Case 1 180126-1 (17B2750)
Conference Coordinator: Wesley Siniard.
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Nine-year-old, male castrated American Cocker Spaniel
This patient was presented for vomiting, inappetence, and diarrhea. He was hypertensive with severe hypoproteinemia, hyperphosphatemia, azotemia, proteinuria, and a markedly elevated urine protein to creatinine ratio. A renal biopsy was taken and submitted for evaluation.
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A core biopsy sample is present on this slide, which contains renal tissue, skeletal muscle and connective tissue is examined. Seven glomeruli are present in the section. Glomerular tufts are hypercellular and fill the urinary spaces. The hypercellularity is centered around the periphery of the glomerular tufts (endocapillary hypercellularity). A few capillary walls are thickened and some of the lumens are obliterated. Karyorrhectic debris is found throughout the glomerular tufts. Podocytes and parietal cells are occasionally hypertrophied. One glomerulus has a broad based synechiae. Tubular epithelia are filled with variably sized vacuoles and the interstitium has mild multifocal aggregates of lymphocytes. Rare tubules have attenuated epithelium with evidence of regeneration (mitotic figure).
Periodic acid Schiff and Jones Methenamine Silver Stain: Duplication of the glomerular basement membrane (GBM) is rarely observed.
Masson’s Trichrome: Fuschinophilic deposits decorate the glomerular basement membrane.
Electron Microscopy Ultrastructural lesions include subepithelial, subendothelial, mesangial and rare intramembranous dense (immune) deposits with the subepithelial deposits predominating. Podocyte foot processes are effaced, and podocyte villous transformation is also observed. Endocapillary hypercellularity obliterates or reduces the size of the capillary lumens.
Kidney: Immune-complex glomerulonephritis, mixed membranoproliferative pattern Kidney: Mild, multifocal tubular epithelial vacuoles and attenuation with regeneration
The glomerular lesions are classified as a mixed membranoproliferative glomerulonephritis (MPGN) based on the histological appearance of MPGN and on the distribution of immune deposits in both subendothelial and subepithelial locations. The lesions appear to be acute because there is little evidence of spike formation or encirclement of the immune deposits into the GBM that would suggest chronicity. Positive binding of fluorescein-labeled IgG specific for IgG, IgM, lambda light chain and complement component C3 was demonstrated along the capillary walls and within the mesangium indicating the presence of immune complexes with the glomeruli. This correlates with the presence of dense (immune) deposits observed by transmission electron microscopy and supports the diagnosis of an immune-mediated glomerulonephritis.
