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. Author manuscript; available in PMC: 2016 Jun 1.
Published in final edited form as: Proteomics Clin Appl. 2015 Jun;9(0):490–500. doi: 10.1002/prca.201400193

Figure 1.

Figure 1

Panel A shows a light microscopy picture of a renal section derived from a child with HIVAN. The black arrows point to a collapsed glomerulus and a tubular microcyst (Jones methenamine silver stain). Panel B shows a renal section from a child with HIV-HUS. The picture shows dilated capillary loops with red blood cell fragments, and tubular microcysts (Hematoxylin-eosin stain). The black arrow points to a renal arteriole with luminal narrowing due to red cell fragments and intraluminal thrombosis (A and B original magnification x 200). Pictures A and B are reproduced with permission from “Kidney disease in HIV-positive children” McCulloch, M.I., Ray P.E. Seminars in Nephrology (2008) 28, 585–594. Panel C, shows representative changes in urinary EGF, MMP-2, FGF-2, and serum creatinine (SCr), seen during the different stages of childhood HIVAN [16]. Panel D shows representative changes in urinary EGF, NGAL, FGF-2, and SCr, seen during different stages of acute kidney injury in HIV-infected children [37,42, 74].