PMC5762945_01
(a,b) Kidney biopsy 1 (performed in 2006). Light microscopy showing tip variant focal segmental glomerulosclerosis (FSGS), with a cellular segmental lesion containing endocapillary foam cells that protrudes into the tubular pole and forms an adhesion to the tubular orifice, consistent with a tip lesion (hematoxylin and eosin, original magnification x600) (a). Another glomerulus contains a segmental cellular lesion of sclerosis with hypertrophy of the overlying podocytes (hematoxylin and eosin, original magnification x600 (b). (c,d) Kidney biopsy 2 (performed in 2015). Light microscopy showing a small synechia (adhesion) between the peripheral glomerular tuft and Bowman capsule at the origin of the tubular pole, forming a tip lesion (Jones methenamine silver, original magnification x400). By electron microscopy, there is diffuse foot process effacement with microvillous transformation of the podocyte cytoplasm. The glomerular basement membrane is unremarkable and no electron-dense deposits are identified (electron micrograph, original magnification x10,000).
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Past medical history included biopsy-documented tip variant FSGS at the age of 25 years that had responded to a 6-week course of corticosteroid therapy (Figure 1a and b). A repeat kidney biopsy performed during this hospitalization showed relapse of tip variant FSGS with severe podocyte foot process effacement (Figure 1c and d).
Time course of nephrotic syndrome response in relation to antihelmintic therapy.
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Figure 2 summarizes the changes in laboratory findings over time following initiation of antihelmintic treatment.