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Influence of severity of illness on neutrophil gelatinase-associated lipocalin performance as a marker of acute kidney injury: a prospective cohort study of patients with sepsis.

Vanmassenhove J, Glorieux G, Lameire N, Hoste E, Dhondt A, Vanholder R, Van Biesen W - BMC Nephrol (2015)

Bottom Line: Transient and intrinsic AKI were respectively defined as AKI according to RIFLE during the first 72 hours that did or did not recover to "no AKI" in the following 72 hours.Prevalence of transient and intrinsic AKI were higher in patients with versus without septic shock (OR (95% CI): 3.3(1.4-8.2)). uNGAL was associated with sNGAL, and this with parallel slopes but different intercepts for AKI (Y = 0.87*X + 314.3, R2 = 0.31) and no AKI (Y = 0.87*X + 20.1, R2 = 0.38).Serum and uNGAL levels are influenced by severity of illness and inflammation, and this was found to be independent of the presence of AKI.

View Article: PubMed Central - PubMed

ABSTRACT

Background: The role of neutrophil gelatinase-associated lipocalin (NGAL) as a diagnostic marker for acute kidney injury (AKI) in sepsis is still debated. We hypothesized that in sepsis, the performance of serum(s) and urinary(u) NGAL can be negatively impacted by severity of illness and inflammation, and that both uNGAL and sNGAL levels can be increased regardless of presence of AKI.

Methods: One hundred and seven patients with sepsis were included. uNGAL and sNGAL were measured at admission (T0) and 4 hours (T4) and 24 hours later (T24). Transient and intrinsic AKI were respectively defined as AKI according to RIFLE during the first 72 hours that did or did not recover to "no AKI" in the following 72 hours. Patients were classified according to tertiles of CRP and APACHE II score increase. The relationship between sNGAL and uNGAL was assessed by linear regression.

Results: Fifty-seven patients developed transient and 22 intrinsic AKI. Prevalence of transient and intrinsic AKI were higher in patients with versus without septic shock (OR (95% CI): 3.3(1.4-8.2)). uNGAL was associated with sNGAL, and this with parallel slopes but different intercepts for AKI (Y = 0.87*X + 314.3, R2 = 0.31) and no AKI (Y = 0.87*X + 20.1, R2 = 0.38). At T4, median uNGAL and sNGAL levels were higher in septic patients with versus without shock but this is independent of AKI ((545 ng/mL vs 196 ng/ml for uNGAL and 474 ng/ml vs 287 ng/ml for sNGAL (both P = 0.003)). Both uNGAL and sNGAL levels increased with tertiles of CRP and APACHE II score increase.

Conclusions: Serum and uNGAL levels are influenced by severity of illness and inflammation, and this was found to be independent of the presence of AKI. There is a strong correlation between sNGAL and uNGAL levels in patients with sepsis, indicating that increased levels of uNGAL can also be due to overspill from the systemic circulation, blurring the discriminative value of NGAL as a biomarker for AKI in patients with sepsis.

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Urinary NGAL in no AKI, transient AKI and intrinsic AKI, stratified according to sepsis severity. (A) At time point T0, urinary NGAL(ng/ml) is not significantly different between no-AKI, transient AKI and intrinsic AKI in sepsis without shock (P = 0.27) and sepsis with shock (P = 0.08). (B) At time point T4, urinary NGAL(ng/ml) is not significantly different between no AKI, transient AKI and intrinsic AKI in sepsis without shock (P = 0.27). (C) At time point T24, urinary NGAL (ng/mL) is not significantly different between no-AKI, transient AKI and intrinsic AKI in sepsis without shock (P = 0.27) and sepsis with shock (P = 0.11). (° = outliers; * = extreme outliers (> three times the height of the boxes)).
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Fig2: Urinary NGAL in no AKI, transient AKI and intrinsic AKI, stratified according to sepsis severity. (A) At time point T0, urinary NGAL(ng/ml) is not significantly different between no-AKI, transient AKI and intrinsic AKI in sepsis without shock (P = 0.27) and sepsis with shock (P = 0.08). (B) At time point T4, urinary NGAL(ng/ml) is not significantly different between no AKI, transient AKI and intrinsic AKI in sepsis without shock (P = 0.27). (C) At time point T24, urinary NGAL (ng/mL) is not significantly different between no-AKI, transient AKI and intrinsic AKI in sepsis without shock (P = 0.27) and sepsis with shock (P = 0.11). (° = outliers; * = extreme outliers (> three times the height of the boxes)).

Mentions: Median urinary and serum NGAL levels were higher in sepsis patients with versus those without shock (Figure 1A, B, C and Table 3). All no AKI patients had serum NGAL levels above the generally accepted cut-off of 150 ng/mL [26,27] at all time points. All sepsis patients with shock had urinary NGAL levels above 150 ng/mL at admission and four hours later, even if they did not have AKI. Urinary and serum NGAL levels were higher in intrinsic versus transient and no AKI patients, but there was substantial overlap limiting discriminative value (Table 3). When classified according to sepsis without versus with shock, discriminative value of NGAL for AKI further decreased (Figure 2A, B and C).Figure 1


Influence of severity of illness on neutrophil gelatinase-associated lipocalin performance as a marker of acute kidney injury: a prospective cohort study of patients with sepsis.

Vanmassenhove J, Glorieux G, Lameire N, Hoste E, Dhondt A, Vanholder R, Van Biesen W - BMC Nephrol (2015)

Urinary NGAL in no AKI, transient AKI and intrinsic AKI, stratified according to sepsis severity. (A) At time point T0, urinary NGAL(ng/ml) is not significantly different between no-AKI, transient AKI and intrinsic AKI in sepsis without shock (P = 0.27) and sepsis with shock (P = 0.08). (B) At time point T4, urinary NGAL(ng/ml) is not significantly different between no AKI, transient AKI and intrinsic AKI in sepsis without shock (P = 0.27). (C) At time point T24, urinary NGAL (ng/mL) is not significantly different between no-AKI, transient AKI and intrinsic AKI in sepsis without shock (P = 0.27) and sepsis with shock (P = 0.11). (° = outliers; * = extreme outliers (> three times the height of the boxes)).
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4352556&req=5

Fig2: Urinary NGAL in no AKI, transient AKI and intrinsic AKI, stratified according to sepsis severity. (A) At time point T0, urinary NGAL(ng/ml) is not significantly different between no-AKI, transient AKI and intrinsic AKI in sepsis without shock (P = 0.27) and sepsis with shock (P = 0.08). (B) At time point T4, urinary NGAL(ng/ml) is not significantly different between no AKI, transient AKI and intrinsic AKI in sepsis without shock (P = 0.27). (C) At time point T24, urinary NGAL (ng/mL) is not significantly different between no-AKI, transient AKI and intrinsic AKI in sepsis without shock (P = 0.27) and sepsis with shock (P = 0.11). (° = outliers; * = extreme outliers (> three times the height of the boxes)).
Mentions: Median urinary and serum NGAL levels were higher in sepsis patients with versus those without shock (Figure 1A, B, C and Table 3). All no AKI patients had serum NGAL levels above the generally accepted cut-off of 150 ng/mL [26,27] at all time points. All sepsis patients with shock had urinary NGAL levels above 150 ng/mL at admission and four hours later, even if they did not have AKI. Urinary and serum NGAL levels were higher in intrinsic versus transient and no AKI patients, but there was substantial overlap limiting discriminative value (Table 3). When classified according to sepsis without versus with shock, discriminative value of NGAL for AKI further decreased (Figure 2A, B and C).Figure 1

Bottom Line: Transient and intrinsic AKI were respectively defined as AKI according to RIFLE during the first 72 hours that did or did not recover to "no AKI" in the following 72 hours.Prevalence of transient and intrinsic AKI were higher in patients with versus without septic shock (OR (95% CI): 3.3(1.4-8.2)). uNGAL was associated with sNGAL, and this with parallel slopes but different intercepts for AKI (Y = 0.87*X + 314.3, R2 = 0.31) and no AKI (Y = 0.87*X + 20.1, R2 = 0.38).Serum and uNGAL levels are influenced by severity of illness and inflammation, and this was found to be independent of the presence of AKI.

View Article: PubMed Central - PubMed

ABSTRACT

Background: The role of neutrophil gelatinase-associated lipocalin (NGAL) as a diagnostic marker for acute kidney injury (AKI) in sepsis is still debated. We hypothesized that in sepsis, the performance of serum(s) and urinary(u) NGAL can be negatively impacted by severity of illness and inflammation, and that both uNGAL and sNGAL levels can be increased regardless of presence of AKI.

Methods: One hundred and seven patients with sepsis were included. uNGAL and sNGAL were measured at admission (T0) and 4 hours (T4) and 24 hours later (T24). Transient and intrinsic AKI were respectively defined as AKI according to RIFLE during the first 72 hours that did or did not recover to "no AKI" in the following 72 hours. Patients were classified according to tertiles of CRP and APACHE II score increase. The relationship between sNGAL and uNGAL was assessed by linear regression.

Results: Fifty-seven patients developed transient and 22 intrinsic AKI. Prevalence of transient and intrinsic AKI were higher in patients with versus without septic shock (OR (95% CI): 3.3(1.4-8.2)). uNGAL was associated with sNGAL, and this with parallel slopes but different intercepts for AKI (Y = 0.87*X + 314.3, R2 = 0.31) and no AKI (Y = 0.87*X + 20.1, R2 = 0.38). At T4, median uNGAL and sNGAL levels were higher in septic patients with versus without shock but this is independent of AKI ((545 ng/mL vs 196 ng/ml for uNGAL and 474 ng/ml vs 287 ng/ml for sNGAL (both P = 0.003)). Both uNGAL and sNGAL levels increased with tertiles of CRP and APACHE II score increase.

Conclusions: Serum and uNGAL levels are influenced by severity of illness and inflammation, and this was found to be independent of the presence of AKI. There is a strong correlation between sNGAL and uNGAL levels in patients with sepsis, indicating that increased levels of uNGAL can also be due to overspill from the systemic circulation, blurring the discriminative value of NGAL as a biomarker for AKI in patients with sepsis.

Show MeSH
Related in: MedlinePlus