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AKI in early sepsis is a continuum from transient AKI without tubular damage over transient AKI with minor tubular damage to intrinsic AKI with severe tubular damage

Jill Vanmassenhove (UGent) , Griet Glorieux (UGent) , Eric Hoste (UGent) , Annemieke Dhondt (UGent) , Raymond Vanholder (UGent) and Wim Van Biesen (UGent)
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Abstract
The pathophysiology of septic acute kidney injury (AKI) is incompletely understood, and there is controversy on the role of renal hypoperfusion in early sepsis. We hypothesized that renal hypoperfusion plays a role in early sepsis and that there is a continuum between transient AKI without tubular damage, transient AKI with minor tubular damage, and intrinsic AKI. A total of 107 consecutive patients with sepsis were included. Fractional excretion of sodium (FENa), urinary, and serum neutrophil gelatinase-associated lipocalin were measured at admission (T0) and 4 h (T4) and 24 h later (T24). Patients were classified according to FENa quartiles (FENaQ). Transient and intrinsic AKI were respectively defined as AKI that did or did not recover to no AKI in the following 5 days. A total of 57 developed transient AKI, 22 developed intrinsic AKI, and 28 did not have AKI. Of the ten patients with transient AKI classified in the two lowest FENa quartiles (FENa < 0.36 %) and without signs of local tubular damage, seven still did not show signs of tubular damage 24 h later. Also, 50 % of patients with intrinsic AKI classified in the same FENaQ did not show signs of local tubular damage at admission but did so 24 h later. There is a continuum between transient AKI without tubular damage, transient AKI with minor tubular damage, and intrinsic AKI in sepsis. Renal hypoperfusion seems to be the instigator for the development of AKI in the majority of patients with early sepsis. Other mechanisms in some patients cannot be excluded.
Keywords
Neutrophil gelatinase-associated lipocalin, ACUTE KIDNEY INJURY, Fractional excretion of sodium, Acute kidney injury, Sepsis, CRITICALLY-ILL PATIENTS, RENAL BLOOD-FLOW, CONSENSUS CONFERENCE, LIPOCALIN, FAILURE, BIOMARKERS, OUTPUT, NGAL

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MLA
Vanmassenhove, Jill, Griet Glorieux, Eric Hoste, et al. “AKI in Early Sepsis Is a Continuum from Transient AKI Without Tubular Damage over Transient AKI with Minor Tubular Damage to Intrinsic AKI with Severe Tubular Damage.” INTERNATIONAL UROLOGY AND NEPHROLOGY 46.10 (2014): 2003–2008. Print.
APA
Vanmassenhove, J., Glorieux, G., Hoste, E., Dhondt, A., Vanholder, R., & Van Biesen, W. (2014). AKI in early sepsis is a continuum from transient AKI without tubular damage over transient AKI with minor tubular damage to intrinsic AKI with severe tubular damage. INTERNATIONAL UROLOGY AND NEPHROLOGY, 46(10), 2003–2008.
Chicago author-date
Vanmassenhove, Jill, Griet Glorieux, Eric Hoste, Annemieke Dhondt, Raymond Vanholder, and Wim Van Biesen. 2014. “AKI in Early Sepsis Is a Continuum from Transient AKI Without Tubular Damage over Transient AKI with Minor Tubular Damage to Intrinsic AKI with Severe Tubular Damage.” International Urology and Nephrology 46 (10): 2003–2008.
Chicago author-date (all authors)
Vanmassenhove, Jill, Griet Glorieux, Eric Hoste, Annemieke Dhondt, Raymond Vanholder, and Wim Van Biesen. 2014. “AKI in Early Sepsis Is a Continuum from Transient AKI Without Tubular Damage over Transient AKI with Minor Tubular Damage to Intrinsic AKI with Severe Tubular Damage.” International Urology and Nephrology 46 (10): 2003–2008.
Vancouver
1.
Vanmassenhove J, Glorieux G, Hoste E, Dhondt A, Vanholder R, Van Biesen W. AKI in early sepsis is a continuum from transient AKI without tubular damage over transient AKI with minor tubular damage to intrinsic AKI with severe tubular damage. INTERNATIONAL UROLOGY AND NEPHROLOGY. 2014;46(10):2003–8.
IEEE
[1]
J. Vanmassenhove, G. Glorieux, E. Hoste, A. Dhondt, R. Vanholder, and W. Van Biesen, “AKI in early sepsis is a continuum from transient AKI without tubular damage over transient AKI with minor tubular damage to intrinsic AKI with severe tubular damage,” INTERNATIONAL UROLOGY AND NEPHROLOGY, vol. 46, no. 10, pp. 2003–2008, 2014.
@article{5748640,
  abstract     = {The pathophysiology of septic acute kidney injury (AKI) is incompletely understood, and there is controversy on the role of renal hypoperfusion in early sepsis. We hypothesized that renal hypoperfusion plays a role in early sepsis and that there is a continuum between transient AKI without tubular damage, transient AKI with minor tubular damage, and intrinsic AKI. 
A total of 107 consecutive patients with sepsis were included. Fractional excretion of sodium (FENa), urinary, and serum neutrophil gelatinase-associated lipocalin were measured at admission (T0) and 4 h (T4) and 24 h later (T24). Patients were classified according to FENa quartiles (FENaQ). Transient and intrinsic AKI were respectively defined as AKI that did or did not recover to no AKI in the following 5 days. 
A total of 57 developed transient AKI, 22 developed intrinsic AKI, and 28 did not have AKI. Of the ten patients with transient AKI classified in the two lowest FENa quartiles (FENa < 0.36 %) and without signs of local tubular damage, seven still did not show signs of tubular damage 24 h later. Also, 50 % of patients with intrinsic AKI classified in the same FENaQ did not show signs of local tubular damage at admission but did so 24 h later. 
There is a continuum between transient AKI without tubular damage, transient AKI with minor tubular damage, and intrinsic AKI in sepsis. Renal hypoperfusion seems to be the instigator for the development of AKI in the majority of patients with early sepsis. Other mechanisms in some patients cannot be excluded.},
  author       = {Vanmassenhove, Jill and Glorieux, Griet and Hoste, Eric and Dhondt, Annemieke and Vanholder, Raymond and Van Biesen, Wim},
  issn         = {0301-1623},
  journal      = {INTERNATIONAL UROLOGY AND NEPHROLOGY},
  keywords     = {Neutrophil gelatinase-associated lipocalin,ACUTE KIDNEY INJURY,Fractional excretion of sodium,Acute kidney injury,Sepsis,CRITICALLY-ILL PATIENTS,RENAL BLOOD-FLOW,CONSENSUS CONFERENCE,LIPOCALIN,FAILURE,BIOMARKERS,OUTPUT,NGAL},
  language     = {eng},
  number       = {10},
  pages        = {2003--2008},
  title        = {AKI in early sepsis is a continuum from transient AKI without tubular damage over transient AKI with minor tubular damage to intrinsic AKI with severe tubular damage},
  url          = {http://dx.doi.org/10.1007/s11255-014-0822-y},
  volume       = {46},
  year         = {2014},
}

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