Membranous Nephropathy 1

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Across
  1. 2. The most common secondary etiology of MGN is membranous ______ nephritis. (5)
  2. 4. Americans MGN is the most common cause of the nephrotic syndrome in Caucasian adults. However, focal segmental glomerulosclerosis (FSGS) is a more common cause of the nephrotic syndrome in ______ _________ and, in some studies, has surpassed MGN in the overall population. (7, 9)
  3. 6. Initially, the spikes may be small and segmental, and a careful search under_________________ is necessary to demonstrate them. (3, 9)
  4. 8. By light microscopy, the earliest change in MGN is ________ of and small depressions in the GBM seen in en face sections stained with JMS. (8)
  5. 9. Eventually, the GBM becomes more prominently expanded by a thick band of argyrophilic material containing abundant nonargyrophilic “______” and imparting a vacuolated appearance (Fig. 7.8). The “_______” represent a normal-thickness GBM beneath the deposits surrounded by a heaped-up matrix around the deposits. (5) (same answer in both the blanks)
  6. 10. Lesions of _______ are present in approximately 20% of renal biopsies with primary MGN (range 13% to 42%). (4) (abbrev)
  7. 11. Based on the limited information available, segmental MGN is most commonly reported in _______. (8)
  8. 12. Potential secondary etiologies of both _____ and MGN include SLE, Sjögren syndrome, sarcoidosis, and treatment with NSAIDs. (3) (abbrev)
  9. 13. By light microscopy, the earliest change in MGN is mottling of and small ____________ in the GBM seen in en face sections stained with JMS. (11)
  10. 15. Megalin/gp330 is expressed in the proximal tubular brush border of the rat, as well as the ______-coated pits at the base of the podocyte foot processes. (8)
  11. 16. The term “_______________MGN” should be reserved for cases with a segmental distribution of the deposits by light microscopy, immunofluorescence, and EM. (9)
  12. 18. This constellation of mixed membranous and membranoproliferative changes is most commonly encountered in the setting of LN (i.e., class IV and V), in patients with HBV or HCV infection, or as the idiopathic entity of membranoproliferative glomerulonephritis (MPGN) type 3, ____________ subtype. (10)
  13. 20. The subepithelial deposits and associated GBM changes that characterize MGN do not typically result in GBM rupture or crescent formation. Nonetheless, crescents are encountered in a small percentage of cases of MGN and, when present, should raise the possibility of concurrent SLE, anti-_____ disease, or systemic vasculitis. (3) (abbrev)
  14. 22. The subepithelial deposits appear to sit on the GBM and are accompanied by a spectrum of GBM changes ranging from intervening projections of the extracellular matrix (“spikes”) to areas where the GBM projections surround and encase the deposits, creating the appearance of a newly formed, overlying “_______________” (11)
  15. 23. Ultrastructural finding that favors a secondary form of MGN is __________ tubuloreticular inclusions. (11)
Down
  1. 1. Combined MGN and IgAN appear to be common in patients with hepatitis B infection, in patients with _______- ethnicity, and in the allograft, where IgAN recurs in a large percentage of cases and MGN is among the most frequent de novo form of glomerular disease. (5)
  2. 3. Podocyte____________ glomerulopathy is a recently described entity that resembles MGN by light microscopy and may or may not exhibit granular positivity for IgG by immunofluorescence. In contrast to MGN, EM reveals podocyte __________ with microspherical and microtubular structures within the GBM. The majority of cases of protein infolding glomerulopathy have occurred in Japan, and many of the patients have evidence of SLE. Although the morphogenesis of this lesion is unknown, the irregular outer contours of the GBM suggest that podocyte cytoplasmic fragments and cell membranes may become trapped in the course of deposit resorption and matrix remodeling. (9) (same answer in both the blanks)
  3. 5. MGN became a distinct entity in 1957 when David ______ , a renal pathologist at Syracuse University, developed the periodic acid-methenamine silver stain to demonstrate textural changes of the GBM and identified spikes as a defining feature of MGN. As a result of his contributions, the ______ methenamine silver stain bears his name. (5) (same answer in both the blanks)
  4. 7. Kerjaschki and Farquhar determined that glycoprotein 330 (gp330) expressed on the proximal tubular brush border was the critical component of FX1a that induced PHN. Specifically, injection of isolated gp330 was able to induce PHN, while injection of FX1a depleted of gp330 did not produce this model. As a result, gp330, also referred to as __________, was identified as the target antigen in Heymann nephritis. (7)
  5. 8. ___________ deposits have been described mainly in SLE, in few patients of HBV infection and rarely in patients with MGN related to metastatic carcinoma and following treatment with penicillamine. (9)
  6. 14. In a review of nine series published between 1975 and 1989, Glassock found that 23% of cases of MGN were secondary with the prevalence higher (35%) in children younger than ______ years and adults older than 60 years. (7)
  7. 16. Great insights into MGN came from the 1959 landmark work of Heymann and Hackel, who utilized ________-_______ rats. (7, 6)
  8. 17. Secondary forms of MGN are more common in the pediatric population (6) and most often relate to SLE or infection, in particular ____ (3) (abbrev)
  9. 19. EM also is needed to accurately determine the ______of MGN. (5)
  10. 21. The nonargyrophilic material deposited within the GBM and on its epithelial side stains red with the _________stain, while the surrounding GBM stains blue or green depending on the method used. (9)