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Sanjeev Sethi
@SethiRenalPath
Professor, Mayo Clinic, MN. 💯renal pathology. Use X to teach, clinical info changed=protect confidentiality. Be kind to animals. Love dogs. Views are mine.
Minnesota, USA
Joined January 2018
Posts
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    Basics of Glomerulonephritis (GN). GBM is key. All patterns can be explained by glomerular basement membrane (GBM) & type of injury. Let’s do one at a time CRESCENTIC GN 1. Results from breach/break of GBM (red arrow) 2. Injury is sudden & severe Eg-ANCA & anti-GBM GN
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    Finally. We figured out the dense deposits in dense deposit disease (DDD). The answer is Apolipoprotein E. You can stain for APOE & make the diagnosis of DDD in >80% cases. Without electron 🔬. DDD was the reason I got into mass spectrometry 17 yrs ago. doi.org/10.1016/j.kint…
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    A very happy and proud moment for me. Our son Amit started medical school at the University of Minnesota Medical School- Primary Care education at its best. @umnmedschool
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    Simple concept of GN. It’s all about location! 1. Subendothelial deposits/injury by Ig, immune-complexes, complement, other mechanism leads to influx of leukocytes= inflammation=GN 2. Subepithelial deposits/injury= protected by GBM & endothelial cells=no inflammation=No GN. 1/3
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    Basics of GN (part 2) Clinical presentation correlates with location of injury & state of GBM 1. Epi/Subepithelial injury=nephrotic 2. GBM breach=RPGN 3. Subendothelial injury:acute/DPGN= nephritic 4. Subendothelial injury: chronic/MPGN & double contour= Nephritic-nephrotic
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    Excited about discovering a new antigen in membranous nephropathy (MN): Semaphorin 3B (Sema3B). Sema3B is a unique antigen detected in mostly childhood MN. Lot of work plus great collaboration. (1/3)
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    Basics of GN (pt 3) I. Epithelial/Subepithelial injury (Podocytopathies) -No inflammation as GBM protects from invasion by leukocytes -Yet, there is podocyte injury 1. Direct sudden injury to podocyte: -Minimal change disease, primary FSGS -anti nephrin/podocin Ab, others 1/3
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    1/6. Here is my approach to work up of the antigens in membranous nephropathy (MN). It’s not perfect. @NephRodby @GlassockJ Start with the common (~60 %) group: This includes: PLA2R, followed by NELL1.
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    I had no idea at first, then it suddenly hit me. 1. Normal glomeruli,no FSGS 2. Tubules filled with large granules 3. IF negative=not light chain tubulopathy Chromogranin +++ in tubules Dx: Neuroendocrine tumor-associated tubulopathy 65-yr, diabetes, HTN, pancreas mass, ⬆️ Cr
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    Never seen this: ? Whipple’s disease in the kidney. Patchy accumulation of aggregates of PAS-positive rods in Bowman’s space, few capillary loops, interstitium & tubules. Initially thought of crystal storing histiocytosis but IF negative for Ig. EM showed bacteria in tubules.
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    A comprehensive review on glomerulonephritis (GN). It’s a huge topic and it took a while, but we enjoyed writing this one. We tried to cover all of GN. An up to date reference for residents and fellows. @MayoClinicNeph @MayoClinicPath @MayoClinicGIM thelancet.com/journals/lance…
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    Thrombotic microangiopathy (TMA) day: 2 types. 1.Vascular TMA: Arteries with fibrin thrombi & onion skinning of media. 45-yr old with AKI, HTN & ? scleroderma 2.Glomerular TMA: double contours (arrow), mesangiolysis and lobular tufts. 50-yr old treated with Gemcitabine for Ca
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    Something other than election results 😀! I had an IgA day. C3 is helpful in determining etiology. In IgA nephropathy (upper row) C3 varies 1-3+. In IgA-dominant infection related GN, C3 is 3+ (lower row). Think infection-related GN when you see super bright C3 in setting of IgA.
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    So IgA on kidney bx: 1. IgA nephropathy 2. IgA vasculitis/HSP 3. IgA-dominant infection related GN (often staphylococcus) Often exudative on LM, IgA= GBM + mesangial, bright C3>IgA, usually humps on EM Most imp: h/o infection, often diabetic 4. IgA in lupus along with other Ig