsening GFR, the relationship between haemoglobin levels and mortality is that of an inverse-J curve; lower haemoglobin concentrations are an independent predictor of cardiovascular disease and mortality [6], while haemoglobin levels beyond the upper limit of normal are also associated with an increased hazard of adverse cardiovascular outcomes [7] [8]. "
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    ABSTRACT: Background: Impaired renal function and anaemia are common among patients with acute myocardial infarction (AMI). While both conditions are known independent risk factors for increased mortality, their interaction as risk factors for increased mortality in AMI is unclear. Methods: We studied 5395 subjects hospitalized for AMI between January 2000 and December 2005. An estimated glomerular filtration rate (GFR) <60 mL/min/1.73 m(2) was defined as impaired GFR and GFR ≥ 60 mL/min/1.73 m(2) was defined as preserved GFR. Anaemia was defined as <13 g/dL (males) and <12 g/dL (females). The odds ratio (OR) for one-year mortality and its 95% confidence interval (CI) were calculated by logistic regression. Results: We identified 758 (14%) patients with impaired GFR and anaemia, 1105 (20.5%) patients with impaired GFR without anaemia, 465 (8.6%) patients with preserved GFR and anaemia, and 3012 (55.8%) patients with preserved GFR without anaemia; one-year mortality rates were 56.5%, 41.8%, 31.8% and 10.3% respectively in these 4 groups. Among patients with impaired GFR, anaemia was associated with an adjusted OR of 1.47 (95% CI=1.17-1.85) for one-year mortality, while among patients with preserved GFR, anaemia was associated with a higher adjusted OR of 2.07 (95% CI=1.54-2.76) for one-year mortality, interaction P<0.001. Conclusion: The combination of impaired GFR and anaemia confers greater than five-fold increased risk of mortality after AMI. The differential effect of anaemia among patients with impaired and preserved GFR on mortality suggests that in patients with preserved GFR anaemia confers a greater relative hazard than in patients with impaired renal function.
    International journal of cardiology 01/2013; 168(2). DOI:10.1016/j.ijcard.2012.12.017 · 4.04 Impact Factor
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    ABSTRACT: Clinical practice guidelines recommend maintaining serum potassium levels between 4.0 and 5.0 mEq/L in patients with acute myocardial infarction (AMI). These guidelines are based on small studies that associated low potassium levels with ventricular arrhythmias in the pre-β-blocker and prereperfusion era. Current studies examining the relationship between potassium levels and mortality in AMI patients are lacking. To determine the relationship between serum potassium levels and in-hospital mortality in AMI patients in the era of β-blocker and reperfusion therapy. Retrospective cohort study using the Cerner Health Facts database, which included 38,689 patients with biomarker-confirmed AMI, admitted to 67 US hospitals between January 1, 2000, and December 31, 2008. All patients had in-hospital serum potassium measurements and were categorized by mean postadmission serum potassium level (<3.0, 3.0-<3.5, 3.5-<4.0, 4.0-<4.5, 4.5-<5.0, 5.0-<5.5, and ≥5.5 mEq/L). Hierarchical logistic regression was used to determine the association between potassium levels and outcomes after adjusting for patient- and hospital-level factors. All-cause in-hospital mortality and the composite of ventricular fibrillation or cardiac arrest. There was a U-shaped relationship between mean postadmission serum potassium level and in-hospital mortality that persisted after multivariable adjustment. Compared with the reference group of 3.5 to less than 4.0 mEq/L (mortality rate, 4.8%; 95% CI, 4.4%-5.2%), mortality was comparable for mean postadmission potassium of 4.0 to less than 4.5 mEq/L (5.0%; 95% CI, 4.7%-5.3%), multivariable-adjusted odds ratio (OR), 1.19 (95% CI, 1.04-1.36). Mortality was twice as great for potassium of 4.5 to less than 5.0 mEq/L (10.0%; 95% CI, 9.1%-10.9%; multivariable-adjusted OR, 1.99; 95% CI, 1.68-2.36), and even greater for higher potassium strata. Similarly, mortality rates were higher for potassium levels of less than 3.5 mEq/L. In contrast, rates of ventricular fibrillation or cardiac arrest were higher only among patients with potassium levels of less than 3.0 mEq/L and at levels of 5.0 mEq/L or greater. Among inpatients with AMI, the lowest mortality was observed in those with postadmission serum potassium levels between 3.5 and <4.5 mEq/L compared with those who had higher or lower potassium levels.
    JAMA The Journal of the American Medical Association 01/2012; 307(2):157-64. DOI:10.1001/jama.2011.1967 · 35.29 Impact Factor
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