Renal neutrophil gelatinase associated lipocalin expression in lipopolysaccharide-induced acute kidney injury in the rat

BMC Nephrol. 2012 Jun 27:13:25. doi: 10.1186/1471-2369-13-25.

Abstract

Background: Neutrophil gelatinase associated lipocalin (NGAL) is a highly predictive biomarker of acute kidney injury. To understand the role of NGAL in renal injury during sepsis, we investigated the temporal changes and biological sources of NGAL in a rat model of acute kidney injury, and explored the relationship between renal inflammation, humoral NGAL and NGAL expression during endotoxemia.

Methods: To induce acute renal injury, rats were treated with lipopolysaccharide (LPS, 3.5 mg/kg, ip), and the location of NGAL mRNA was evaluated by in situ hybridization. Quantitative RT-PCR was also used to determine the dynamic changes in NGAL, tumor necrosis factor α (TNFα) and interleukin (IL)-6 mRNA expression 1, 3, 6, 12, and 24 hours following LPS treatment. The correlation among NGAL, TNFα and IL-6 was analyzed. Urinary and plasma NGAL (u/pNGAL) levels were measured, and the relationship between humoral NGAL and NGAL expression in the kidney was investigated.

Results: Renal function was affected 3-12 hours after LPS. NGAL mRNA was significantly upregulated in tubular epithelia at the same time (P < 0.001). The course of NGAL mRNA upregulation occurred in parallel with renal damage. There was a transient increase in TNFα and IL-6 mRNA levels within 3 hours following LPS administration, and a strong correlation between TNFα and NGAL mRNA (r = 0.995, P <0.001) but not with IL-6 mRNA. Both pNGAL and uNGAL levels were markedly increased compared with those in the control group (P < 0.001); however, only uNGAL levels were correlated with NGAL mRNA (r = 0.850, P <0.001).

Conclusions: NGAL upregulation is sensitive to LPS-induced renal TNFα increase and injury, which are observed in the tubular epithelia. Urinary NGAL levels accurately reflect changes in NGAL in the kidney.

MeSH terms

  • Acute Kidney Injury / chemically induced
  • Acute Kidney Injury / metabolism*
  • Acute Kidney Injury / pathology
  • Acute-Phase Proteins / genetics*
  • Acute-Phase Proteins / metabolism*
  • Acute-Phase Proteins / urine
  • Analysis of Variance
  • Animals
  • Biomarkers / blood
  • Biomarkers / urine
  • Creatinine / blood
  • Gene Expression
  • Interleukin-6 / metabolism
  • Kidney Glomerulus / pathology
  • Kidney Tubules / metabolism
  • Kidney Tubules / pathology
  • Lipocalin-2
  • Lipocalins / blood
  • Lipocalins / genetics*
  • Lipocalins / metabolism*
  • Lipocalins / urine
  • Lipopolysaccharides
  • Male
  • Proto-Oncogene Proteins / blood
  • Proto-Oncogene Proteins / genetics*
  • Proto-Oncogene Proteins / metabolism*
  • Proto-Oncogene Proteins / urine
  • RNA, Messenger / metabolism*
  • Rats
  • Rats, Sprague-Dawley
  • Time Factors
  • Tumor Necrosis Factor-alpha / metabolism*
  • Up-Regulation
  • Urothelium / metabolism

Substances

  • Acute-Phase Proteins
  • Biomarkers
  • Interleukin-6
  • Lcn2 protein, rat
  • Lipocalin-2
  • Lipocalins
  • Lipopolysaccharides
  • Proto-Oncogene Proteins
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Creatinine