Pradeep shenoy m

Renal biopsy IF patterns can provide powerful diagnostic clues. 🔹 Linear IgG staining → think anti-GBM disease, monoclonal deposition disease, immunotactoid GN 🔹 Granular IgG staining → suggests immune complex diseases like lupus nephritis, IgA nephropathy, membranous nephropathy & post-infectious GN Always correlate IF with LM, EM, serology & clinical presentation for accurate diagnosis. #GSR #BuddingNephros #Nephrology #RenalBiopsy #Immunofluorescence #KidneyDisease #MedTwitter

🩺 Podocyte-protecting drugs are changing modern nephrology practice. Podocyte injury is a key driver of proteinuria and CKD progression. Important podocyte-protective therapies include: ✅ RAAS blockers (ACEi/ARBs) ✅ SGLT2 inhibitors ✅ Finerenone & other MRAs ✅ Calcineurin inhibitors ✅ Endothelin pathway inhibitors ✅ Rituximab in selected glomerular diseases 🎯 Goals: • Reduce proteinuria • Preserve glomerular filtration barrier • Slow CKD progression • Improve long-term renal outcomes The strongest evidence today supports: 🛡️ RAAS blockade + SGLT2 inhibitor ± Finerenone #GSR #BuddingNephros #Nephrology #Proteinuria #KidneyDisease #GlomerularDisease #MedTwitter

@priti899 @DrSamB21 @kdjhaveri @myadla @arvindcanchi @thisis_drgsp @BeheraVineet @valerie_luyckx @silvishah @SwarnalathaGud2 @DivyaveerSSNeph @Kavitasv20 Congratulations

⚡️A surreal, full-circle moment ✨📚🩺 ☀️From learning nephrology through Brenner & Rector’s The Kidney during residency 👩🏻‍⚕️ to contributing to its 12th edition 🌍📖 — Chapter 59. Honored and deeply grateful to co-author “Infectious Diseases and the Kidney” alongside Prof. Vivekanand Jha 🙏🏻✨📘 ❤️🩺🌟 #Nephrology #AcademicMedicine #BrennerAndRectors #KidneyDisease

ANCA Vasculitis made simple 🔥 🔹 GPA → ENT + lung nodules + c-ANCA(PR3) 🔹 MPA → renal + pulmonary capillaritis + p-ANCA(MPO) 🔹 EGPA → asthma + eosinophilia + neuropathy One of the highest-yield topics in rheumatology & medicine. Which pattern do you find hardest to remember? #Rheumatology #Vasculitis @docakx @IhabFathiSulima #MedTwitter #InternalMedicine #Nephrology

Management of gout

🔬 Significance of Serum Free Light Chain (SFLC) in Multiple Myeloma My latest comprehensive infographic on this key biomarker that has transformed diagnosis, prognosis, renal monitoring & treatment decisions in MM. Covers everything in one visual: ✅ Basic concept & what SFLC actually measures ✅ Normal ranges + κ/λ ratio ✅ IMWG myeloma-defining event (involved/uninvolved SFLC ratio ≥100) ✅ Light-chain, oligosecretory & non-secretory myeloma + AL amyloidosis ✅ Risk stratification & prognostic implications ✅ Myeloma cast nephropathy & renal failure ✅ Rapid treatment monitoring (half-life 2–6 hrs!) ✅ Early relapse detection & practical clinical pearls Save 📌 this as your quick reference guide! Cancer Concepts Explained by Dr Rupam Manna Follow for more → @DrRupamOncology #MultipleMyeloma #SFLC #Myeloma #Oncology #HemOnc #MedEd #MedTwitter #Hematology

Confused about osteoporosis drugs in CKD? 👉 Low PTH = build bone → Teriparatide 👉 Any CKD = use safely → Denosumab (watch Ca!) 👉 Early CKD only → Bisphosphonates Simple rule: Turnover guides therapy #GSR #BuddingNephros #Nephrology #CKD

You know APS is antibody-mediated. We test anti-β2GPI. We test anticardiolipin. We test lupus anticoagulant. In pregnancy, we give heparin. But lupus anticoagulant isn’t a single antibody. And heparin isn’t just a blood thinner. Yet both revolve around one molecule: β2GPI. Let me explain.🧵👇 1-APS is NOT truly about phospholipids Despite the name “antiphospholipid,” the main pathogenic target is β2-glycoprotein I (β2GPI) -a phospholipid-binding protein. Cardiolipin is the surface. β2GPI is the antigen. 2-What is lupus anticoagulant (LA)? LA is not a specific antibody. It is a functional laboratory phenomenon: An antibody that prolongs phospholipid-dependent clotting assays (like dRVVT or aPTT) and corrects with excess phospholipid. 3-Why does LA prolong clotting in vitro? Clotting assays require phospholipid surfaces. In many APS patients: • β2GPI binds phospholipid • Anti-β2GPI antibodies bind β2GPI • This interferes with coagulation complex assembly → Clotting time prolongs. That’s why it’s called “anticoagulant.” 4-But not all LA is anti-β2GPI Important nuance: Some LA activity is prothrombin-dependent (e.g., aPS/PT antibodies). So LA is heterogeneous. But in high-risk APS (especially triple positive patients), LA is often β2GPI-dependent — and strongly associated with thrombosis. 5-Now shift to obstetric APS Pregnancy loss in APS is not just thrombosis. Placental studies and animal models show: • Complement activation • Trophoblast injury • Impaired placental remodeling Sometimes with minimal thrombosis. This is immune-mediated placental dysfunction. 6-β2GPI at the maternal–fetal interface β2GPI binds trophoblast membranes. Anti-β2GPI antibodies: • Inhibit trophoblast invasion • Increase apoptosis • Trigger complement cascade The placenta becomes the target. 7-So why does heparin help? If pregnancy loss were purely thrombotic, aspirin alone should be enough. But aspirin + heparin improves live birth rates. Because heparin does more than anticoagulation.. 8-Heparin disrupts β2GPI biology Heparin binds a heparin-binding region in domain V of β2GPI. This can: • Reduce β2GPI binding to phospholipids • Interfere with antibody clustering • Promote β2GPI inactivation in some settings 9-Complement may be the key Animal models show: Block complement → prevent aPL-mediated fetal loss. Heparin reduces complement activation at the placenta. This may be central to its benefit in obstetric APS. 10- The concept APS revolves around β2GPI. Lupus anticoagulant is a functional manifestation, often reflecting antibodies that disrupt phospholipid surfaces (frequently β2GPI-dependent, but not always). And in pregnancy: Heparin works not only by preventing clots.. but by modulating β2GPI interactions and complement activation. Same axis. Different angles. One central protein. β2GPI. #Rheumatology #APS #ObstetricAPS #Lupus #Immunology @DrAkhilX @IhabFathiSulima

7 ideas about mycophenolate that every rheumatologist should know.👇 Concept 1: What we prescribe is not the active drug We prescribe MMF MMF → (in stomach) → MPA (active drug) Only MPA suppresses immunity. If this step is inefficient → drug effect falls. Concept 2: Stomach acid decides how much drug works Low gastric pH (acidic stomach) → MMF dissolves properly → more MPA enters blood High gastric pH → MMF dissolves poorly → less MPA absorbed This step happens before we ever think of doses. Concept 3: Why PPIs quietly reduce MMF effect PPI → raises gastric pH → MMF does not dissolve well → ↓ MPA exposure by ~25–30% Dose unchanged. Patient compliant. But effective drug level is lower. Concept 4: Formulation changes the entire pathway MMF → dissolves in stomach → highly pH dependent EC-MPS → bypasses stomach → releases in intestine → much less affected by PPIs Same drug. Different route. Different outcome. Concept 5: Mycophenolate has a “second absorption” After first absorption: MPA → liver → MPAG MPAG → bile → gut Gut bacteria → MPAG back to MPA MPA → reabsorbed This loop → creates a second peak → contributes 30–40% of total drug exposure This is not a minor effect. Concept 6: Kidney disease and albumin change lab numbers MPA is 97–99% bound to albumin Renal failure or low albumin → less protein binding → ↓ total MPA level But → free (active) MPA may be unchanged So low numbers do not always mean low efficacy. Concept 7: The gut has silent thieves Sevelamer → binds MPA in gut → −25–35% exposure Laxatives → speed transit / bind drug → −50% or more Iron supplements → chelate MPA → up to −90% absorption These are common, overlooked causes of failure. Clinical moment: patient flares on MMF Before increasing dose → pause and ask: ➡ On a PPI? ➡ MMF or EC-MPS? ➡ Taking sevelamer, iron, laxatives? ➡ Low albumin? Renal impairment? Often, the answer is here. Final teaching pearl Mycophenolate works well when the stomach, gut, liver, kidney, and proteins cooperate. If any step is disturbed → drug exposure quietly falls. Understand the journey, and mycophenolate becomes predictable. #Rheumatology #MedTwitter #Mycophenolate #ClinicalPharmacology #MedEd #RheumPearls #Immunosuppression @DrAkhilX @IhabFathiSulima @CelestinoGutirr @nileshnolkha

This young girl's quest for a diagnosis ended today. She came to us after a 2.5 year ordeal in different places. 🌟This 23 year old 👩‍🚒bariatric Surgery (Sleeve Gastrectomy) in October 2022 after which her weight ⬇️⬇️ from 120 kg to 72 kg in 8 months. 🌟Experienced GERD and was bedbound for 6 months. She developed emotional disturbances requiring Qutipin. 🌟2 months later, she developed progressive weakness in hands (2 months). 🌟o/e weakness in distal hand muscles (extensors > flexors). Brisk DTRs, flexor plantar response, normal sensory function. 🌟NCS showed a generalized motor CMAP reduction, predominantly affecting radial nerves. 🌟She was diagnosed with a unclear myeloneuropathy vs. Progressive Motor Neuropathy post-bariatric surgery. 🌟MRI Spine: normal. Holo vitamin panel normal, except high Pantothenic Acid. 🌟Creatinine 1.6 (Medical Renal Disease - ? etiology).

CRP -a story we all live daily (but rarely understand) Today I asked my student: “What is CRP? What is its normal function?” He said confidently: “Sir, it’s an acute-phase reactant. It increases in infection.” Then I asked: “What do you mean by acute-phase reactant?” He paused… thinking… stuck. And honestly-most of us would also pause if we had to explain it properly. Because we order CRP every day to “see inflammation”… …but many of us don’t know CRP’s real identity. So let’s see. 👇 First: why the name C-reactive? Because CRP was discovered as a serum factor that reacted with the “C-polysaccharide” of pneumococcus during acute infection. Second: what is CRP, conceptually? CRP is a pattern recognition receptor (PRR)—but unlike TLR/CLR (membrane) or RLR (cytosolic)… 👉 CRP is a soluble, secreted PRR that patrols from the bloodstream. What does this “soluble PRR” recognize? Signals of danger: microbes + damaged self. CRP binds targets like phosphorylcholine on microbes and on apoptotic/necrotic membranes—basically, “this needs cleanup.” Then CRP does the work: 🧹 Opsonization (tags for phagocytosis) 🧩 Classical complement activation (via C1q) ➡️ Better clearance of debris & immune complexes. Now the clinical beauty: CRP kinetics. CRP is made fast—rises by ~6 hours, peaks around ~48 hours after a stimulus. The golden fact most people miss: CRP has a constant half-life ~19 hours (in health and disease). So the CRP value mainly reflects how much the liver is producing, i.e., inflammatory drive. So when should you repeat CRP? If you want the repeat to mean something, match biology: ✅ Repeat in 24–48 hours to judge trend/response (rise/peak/fall dynamics). When is repeating too early? <12 hours usually adds noise, not insight—CRP hasn’t had time to change meaningfully given its kinetics and half-life. CRP isn’t just “an acute phase reactant.” It’s a secreted PRR + complement-linking opsonin + a real-time reporter of inflammatory production. We order it daily. It’s worth knowing what it really does. 👉 #MedTwitter #RheumTwitter #Immunology #CRP #ClinicalPearls #MedEd @DrAkhilX @IhabFathiSulima @CelestinoGutirr @Urchilla01 @schowardjd

Here is an app that I’ve created for cognitive testing. It’s freely available and collates most of the commonly used bedside tests in Neurology/Neurosurgery. Let me know if anyone has any suggestions, recommendations or questions! mindmap-lobes-app.lovable.app

🧵 1️⃣ Inpatient Hyperglycemia 25% of hospitalized patients have diabetes. But even non-diabetics with hyperglycemia face worse outcomes — higher infection rates, longer stays, more readmissions, and higher mortality. Hyperglycemia isn’t just a number. It’s a prognostic marker and a modifiable target. Let’s break it down 👇 #MedTwitter #Endocrinology @DrAkhilX @prarit_v @Doctors__squad @DoctorLFC @drkeithsiau

😻Favourite Nutritional Councelling for a Rheumatologist #GOUT diet 🍛A disease with robust evidence for dietary modifications A thread…. Do 🔖 bookmark! 🚨‼️

💡 When lupus meets minimal change disease… think Lupus Podocytopathy 🧬 Nephrotic-range proteinuria 🔬 Normal LM, negative IF 🧠 EM: podocyte foot process effacement 🎯 Steroid-sensitive but relapsing — CNI or Rituximab if recurrent #LupusNephritis #Rheumatology #Nephrology #MedEd @DrAkhilX @IhabFathiSulima @Renalpathsoc @JasmineNephro @arvindcanchi @sundar_s1955

Think a normal uric acid rules out gout? Not so fast. Nearly 1 in 3 gout flares happen with normal urate levels. Here’s why your “normal” report might be lying to you 👇 1- The twist During a flare, inflammation itself changes uric acid handling. Cytokines like IL-6 and stress hormones like ACTH make the kidneys dump more urate — a temporary uricosuric effect. 2- The clinical pearl So when should you check uric acid? 🧾 At least 2 weeks after the flare settles. Only then does the true baseline appear. Otherwise, you might miss the diagnosis entirely. 3- Summary (save-worthy) 🔍 Serum uric acid in acute gout: – May be normal (~33 %) – ACTH + IL-6 lower urate via uricosuria – Re-check ≥ 2 weeks post-flare 👉 Save this before your next “normal uric acid” surprise. Rheumatology is full of beautiful paradoxes. Follow @IlliasulK for more 🩸🦴 #Rheumatology #Immunology #Sullysrounds #MedX #Medtwitter #Mnemonics #Medicine #History @DrAkhilX @IhabFathiSulima @Janetbirdope #MedTwitter #rheumtwitter @CelestinoGutirr

🆕 Bench to Bedside: Diagnosis & Treatment of #SLE Nephritis #ACR25 🎤 Talks by Dr. Andrea Fava, Dr. Maria Dall’Ara, & Dr. Anca Askanase 🔹Limitations of Using Proteinuria 🔹Applying 2024 ACR LN Guidelines 🔹How to Treat Refractory Disease #LupusNephritis #Lupus #ACR2025

ACR Convergence 2025 | Inflammatory Brain Disease for the Clinical Rheumatologist 👨‍⚕️ Eyal Muscal, MD – Baylor College of Medicine ⸻ 🧩 CLINICAL SNAPSHOTS — WHEN RHEUMATOLOGY MEETS THE BRAIN 🧠 🧠 NPSLE (Neuropsychiatric SLE) Seizures, psychosis, cognitive dysfunction. 💊 Cyclophosphamide | Rituximab | PLEX 🌿 Neurosarcoidosis Cranial neuropathies, myelitis, hypothalamic lesions. 💊 TNF-α blockade | Corticosteroids | Cyclophosphamide 🩸 CNS Vasculitis Stroke-like episodes, headache, encephalopathy. 💊 Cyclophosphamide ± MMF | IL-6 blockade 🔥 Autoinflammatory Syndromes (VEXAS, DADA2, NOMID, TRAPS) Periodic fevers, vasculitis, aseptic meningitis. 💊 IL-1 / IL-6 / TNF inhibitors 💎 IgG4-Related CNS Disease Pachymeningitis, tumefactive lesions, CSF IgG4 elevation. 💊 Rituximab — cornerstone therapy ⸻ ✨ Key Insight: Neuroinflammation often mirrors systemic autoimmunity — early recognition enables precision, collaboration, and recovery. ⸻ 🔖 #ACR25 #ACRConvergence2025 #NeuroRheum #ACRAmbassador #BrainInflammation #Autoimmunity #Rheumatology #NeuroImmunology #PrecisionMedicine

⚡EULAR 2025 Update: Lupus Nephritis (SLE Kidney Involvement) 1️⃣ New Structure: 4 principles + 13 recommendations (evidence-graded). 2️⃣ Core Approach: 🔹 Early biopsy, expert care, & HCQ for all. 🔹 Rheumatology–nephrology team care. 🔹 Aim: prevent CKD, reduce flares, improve QoL. 3️⃣ Targets: 🎯 Proteinuria ↓ ≥25% (3 mo), ≥50% (6 mo), <700 mg/g (12 mo). 🎯 Preserve/improve GFR ≥ 80% baseline by 3 mo. 4️⃣ Steroids: Pulse IV MP → taper ≤5 mg/d @ 4–6 mo → stop by 12–24 mo if stable. 5️⃣ First-line (Major Change): ✅ Combination therapy preferred: •MMF / low-dose CYC + Belimumab, OR •MMF + CNI (Voclosporin/Tacrolimus), OR •MMF + Obinutuzumab (NEW). ➡️ Single-agent MMF or CYC only if limited options or mild LN. 6️⃣ Maintenance: Continue ≥3 yrs; replace CYC → MMF/AZA. 7️⃣ Tapering: Withdraw IS after ≥3 yrs sustained remission; watch for flare risks (active serology, short duration). 8️⃣ Refractory LN: Switch class/biologic; consider Obinutuzumab / Rituximab / CAR-T (future). 9️⃣ Nonimmune Care: RAAS blockers, SGLT2i, Statins, Bone protectants, Vaccines (Flu / Pneumo / COVID / HZV) + Lifestyle control. 🔟 Special Situations: •TMA: treat per mechanism (TTP→Plasma exchange; CM-HUS→Complement blockade). •Pregnancy: plan after ≥6 mo remission; use HCQ, AZA, CNI; avoid MMF, CYC, RAASi. •Kidney Failure: all replacement options ok; transplant if extrarenal SLE inactive ≥6 mo. 📘 DOI: 10.1016/j.ard.2025.09.007 🔖 #EULAR2025 #LupusNephritis #SLE #Belimumab #Voclosporin #Obinutuzumab #RheumTwitter

🧵100 timeless bedside gems every doctor should know. Straight from Hutchison’s Clinical Methods — distilled into 10 clean infographics. If you love real clinical medicine, this thread will remind you why you chose it. 🩺 Let’s bring back the art of examination 👇 (Save this thread — it’ll outlive most AI tools.) #MedTwitter #MedEd #FOAMed @DrAkhilX @IhabFathiSulima @drkeithsiau @DurgaPrasannaM1 @JasmineNephro