BibTex format
@article{Arunkumaran:2017:10.1097/CCM.0000000000002381,
author = {Arunkumaran, N and Sixma, M and Jentho, E and Ceravola, E and Bass, P and Kellum, JA and Unwin, RJ and Tam, FWK and Singer, M},
doi = {10.1097/CCM.0000000000002381},
journal = {Critical Care Medicine},
pages = {e821--e830},
title = {Sequential analysis of a panel of biomarkers and pathologic findings in a resuscitated rat model of sepsis and recovery},
url = {http://dx.doi.org/10.1097/CCM.0000000000002381},
volume = {45},
year = {2017}
}
RIS format (EndNote, RefMan)
TY - JOUR
AB - Objective:To characterize the temporal pattern of a panel of blood and urinary acute kidney injury (AKI) biomarkers in ananimal model of fecal peritonitis and recoveryDesign: Prospective observational animal study Setting: University research laboratorySubjects: Male Wistar ratsInterventions:Afluid-resuscitated, long-term (3 day)rat model of sepsis (fecal peritonitis) and recovery was used to understand the temporal association ofAKI biomarkers in relation to systemic hemodynamics, inflammation, and renal function.At pre-defined time points (3, 6, 12, 24, 48, 72h), animals (≥6 per group) underwent echocardiography, blood and urine sampling, and had kidneys taken for histological analysis. Comparison was made against sham-operated controls and naïve animals.Measurements and main results:Thesystemic pro-inflammatory response was maximal at 6 hours, corresponding with the nadirof stroke volume. Serum creatinine peaked late (24h), whenclinicalrecovery was imminent. Histological evidence of tubular injury and cell death was minimal. After a recovery period, all biomarkers returned to levels approaching those observed in sham animals. Apart from urine clusterin and IL-18, all other urinarybiomarkers were elevated at earlier time-points comparedto serum creatinine. Urine NGAL was the most sensitive marker among those studied, rising from 3h. While serum creatinine fell at 12h, serum cystatin C increased, suggestive of decreased creatinine production.Conclusions:Novel information is reported on the temporal profile of a panel of renal biomarkers in sepsis in the context of systemic and renal inflammation and recovery. Insight into the pathophysiology of AKI is gleaned from the temporal change markers ofrenalinjury (urine NGAL, KIM-1, calbindin),followed by a marker of cell cycle arrest (urine IGFBP7) and,finally,by functionalmarkers of filtration (serum creatinine and cystatin C). Thes
AU - Arunkumaran,N
AU - Sixma,M
AU - Jentho,E
AU - Ceravola,E
AU - Bass,P
AU - Kellum,JA
AU - Unwin,RJ
AU - Tam,FWK
AU - Singer,M
DO - 10.1097/CCM.0000000000002381
EP - 830
PY - 2017///
SN - 1530-0293
SP - 821
TI - Sequential analysis of a panel of biomarkers and pathologic findings in a resuscitated rat model of sepsis and recovery
T2 - Critical Care Medicine
UR - http://dx.doi.org/10.1097/CCM.0000000000002381
VL - 45
ER -