1/6. Here is my approach to work up of the antigens in membranous nephropathy (MN). It’s not perfect. Roger Rodby Richard J. Glassock Start with the common (~60 %) group: This includes: PLA2R, followed by NELL1.

APPLAUSE-IgAN: Iptacopan for IgA Nephropathy (IgAN) from KIReports #GlomConHawaii 🇺🇸 #Nephpearls How it started How it’s going 👉🏼 pubmed.ncbi.nlm.nih.gov/37180505/

Monoclonal Gammopathy of Renal Significance (MGRS) by the expert Ladan Zand Mayo Clinic Nephrology GlomCon Fellowship Program ⭐️ #Glomlovers #NephX Joselyn Reyes Bahamonde

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

Facilitated our Journal Club today on APPLAUSE-IgAN Trial’s interim analysis. 🔗 nejm.org/doi/full/10.10… Vlado Perkovic Exciting times — there is always more to learn & this fellow is here for all of it! 🤓🔬🫘 #GlomerularDiseases #Nephrology

🫘✅Management of Renal Amyloidosis academic.oup.com/ndt/article-ab… NDT Hans-Joachim Anders

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

🫘💊How to initiate ACEi or ARB and how to monitor hyperkalemia/Creatinine Int Society of Nephrology KDIGO

Albuminuria: The CKM biomarker we’re overlooking❗️ 💡The best risk stratifying biomarker 🔹 Even UACR <3.4 mg/mmol = ⤴️ #CVD, #CKD & mortality risk 🔸 Signals early endothelial dysfunction across HTN, #T2D, #HF & #MASLD 🔹 Yet 💧screening rates low, esp. in primary care 🔸

Basics of GN (part 4) CRESCENTIC GN Severe sudden injury= Rupture of GBM=necrosis & crescent Clinical syndrome: RPGN 1. Anti-GBM GN LM:Large number of huge crescents IF:linear staining for IgG along GBM Due to antibodies to a3 (IV) collagen Goodpasture=lung involved too 1/3

Schematic view illustrating the events leading to crescent 🌙 formation #Nephpearls (a) Normal glomerulus (b) Glomerular disease leads to gaps or holes in the glomerular basement membrane (GBM), resulting in (c) proliferation of parietal epithelial cells and ultimately (d)

The pathophysiology and treatment strategies for Hepatorenal Syndrome (HRS-AKI) in the context of cirrhosis with ascites. nejm.org/doi/full/10.10…

Secondary TMAs

This Dx often not the mind of nephrologist- always surprised by Dx Fibrillary Glomerulonephritis LM: Membranoproliferative GN IF: IgG 3+, polyclonal=3+ kappa & lambda EM: fibrillary deposits DNAJB9 positive, Congo red negative 65 yr obese lady, hematuria & proteinuria. Cr 2

🎉 NYU Nephrology Batch 2025 🎓 That’s a wrap 🥹 — Trisha Laxamana MD ❄️🗽🇵🇭 Niveda Shekar Rahul Abraham #amir 🤍💜

but wait — some #throwback: 1. NYC Bootcamp early first year 🤓 2. Us passing ABIM in 2023 💪🏼 3. Video documentation of above 🙈 4. A conference in second year 😋 So much high yield memories to carry forward 💜

The cake made it! And it was our GN fellow’s Trisha Laxamana MD ❄️🗽🇵🇭 birthday which we got to celebrate! So happy to have you on our team Trisha!

Trisha Laxamana MD ❄️🗽🇵🇭

Membranous nephropathy has undergone a paradigm shift due to the discovery of unique MN antigens. MN has gone from idiopathic to ➡️ primary vs. secondary ➡️ where an antigen can be detected in ~80% of MN. This is a comprehensive review of each antigen. nature.com/articles/s4158…

A sumptuous dinner graciously hosted by Dr. Ladan Zand with the Mayo Clinic Glomerular Diseases team ✨ Such an honor to enjoy her exquisite cooking and delicious cake! 😍 fernando fervenza Anila Cara Helio Vida Cassi Junior