Epidemiology of Acute Kidney Injury

Cerdá, Jorge; Lameire, Norbert; Eggers, Paul W.; Pannu, Neesh; Uchino, Sigehiko; Wang, Haiyan; Bagga, Arvind; Levin, Adeera

doi:10.2215/cjn.04961107

Cited by 247 publications

(175 citation statements)

References 63 publications

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“…Although adult AKI epidemiologic data exist (13), the epidemiology of pediatric AKI remains inadequately described. Most pediatric studies have been from single centers and are limited by small sample size and a propensity to focus only on critical care populations or children who require dialysis (2,(14)(15)(16)(17)(18)(19)(20)(21)(22).…”

Section: Introductionmentioning

confidence: 99%

AKI in Hospitalized Children

Sutherland

Ji²,

Sheikhi³

et al. 2013

Clinical Journal of the American Society of Nephrology

229

154

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SummaryBackground and objectives Although AKI is common among hospitalized children, comprehensive epidemiologic data are lacking. This study characterizes pediatric AKI across the United States and identifies AKI risk factors using high-content/high-throughput analytic techniques.Design, setting, participants, & measurements For the cross-sectional analysis of the 2009 Kids Inpatient Database, AKI events were identified using International Classification of Diseases, Ninth Revision, Clinical Modification codes. Demographics, incident rates, and outcome data were analyzed and reported for the entire AKI cohort as well as AKI subsets. Statistical learning methods were applied to the highly imbalanced dataset to derive AKI-related risk factors.Results Of 2,644,263 children, 10,322 children developed AKI (3.9/1000 admissions). Although 19% of the AKI cohort was #1 month old, the highest incidence was seen in children 15-18 years old (6.6/1000 admissions); 49% of the AKI cohort was white, but AKI incidence was higher among African Americans (4.5 versus 3.8/1000 admissions). In-hospital mortality among patients with AKI was 15.3% but higher among children #1 month old (31.3% versus 10.1%, P,0.001) and children requiring critical care (32.8% versus 9.4%, P,0.001) or dialysis (27.1% versus 14.2%, P,0.001). Shock (odds ratio, 2.15; 95% confidence interval, 1.95 to 2.36), septicemia (odds ratio, 1.37; 95% confidence interval, 1.32 to 1.43), intubation/mechanical ventilation (odds ratio, 1.2; 95% confidence interval, 1.16 to 1.25), circulatory disease (odds ratio, 1.47; 95% confidence interval, 1.32 to 1.65), cardiac congenital anomalies (odds ratio, 1.2; 95% confidence interval, 1.13 to 1.23), and extracorporeal support (odds ratio, 2.58; 95% confidence interval, 2.04 to 3.26) were associated with AKI.Conclusions AKI occurs in 3.9/1000 at-risk US pediatric hospitalizations. Mortality is highest among neonates and children requiring critical care or dialysis. Identified risk factors suggest that AKI occurs in association with systemic/multiorgan disease more commonly than primary renal disease.

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Section: Introductionmentioning

confidence: 99%

AKI in Hospitalized Children

Sutherland

Ji²,

Sheikhi³

et al. 2013

Clinical Journal of the American Society of Nephrology

229

154

View full text Add to dashboard Cite

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“…Three areas of epidemiology lack data. First, there are comparatively few good epidemiology studies in countries other than in Europe, North America or Australasia (Cerda et al (2008)). The incidence of AKI in countries with large populations such as China, India, Indonesia, Nigeria has significance beyond their own borders.…”

Section: Epidemiologymentioning

confidence: 99%

The Metamorphosis of Acute Renal Failure to Acute Kidney Injury

Pickering¹,

Endre²

2012

Basic Nephrology and Acute Kidney Injury

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“…1,2 This has piqued the interest of renal researchers, leading to a massive surge in our knowledge of its pathogenesis, systemic effects, and clinical course. Consequently, there has been a paradigm shift in our appreciation of AKI.…”

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confidence: 99%

“…In addition to their potential contribution to oxidant stress, NOX ROS production is now recognized to play a fundamental role in cell signaling, with diverse effects on cell growth, differentiation, motility, and survival. 2 These insights have motivated significant interest in nonphagocytic NOX in human health and disease.…”

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confidence: 99%

Mineralocorticoid Receptor Antagonism in AKI

Juncos

2016

Journal of the American Society of Nephrology

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AKI is a leading cause of morbidity and mortality in hospitalized patients, particularly among the critically ill, and its incidence is increasing. 1,2 This has piqued the interest of renal researchers, leading to a massive surge in our knowledge of its pathogenesis, systemic effects, and clinical course. Consequently, there has been a paradigm shift in our appreciation of AKI. Classically, AKI was assumed to be a renal-specific, self-limited, reversible condition easily supported by dialysis. Conversely, we now recognize it as a systemic entity that modulates the underlying disease process and causes dysfunction of other organs. 3,4 Moreover, survivors of AKI are at increased risk of long-term adverse outcomes, including CKD, ESRD, cardiovascular events, gastrointestinal bleeding, bone fractures, and premature death. 5,6 Hence, identifying effective therapeutic targets in AKI is of paramount importance. In search of effective therapies, we have vastly increased our mechanistic understanding of AKI; however, we have been less successful at translating this knowledge into clinically relevant therapies, perhaps because of its intricate pathophysiology.AKI is often instigated by a drop in renal perfusion to a level that prevents renal cells from producing sufficient ATP to maintain essential processes. This ischemic injury initiates a response that increases generation of reactive oxygen species, cytokines, chemokines, and leukocyte activation and decreases nitric oxide (NO), thus propagating renal injury. Injury of the endothelial cells leads to microvascular dysfunction characterized by diminished vasodilation and enhanced vasoconstriction. 7 This imbalance between vasoconstriction and vasodilation contributes to the persistent hypoperfusion of the outer medullary region, causing extension of renal injury. 8 Consequently, strategies that diminish this imbalance have attracted much interest. Vasodilators that preferentially increase medullary perfusion, such as NO, may be particularly effective. NO is especially appealing because of its antioxidant, anti-inflammatory, and other beneficial effects. Indeed, agents that augment NO activity (e.g., endothelial nitric oxide synthase [eNOS] -expressing surrogate cells, nitrite, and phosphodiesterase 5 inhibitors) protect against ischemia-reperfusion-induced AKI (I/R-AKI). 7 Alternatively, the imbalance can be improved by blocking vasoconstrictors (e.g., angiotensin II and endothelin [ET]). Because aldosterone has vasoconstrictor, profibrotic, and proinflammatory properties, it may also be an attractive target.In this issue of JASN, Barrera-Chimal et al. 8 provide compelling evidence that BR-4628, a third generation mineralocorticoid receptor (MR) antagonist, is highly protective against experimental I/R-AKI. Moreover, Barrera-Chimal et al. 8 uncover a novel mechanism by which it extends its protection; it prevents AKI-induced inactivation of the ET B receptor, thus normalizing generation of NO. The concept that MR antagonists may be effective against AKI is not novel. I...

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Epidemiology of Acute Kidney Injury

Cited by 247 publications

References 63 publications

AKI in Hospitalized Children

AKI in Hospitalized Children

The Metamorphosis of Acute Renal Failure to Acute Kidney Injury

Mineralocorticoid Receptor Antagonism in AKI

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