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Neutrophil gelatinase-associated lipocalin as a marker of tubular damage appears to be unrelated to fractional excretion of sodium as a marker of tubular function in septic patients, with or without AKI
- Published: 27 October 2011
Keywords
- Acute Kidney Injury
- Septic Patient
- Fractional Excretion
- Tubular Damage
- Sodium Resorption
Introduction
The utility of urinary biochemistry has recently been challenged [1], while there is emerging evidence that renal biomarkers may accurately quantify the risk of development of acute kidney injury (AKI) [2]. Neutrophil gelatinase-associated lipocalin (NGAL) is a marker of renal tubular damage [3]. Fractional excretion of sodium (FENa) is a marker of renal tubular function, and is a significantly cheaper investigation [4]. Insults damaging the tubules and resulting in AKI should both stimulate NGAL production and prevent resorption of sodium. Given the different pathological mechanisms underlying septic and nonseptic AKI, it is plausible that the relationship between these variables could be different in these two groups of patients [5].
Methods
To test this hypothesis, we studied ICU patients developing SIRS and oliguria or a 25 μmol/l increase in serum creatinine within 48 hours of ICU admission. We sought to determine if a relationship existed between FENa and NGAL in patients, with and without sepsis, developing AKI. We measured the serum and urinary NGAL, creatinine and sodium of patients with SIRS and either oliguria or an increase in creatinine within 48 hours of admission to a tertiary referral ICU. Point-of-care creatinine measurements were used to identify the maximum RIFLE category of AKI developed within the first 5 days of admission. The strength of the relationship between variables was determined using Spearman's rank correlation coefficient.
Results
Relationships between NGAL, FENa and AKI
Urinary NGAL | Urinary NGAL corrected for urinary creatinine | Serum NGAL | Urine:serum NGAL ratio | |||||||
|---|---|---|---|---|---|---|---|---|---|---|
FENa | n | Spearman | P value | Spearman | P value | Spearman | P value | Spearman | P value | |
Nonseptic | No AKI | 43 | 0.153 | 0.328 | 0.587 | <0.0001 | 0.450 | 0.002 | -0.009 | 0.953 |
AKI | 33 | -0.039 | 0.830 | 0.438 | 0.011 | 0.258 | 0.148 | -0.235 | 0.188 | |
RIFLE R-F | 14 | 0.015 | 0.958 | 0.235 | 0.418 | -0.077 | 0.793 | -0.068 | 0.817 | |
Septic | No AKI | 12 | -0.168 | 0.602 | -0.007 | 0.983 | 0.232 | 0.467 | -0.427 | 0.167 |
RIFLE R-F | 5 | -0.300 | 0.624 | 0.500 | 0.391 | 0.112 | 0.858 | -0.400 | 0.505 | |
Conclusion
The lack of a strong correlation FENa and NGAL in patients developing RIFLE I and F AKI suggests that changes in NGAL and changes in sodium resorption occur as a consequence of different stimuli in the pathogenesis of the syndrome. The absence of any observed relationship between NGAL and FENa in septic patients suggests a pathological process different from that underlying nonseptic AKI. The small sample size may be a confounding factor.
Authors’ Affiliations
References
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Copyright
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
