Anagha Shreyas

I was in my first month of residency....standing in front of a shouting relative who wanted answers I didn’t have yet. I was nervous, sleep-deprived and trying to explain the "pathophysiology" and "prognosis" using every textbook term I knew. The more I talked about lab values, the angrier they got. I was losing control of the room. The senior staff nurse, who had probably seen hundreds of residents like me come and go, quietly walked over. She didn't interrupt me. She just put a hand on the relative’s arm, looked them in the eye, and spoke two sentences in their local dialect. She didn't mention a single medical term. She talked about comfort, about the small progress made since the morning, and promised to keep a close eye on him through the night. The tension in the room vanished instantly. The shouting stopped. The relative finally exhaled. In five minutes, she did what I couldn't do with an hour of medical counseling. Medical school taught me how to treat a disease. But in that first month, the nurses in my ward began teaching me how to treat a human being. We sign the discharge papers, but they are the ones who guide the family through the storm. To the teachers who don’t wear a professor’s gown: Happy International Nurses Day.

🧠 Post Renal Transplant Infections Timeline – Must Know! 🕒 0–1 month (Surgical phase) • Nosocomial infections dominate • UTI, SSI, pneumonia • Not immunosuppression-driven 🕒 1–6 months (🔥 Peak immunosuppression) • Opportunistic infections • Cytomegalovirus infection (most common) • Pneumocystis jirovecii pneumonia, TB, fungi • BK virus nephropathy 🕒 >6 months (Community phase) • CAP, UTI, influenza • Late CMV, PCP (if no prophylaxis) • Post-transplant lymphoproliferative disorder 💡 Pearls: ✔ Timeline = diagnosis shortcut ✔ CMV = key player ✔ Think TB in India ✔ TMP-SMX prophylaxis saves lives #GSR #BuddingNephros #Transplant #Infection

Diabetes Inspidus ❌ AVP deficiency ♈️ Water deprivation is out. Copeptin is in.
Hypertonic saline + copeptin → ~97% accuracy for AVP deficiency💧 
Desmopressin works—but watch hyponatremia ⚠️ #NephTwitter #FOAMed #MedEd #MedTwitter

Snakebite isn’t just a toxin problem—it’s a kidney story 🐍🩺 🫘 AKI occurs in 8–60%, with up to 92% needing dialysis in severe cases. Time to antivenom = kidney survival. Survivors ≠ safe → CKD risk persists. #NephTwitter #FOAMed #AKI #Snakebiteaki #MedTwitter

🚨 Abnormal Bladder before Renal Transplant – Don’t Miss This! A poorly functioning bladder can silently damage your graft. 🔍 Evaluate properly: ✔️ Urodynamics (MOST IMPORTANT) ✔️ Post-void residual (PVR) ✔️ Urine culture (treat all infections) ✔️ Imaging (USG, MCUG, cystoscopy) ⚠️ Red flags: ❌ High-pressure bladder ❌ Low compliance ❌ Severe reflux 🛠️ Fix before transplant: • Anticholinergics • CIC • Augmentation cystoplasty 🎯 Target: Low-pressure + good capacity + complete emptying 👉 Optimize bladder FIRST → Protect graft LONG TERM #GSR #BuddingNephros #Bladder #transplant #kidney

Clinical Indications for ANCA Testing ANCA testing should be considered when there is suspicion of ANCA-associated vasculitis (AAV), particularly in the following scenarios: 🫘 Renal •Glomerulonephritis (especially rapidly progressive GN) 🫁 Pulmonary •Pulmonary hemorrhage •Pulmonary–renal syndrome •Multiple lung nodules 🧴 Cutaneous •Cutaneous vasculitis with systemic features 👃 ENT / Upper airway •Chronic destructive disease of upper airways •Long-standing sinusitis or otitis •Subglottic tracheal stenosis 🧠 Neurological •Mononeuritis multiplex •Peripheral neuropathy 👁️ Ocular / Orbital •Retro-orbital mass •Scleritis Order ANCA only when there is strong clinical suspicion of AAV-not as a screening test. Source: Revised 2017 international consensus on testing of ANCAs in granulomatosis with polyangiitis and microscopic polyangiitis #RheumattDoc #MedTwitter #RheumTwitter #Medicine #rheumatology @docakx @IhabFathiSulima @CelestinoGutirr @DurgaPrasannaM1

Failed kidney graft post transplant What to do? Do we continue immunosuppressant? Or stop? Do we remove non functioning kidney graft Answer depends on what is the future plan

Furosemide Stress Test(FST): Clinical Protocol and interpretation . #KDIGO AKI Guidelines 2026

Diffusion 💨 clears Ultrafiltration 💧 dries Convection 🔄 refines #NephTwitter #Dialysis #FOAMed

Membranous Nephropathy 🔬Anti-PLA2R = used for Diagnosis , Prognosis, Monitoring 📊 Risk stratify: Based on Proteinuria + eGFR + AntiPLA2R 🟢 Low risk→ Supportive 🟡 Mod→ Observe ± RTX 🔴 High→ Rituximab / Cyclophosphamide+Steroid 👍for Antigens: VA @KKNephBytes 💯 #KDIGO

🩻Contrast-induced AKI: one of the biggest myths still shaping clinical decisions For decades we were taught: 👉 “Contrast damages the kidneys” 👉 “Avoid CT with contrast in CKD” 👉 “Hydrate, protect, delay imaging if needed” But what if… most of this is wrong?🤔 ->The uncomfortable reality Modern evidence shows: 👉 Low-osmolar contrast rarely causes true nephrotoxicity 👉 Even in CKD, AKI, and ICU patients 👉 The risk is often overestimated—or nonexistent So where did the fear come from? 📍 1950s high-osmolar contrast (actually toxic) 📍 Poorly controlled observational studies 📍 “Creatinine rise = contrast injury” assumption 👉 Correlation became causation 👉 And the dogma stayed ⚠️What recent data tells us ✔ No difference in AKI rates with vs without contrast ✔ No benefit from bicarbonate, NAC, or aggressive hydration ✔ Even ICU and AKI patients show no worsening outcomes ->Translation to real life 👉 The patient was going to develop AKI anyway...Not because of contrast!! ->The real problem: “Renalism” 👉 Avoiding necessary imaging 👉 Delaying diagnosis 👉 Choosing inferior tests And that leads to: ❌ Missed PE ❌ Delayed sepsis source control ❌ Worse outcomes ->Clinical mindset shift Instead of asking: 👉 “Will contrast harm the kidneys?” We should ask: 👉 “Will NOT doing the scan harm the patient?” ->Who still deserves caution? ✔ eGFR <30 ✔ Severe hemodynamic instability ✔ Multiple nephrotoxins Even then: 👉 Optimize volume 👉 Minimize dose 👉 Don’t delay critical imaging 🤓Bottom line ✔ Contrast nephrotoxicity exists… but is rare ✔ The fear is bigger than the risk ✔ The harm of NOT imaging is often greater In critical care 👉 We don’t treat creatinine 👉 We treat patients And sometimes… 👉 The most dangerous thing is NOT the contrast 👉 It’s hesitation. 📃Reference Florens N, Demiselle J. Kidney360 7: 445–449, 2026. doi: doi.org/10.34067/KID.0…

Prevention of Urinary Stones with Hydration - PUSH Trial 1. Didn't work 2. Tough to get pts to drink more water. The PUSH Trial in Lancet - thelancet.com/journals/lance… A nice synopsis of the trial here - nephjc.com/news/2026/4/2/…

Even in dialysis, the story of SGLT2 inhibitors doesn’t end at the tubule 🌿 > Cardiac protection ❤️ > Anti-inflammatory effects 🧬 > Gut–kidney axis modulation 🦠 > Volume & RKF benefits 💧 #NephTwitter #MedTwitter #FOAMed @CKJsocial @ISNeducation @ISNkidneycare

Beyond glucose — SGLT2 inhibitors are redefining kidney protection! #NephTwitter #MedTwitter #FOAMed

@DrSyeda_hurmath @arvindcanchi Congratulations 🥳

My first WCN conference in beautiful Japan—an enriching experience. Grateful for the opportunity to present my abstract. Thank you @arvindcanchi sir and Dr. Vinod Dibbur sir for your constant support, opportunity and guidance.#WCN2026

Rituximab In Membranous Nephropathy ! #glomseries #NephTwitter #FOAMed #MedTwitter

New clinical def for CKDu #isnwcn presentation by Ramon Trabanino

How to modify immunosuppressive on pregnancy #isnwcn

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

HF + CKD = treat by EF + eGFR 🎯 ✅HFrEF: <15 → β-blocker + nitrates 15–29 → + SGLT2i (>20) ± vericiguat 30–59 → + ARNI/ACEi/ARB + MRA ≥60 → full GDMT ✅HFpEF: SGLT2i backbone; add nsMRA (>25), ARNI if EF ~50% @goKDIGO pubmed.ncbi.nlm.nih.gov/41793402/