[1703] Anatomy of the [Non Kimmelstiel-Wilson Nodule (KWN)] Segmental Mesangial Expansion (SME) in Diabetic Glomeruli

L Clarke Stout. University of Texas Medicall Branch, Galveston, TX

Background: SMEs occurred in the same location in the glomerulus as KWNs, but differed in that the expanded mesangium was morphologically normal and admixed with mesangial nuclei and vascular spaces. This study describes their 3 dimensional structure using 4 µm paraffin step serial sections in 10 diabetic cases, and 1 µm plastic serial sections in 1 of the cases.
Design: The study population consisted of 74 diabetics and 59 matched controls retrieved from consecutive autopsies at our hospital. Twenty five of the diabetics with any degree of diabetic glomerular change ranging from minimal to severe (end stage cases were omitted) were studied with 18 4 µm serial sections stained as follows: periodic acid-Schiff (PAS), IgG, IgM, Jones' periodic acid-methenamine silver (PAM), Masson's trichrome, IgA, albumin, lysozyme, PAS, fibrinogen, fibronectin, PAM, trichrome, kappa light chains, lambda light chains, leukocyte common antigen, PAS, and smooth muscle actin. SMEs >40 µm were traced through the 4 µm sections starting with PAS 9 in 102-108 glomeruli per case in 10 of the 25 diabetics with minimal to mild changes. They were traced through 1 µm PolyBed 812 embedded toluidine blue stained serial sections in 3 complete glomeruli in 1 of the cases.
Results: In the 4 µm sections 6/10 cases had 19 (1-7) SMEs that were 30 x 40 to 60 x 70µm in area and occupied 3 to 9 levels. The SME mesangium was reticular, contained mesangial/endothelial nuclei, and vascular spaces without glomerular capillary basement membranes (GBMs) that eventually opened into capillaries at the SME periphery. SMEs arose at capillary branch points, with the involved capillaries having no or partial GBMs. In the 1 µm sections 3 glomeruli from 1 case had 6 SMEs, 2 of which were fed by an afferent arteriolar branch (AAB) with complete mesangial interposition (MI). MI was confirmed by electron microscopy in another AAB, and the 1 µm sections confirmed the absence of GBMs in intra-SME vascular spaces, some of which were as tiny as the SME reticular spaces. Most intra SME vascular spaces could be traced from feeding to peripheral or peripheral to peripheral capillaries.
Conclusions: The little known SMEs are large mesangial proliferations that appear capable of reducing free capillary filtration surfaces and increasing mesangial-capillary surfaces. The presence of MI in some feeding capillaries, the origin of SMEs at branch points, and the apparently normal SME mesangium suggests that SMEs may be a reaction to increased glomerular capillary flow/pressure.
Category: Kidney (does not include tumors)

Wednesday, March 21, 2012 1:00 PM

Poster Session VI # 274, Wednesday Afternoon


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