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Volume 15 Supplement 3

Sepsis 2011

  • Poster presentation
  • Open Access

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

  • 1,
  • 1,
  • 1,
  • 1,
  • 1 and
  • 1
Critical Care201115 (Suppl 3) :P10

https://doi.org/10.1186/cc10379

  • Published:

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

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

   

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

(1)
Department of Intensive Care, Austin Hospital, Heidelberg, VIC, Australia

References

  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.0000266684.17500.2FView ArticlePubMedGoogle Scholar
  2. Siew ED, Ware LB, Ikizler TA: Biological markers of acute kidney injury. J Am Soc Nephrol 2011, 22: 810-820. 10.1681/ASN.2010080796View ArticlePubMedGoogle Scholar
  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/s00134-009-1711-1PubMed CentralView ArticlePubMedGoogle Scholar
  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/s11255-009-9673-3View ArticlePubMedGoogle Scholar
  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.View ArticlePubMedGoogle Scholar

Copyright

© Glassford et al. 2011

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.

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