Diagnosis, Epidemiology and Outcomes of Acute Kidney Injury

Waikar, Sushrut S.; Liu, Kathleen D.; Chertow, Glenn M.

doi:10.2215/cjn.05191107

Cited by 455 publications

(338 citation statements)

References 159 publications

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“…globally, affecting about 6% of all hospitalized patients in whom it is an independent predictor of mortality and morbidity (1). Much is now known about the epidemiology of AKI in the hospital-acquired and critical care settings (2).…”

Section: T He Incidence Of Acute Kidney Injury (Aki) Is Increasingmentioning

confidence: 99%

Cystatin C as a Marker of Acute Kidney Injury in the Emergency Department

Soto

Coelho

Rodrigues

et al. 2010

Clinical Journal of the American Society of Nephrology

110

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Background and objectives: The diagnosis of acute kidney injury (AKI) is usually based on changes in serum creatinine, which is a poor marker of early renal dysfunction. The discriminative and predictive abilities of serum and urinary cystatin C were examined for the prediction of AKI.Design, setting, participants, & measurements: In this prospective cohort study, serum and urinary cystatin C were serially measured in a heterogeneous group of patients (n ‫؍‬ 616) presenting to a tertiary care emergency department. The primary outcome was AKI, classified according to RIFLE and AKIN criteria. The secondary outcome was an adjudication based on clinical criteria to AKI, prerenal azotemia, chronic kidney disease (CKD), and normal kidney function.Results: Patients were adjudicated to have AKI in 21.1%, prerenal azotemia in 25.8%, CKD in 2.4%, and normal kidney function in 50.7%. For the diagnosis of AKI, the discriminatory ability of urinary creatinine and cystatin C was marginal. Both serum cystatin C and serum creatinine (at presentation and 6 hours later) showed high discriminatory ability for the diagnosis of AKI. However, only serum cystatin C attained a significant early predictive power (Hosmer-Lemeshow P value > 0.05). Serum cystatin C could differentiate between AKI and prerenal azotemia, but not between AKI and CKD.Conclusions: Serum cystatin C is an early, predictive biomarker of AKI, which outperforms serum creatinine in the heterogeneous emergency department setting. However, neither biomarker discriminated between AKI and CKD. Additional biomarkers continue to be needed for improved specificity in the diagnosis of community-acquired AKI.

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Section: T He Incidence Of Acute Kidney Injury (Aki) Is Increasingmentioning

confidence: 99%

Cystatin C as a Marker of Acute Kidney Injury in the Emergency Department

Soto

Coelho

Rodrigues

et al. 2010

Clinical Journal of the American Society of Nephrology

110

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“…From 5% to 7% of hospitalized patients are reported to experience AKI (2,3); the estimated annual health care expenditures attributable to hospital-acquired AKI exceed $10 billion (4). Renal ischemia reperfusion injury (IRI) associated with renal transplantation, postcardiopulmonary bypass surgeries, and other major vascular surgeries is the leading cause of AKI; sepsis and nephrotoxic drug injury are other major contributory factors (5,6).…”

Section: Introductionmentioning

confidence: 99%

Cell-specific translational profiling in acute kidney injury

et al. 2014

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Acute kidney injury (AKI) promotes an abrupt loss of kidney function that results in substantial morbidity and mortality. Considerable effort has gone toward identification of diagnostic biomarkers and analysis of AKI-associated molecular events; however, most studies have adopted organ-wide approaches and have not elucidated the interplay among different cell types involved in AKI pathophysiology. To better characterize AKI-associated molecular and cellular events, we developed a mouse line that enables the identification of translational profiles in specific cell types. This strategy relies on CRE recombinase-dependent activation of an EGFP-tagged L10a ribosomal protein subunit, which allows translating ribosome affinity purification (TRAP) of mRNA populations in CRE-expressing cells. Combining this mouse line with cell type-specific CRE-driver lines, we identified distinct cellular responses in an ischemia reperfusion injury (IRI) model of AKI. Twenty-four hours following IRI, distinct translational signatures were identified in the nephron, kidney interstitial cell populations, vascular endothelium, and macrophages/monocytes. Furthermore, TRAP captured known IRI-associated markers, validating this approach. Biological function annotation, canonical pathway analysis, and in situ analysis of identified response genes provided insight into cell-specific injury signatures. Our study provides a deep, cell-based view of early injury-associated molecular events in AKI and documents a versatile, genetic tool to monitor cell-specific and temporal-specific biological processes in disease modeling.

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“…Early AKI detection, optimal patient risk stratification and adequate treatment may improve outcomes [130,131].…”

Section: Acute Kidney Injurymentioning

confidence: 99%