Skip to main content

Volume 15 Supplement 3

Sepsis 2011

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

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

We enrolled 93 patients between 31 August 2010 and 17 November 2010; 17 had an APACHE III diagnosis of sepsis. Serum NGAL and urinary NGAL when corrected for urinary creatinine were found to correlate moderately well with FENa in patients without sepsis, a relationship that weakens with the progression of AKI in this group. No other correlation showed a significant relationship (Table 1).

Table 1 Relationships between NGAL, FENa and AKI

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.

References

  1. 1.

    Bagshaw SM, Langenberg C, Wan L, May CN, Bellomo R: A systematic review of urinary findings in experimental septic acute renal failure. Crit Care Med 2007, 35: 1592-1598. 10.1097/01.CCM.0000266684.17500.2F

    Article  PubMed  Google Scholar 

  2. 2.

    Siew ED, Ware LB, Ikizler TA: Biological markers of acute kidney injury. J Am Soc Nephrol 2011, 22: 810-820. 10.1681/ASN.2010080796

    Article  PubMed  Google Scholar 

  3. 3.

    Cruz DN, de Cal M, Garzotto F, Perazella MA, Lentini P, Corradi V, Piccinni P, Ronco C: Plasma neutrophil gelatinase-associated lipocalin is an early biomarker for acute kidney injury in an adult ICU population. Intensive Care Med 2010, 36: 444-451. 10.1007/s00134-009-1711-1

    PubMed Central  CAS  Article  PubMed  Google Scholar 

  4. 4.

    Kanbay M, Kasapoglu B, Perazella MA: Acute tubular necrosis and pre-renal acute kidney injury: utility of urine microscopy in their evaluation - a systematic review. Int Urol Nephrol 2010, 42: 425-433. 10.1007/s11255-009-9673-3

    Article  PubMed  Google Scholar 

  5. 5.

    Ishikawa K, May CN, Gobe G, Langenberg C, Bellomo R: Pathophysiology of septic acute kidney injury: a different view of tubular injury. Contrib Nephrol 2010, 165: 18-27.

    Article  PubMed  Google Scholar 

Download references

Author information

Affiliations

Authors

Corresponding author

Correspondence to NJ Glassford.

Rights and permissions

This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and Permissions

About this article

Cite this article

Glassford, N., Schneider, A., Eastwood, G. et al. 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. Crit Care 15, P10 (2011). https://doi.org/10.1186/cc10379

Download citation

Keywords

  • Acute Kidney Injury
  • Septic Patient
  • Fractional Excretion
  • Tubular Damage
  • Sodium Resorption