Received January 16, 2009
Accepted on April 22, 2009

BRIEF COMMUNICATION

Urinary NGAL Marks Cystic Disease in HIV-Associated Nephropathy

Neal Paragas ^*, Thomas L. Nickolas ^*, Christina Wyatt , Catherine S. Forster ^*, Meghan Sise ^*, Susan Morgello , Bernd Jagla ^*, Charles Buchen ^*, Peter Stella ^*, Simone Sanna-Cherchi ^*, Maria Luisa Carnevali , Silvia Mattei , Achiropita Bovino , Lucia Argentiero , Andrea Magnano , Prasad Devarajan , Kai M. Schmidt-Ott ^||, Landino Allegri , Paul Klotman , Vivette D’Agati ^*, Ali G. Gharavi ^*, and Jonathan Barasch ^*1

*College of Physicians and Surgeons, Columbia University, New York, New York; The Mount Sinai School of Medicine, New York, New York; University of Parma, Parma, Italy; Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio; and ||Max Delbruck Center for Molecular Medicine, Berlin, Germany

¹ To whom correspondence should be addressed. E-mail: jmb4{at}columbia.edu.

	Abstract

Nephrosis and a rapid decline in kidney function characterize HIV-associated nephropathy (HIVAN). Histologically, HIVAN is a collapsing focal segmental glomerulosclerosis with prominent tubular damage. We explored the expression of neutrophil gelatinase-associated lipocalin (NGAL), a marker of tubular injury, to determine whether this protein has the potential to aid in the noninvasive diagnosis of HIVAN. We found that expression of urinary NGAL was much higher in patients with biopsy-proven HIVAN than in HIV-positive and HIV-negative patients with other forms of chronic kidney disease. In the HIV-transgenic mouse model of HIVAN, NGAL mRNA was abundant in dilated, microcystic segments of the nephron. In contrast, urinary NGAL did not correlate with proteinuria in human or in mouse models. These data show that marked upregulation of NGAL accompanies HIVAN and support further study of uNGAL levels in large cohorts to aid in the noninvasive diagnosis of HIVAN and screen for HIVAN-related tubular damage.