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Clin J Am Soc Nephrol. 2016 Jun 6;11(6):938-46. doi: 10.2215/CJN.10551015. Epub 2016 Mar 29.

Association of Renal Stress/Damage and Filtration Biomarkers with Subsequent AKI during Hospitalization among Patients Presenting to the Emergency Department.

Author information

1
Department of Internal Medicine, Division of General Internal Medicine and Nephrology, Robert-Bosch Hospital, Stuttgart, Germany; and martin.kimmel@rbk.de.
2
Walker Bioscience, Carlsbad, California.
3
Department of Internal Medicine, Division of General Internal Medicine and Nephrology, Robert-Bosch Hospital, Stuttgart, Germany; and.

Abstract

BACKGROUND AND OBJECTIVES:

Emergency departments (EDs) have a growing role in hospital admissions, but few studies address AKI biomarkers in the ED.

DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS:

Patients admitted to the internal medicine service were enrolled during initial workup in the ED at Robert-Bosch-Hospital, Stuttgart, Germany. Daily serum creatinine (sCr) and urine output (UO) were recorded for AKI classification by Kidney Disease Improving Global Outcomes (KDIGO) criteria. Cystatin C, kidney injury molecule-1, liver-type fatty acid-binding protein, and neutrophil gelatinase-associated lipocalin were measured in blood and urine, and IL-18, insulin-like growth factor-binding protein 7 (IGFBP7), tissue inhibitor of metalloproteinases-2 (TIMP-2) and [TIMP-2]⋅[IGFBP7] were measured in urine collected at enrollment, after 6 hours, and the following morning. Association between these biomarkers and the end point of moderate-severe AKI (KDIGO stage 2-3) occurring within 12 hours of each sample collection was examined using generalized estimating equation logistic regression. Performance for prediction of the AKI end point using two previously validated [TIMP-2]-[IGFBP7] cutoffs was also tested.

RESULTS:

Of 400 enrolled patients, 298 had sufficient sCr and UO data for classification by KDIGO AKI criteria: AKI stage 2 developed in 37 patients and AKI stage 3 in nine patients. All urinary biomarkers, sCr, and plasma cystatin C had statistically significant (P<0.05) odds ratios (ORs) for the AKI end point. In a multivariable model of the urine biomarkers and sCr, only [TIMP-2]⋅[IGFBP7] and sCr had statistically significant ORs. Compared with [TIMP-2]⋅[IGFBP7]<0.3 (ng/ml)(2)/1000, values between 0.3 and 2.0 (ng/ml)(2)/1000 indicated 2.5 (95% confidence interval [95% CI], 1.1 to 5.2) times the odds for the AKI end point and values >2.0 (ng/ml)(2)/1000 indicated 11.0 (95% CI, 4.4 to 26.9) times the odds. Addition of [TIMP-2]⋅[IGFBP7] to a clinical model significantly improved area under the receiver-operating characteristic curve from 0.67 (95% CI, 0.61 to 0.78) to 0.77 (95% CI, 0.72 to 0.86) (P<0.001); however, including both markers in the model was not significantly different from including either marker alone.

CONCLUSIONS:

Urinary [TIMP-2]⋅[IGFBP7] with pre-established cutoffs provides valuable information about risk for imminent AKI in the ED that is complementary to sCr and clinical risk factors.

KEYWORDS:

acute kidney injury; biomarkers; emergency departments; emergency service, hospital; humans; insulin like-growth factor binding protein-7; kidney risk factors; tissue inhibitor of metalloproteinase-2

PMID:
27026519
PMCID:
PMC4891754
DOI:
10.2215/CJN.10551015
[Indexed for MEDLINE]
Free PMC Article

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