Pediatric Nephrology

, Volume 21, Issue 7, pp 989–994 | Cite as

Urinary neutrophil gelatinase-associated lipocalcin in D+HUS: a novel marker of renal injury

  • Howard TrachtmanEmail author
  • Erica Christen
  • Avital Cnaan
  • Jilma Patrick
  • Volker Mai
  • Jaya Mishra
  • Aditya Jain
  • Nathan Bullington
  • Prasad Devarajan
  • Investigators of the HUS-SYNSORB Pk Multicenter Clinical Trial
Original Article


Background: Diarrhea-associated hemolytic uremic syndrome (D+HUS) causes acute renal failure. Neutrophil gelatinase-associated lipocalcin (NGAL) is an early indicator of kidney injury. Objective: To determine if urinary NGAL excretion is a biomarker of severe renal injury and predicts the need for dialysis in D+HUS. Methods: Patients were randomly selected from among participants in the SYNSORB Pk trial. Urine samples were collected daily if available during the first week of hospitalization. NGAL levels were determined by ELISA. Results: 34 children, age 5.9±3.9 yr, were studied; ten (29%) required dialysis. Patients were categorized based on urinary NGAL concentration within five days of hospitalization - <200 ng/ml and ≥200 ng/ml. Twenty patients (58%) had increased urinary NGAL excretion. The severity of D+HUS at enrollment was similar in the two groups. However, children with increased urinary NGAL levels had higher peak BUN and creatinine concentrations (P<0.01) and required dialysis more often, 9/20 versus 1/14 (P=0.024) compared to children with normal excretion. Conclusion: The majority of patients with D+HUS have renal tubular epithelial injury, as evidenced by elevated urinary NGAL excretion. Urinary NGAL levels below 200 ng/ml within five days of hospitalization may be an adjunctive marker that defines less severe renal involvement.


Diarrhea-associated hemolytic uremic syndrome (D+HUS) Neutrophil gelatinase-associated lipocalcin (NGAL) Acute renal failure Dialysis Biomarker 



This work was presented at the Annual Meeting of the American Society of Nephrology, Philadelphia, PA, November 2005. It was supported, in part, by grant DK52147 (HT). PD is supported by grants from the NIH-NIDDK (RO1-DK53289, P50-DK52612, R21-DK070163), a Grant-in-Aid from the American Heart Association Ohio Valley Affiliate, and a Translational Research Initiative Grant from Cincinnati Children’s Hospital Medical Center.


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Copyright information

© IPNA 2006

Authors and Affiliations

  • Howard Trachtman
    • 1
    Email author
  • Erica Christen
    • 1
  • Avital Cnaan
    • 2
  • Jilma Patrick
    • 3
  • Volker Mai
    • 3
  • Jaya Mishra
    • 4
  • Aditya Jain
    • 4
  • Nathan Bullington
    • 4
  • Prasad Devarajan
    • 4
  • Investigators of the HUS-SYNSORB Pk Multicenter Clinical Trial
  1. 1.Department of Pediatrics (Division of Nephrology)Schneider Children’s Hospital of the North Shore-Long Island Jewish Medical CenterNew YorkUSA
  2. 2.Department of Biostatistics and EpidemiologyChildren’s Hospital of PhiladelphiaPhiladelphiaUSA
  3. 3.Department of Epidemiology and Preventive MedicineUniversity of MarylandBaltimoreUSA
  4. 4.Department of Pediatrics (Division of Nephrology)Cincinnati Children’s Hospital Medical CenterCincinnatiUSA

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