Nephro

🚨 ADPKD & CKD Management part 2 #KDIGO Thread 🧵 🚨

ADPKD—Kidney replacement therapy (Dialysis) 📍Dialysis modality choice = shared decision-making 📍Choose HD vs PD based on patient factors + patient choice + facility availability (2C) 📍No survival difference between PD & HD. 📍PD is a viable option in ADPKD kidney failure ✅ ▪️Use caution only if massive kidney/liver enlargement or other standard PD contraindications 📍HD prescription + supportive care (e.g., anticoagulation) = same as non-ADPKD 📍Evidence summary (PD vs HD in ADPKD): ▪️Mortality: no significant difference ( ▪️On PD (ADPKD vs non-ADPKD): no significant differences in Kt/V, peritoneal leaks, peritonitis, switch to HD, technique failure, exit-site infection, or mortality ▪️Hernias: more common in ADPKD on PD ▪️Median technique failure: 6.2 yrs (ADPKD) vs 6.5 yrs (non-ADPKD) ▪️Median time to death: 6.04 yrs (ADPKD) vs 5.57 yrs (non-ADPKD) ▪️More switching PD → HD ▪️One study: hospitalization for infection higher with PD vs HD (58% vs 44%); possible ↑ hernia surgery (7% vs 4%)

Cont. ADPKD—Kidney transplantation cont ⚫️Nephrectomy 📍 Native nephrectomy NOT routine ▪️do only for specific indications when benefit > risk (2C) ▪️ 9 studies—no clear benefit for graft loss or all-cause mortality after Nephrectomy ▫️possible higher transfusion risk if nephrectomy done at time of transplan ▫️note kidneys often shrink up to ~30% in 1st year post-Tx (may improve symptoms) 📍Prefer unilateral over bilateral nephrectomy when appropriate (2D) ✅ (lack of benefit for bilateral + concern for higher complications, e.g., refractory hypotension) 📍Pre-Tx nephrectomy: meta-analysis shows near-significant ↑ long-term mortality; large database suggests ↑ in-hospital post-Tx death 📍Consider longer operative time + transfusion risk → individualized planning 📍 Timing when nephrectomy needed 🕰️: suggested at time of or after transplant, not before, whenever possible (2C) 📍 Surgical approach 🔧: ▪️when feasible, hand-assisted laparoscopic over open nephrectomy (2D) ✅ (similar complications overall, less transfusion) ⚫️(RCC screening pre tx): 📍Individualize RCC evaluation; consider kidney imaging (e.g., abdominal MRI) within 1 year before anticipated transplant 📍Most studies: significant RCC risk not increased vs other etiologies ▪️some cohorts suggest increased RCC in ADPKD 📍Prefer noncontrast MRI in kidney failure/dialysis ▪️give gadolinium (group II) only if necessary  📍MRI advantages: ▪️better soft tissue ▪️can classify simple vs hemorrhagic/proteinaceous cysts ▪️solid lesions have intermediate signals + DWI helps 📍if solid lesion suspected (not AML), consider contrast for enhancement/staging; CEUS possible but often limited in ADPKD due to size/multiplicity

🚨 ADPKD & CKD Management part 2 #KDIGO Thread 🧵 🚨

IgA Nephropathy #IgAN: An Overview of the Clinical Trials ca. 2025 from @KidneyMed @ZohrehGh7 @haresh11 @NWiegley @Alexgr23 @rahaai @SaynaNorouzi @JEGAYTAN90 #Nephpearls 👉 kidneymedicinejournal.org/article/S2590-…

@goKDIGO @kidneydoc101 @BradRovin @ISNWCN @ISNkidneycare Which time zone?

Are you attending #ISNWCN? Join us for the KDIGO session: 📌 IgA Nephropathy in 2025: Bridging the Gap Between Knowledge & Practice 🗓️ Saturday, February 8, 13:00-14:00 📍 Amaltas B Hall – B101B 📺 Livestream: #industry-symposia-saturday" target="_blank" rel="nofollow noopener">theisn.org/wcn/industry/l… Moderated by Liz Lightstone, the session features Hernán Trimarchi on #IgAN pathophysiology, diagnosis, prognosis & global implementation. Brad Rovin will present case-based treatment strategies, followed by a 15-minute Q&A-- a great opportunity to learn & engage. We hope to see you there! #WCN25 🇮🇳

@DrNeilStone And all from IT and research centre 😑

Clearing email inbox after a break from work

@teachplaygrub Do you know AI websites that can help with imaging?"

1/Radiologist not answering the phone? Just want a quick read on that stat head CT? Here's a little help on how to do it yourself w/a thread on how to read a head CT!

Differential Diagnosis ▪️Acquired Kidney Cysts: ↑ with age, no family history •0% (15-29 yrs) •1.7% (30-49 yrs) •11.5% (50-70 yrs) •22.1% (≥70 yrs) •Bilateral cysts rare <50 yrs ▪️ Localized Cystic Disease: Single kidney, no family history, non-progressive. ▪️ Acquired Cystic Kidney Disease: Small bilateral cysts in CKD, ↑ risk of RCC, normal/small kidney size. ▪️ Drug/Metabolic Cysts: Lithium, crizotinib, dRTA, Carney complex, rickets. ▪️ Collagen Mutations: HANAC, thin basement disease → cysts + microhematuria. ▪️ Parapelvic Cysts: Lymphatic cysts sparing cortex (≠ADPKD). ▪️ Medullary Sponge Kidney: Medulla cysts, stones, nephrocalcinosis, normal cortex. ▪️ Genetic Cystic Diseases: •ARPKD •TSC: Angiomyolipomas, facial signs. •VHL: Cysts + retinal, clear cell cancer. •ADTKD: Small kidneys, gout. •HNF-1B: Cysts + systemic signs. •OFD1: Cysts + oral, facial, digital anomalies.

Here’s a comprehensive review of biomarkers of kidney disease progression in adults and children with ADPKD @fouadchebib 📍eGFR → Indexed for age, identifies rapid vs. slow progressors. 📍Sex → Sex: Males have ↑ TKV, more severe ADPKD, reach KF ~5 yrs earlier. 📍PROPKD score → Combines sex, HTN, genotype for KF risk stratification. 📍BMI → ↑ BMI linked to faster TKV growth and eGFR decline. visceral fat is a better predictor of progression. 📍Macrovascular Disease → ↑ HTN, stroke, CV disease with age = faster kidney decline. 📍Salt Intake → ↑ intake → ↑ eGFR. 📍KFRE → Predicts eGFR decline or RRT need using age, sex, eGFR, ACR. 📍TKV/htTKV → predicts CKD 3 within 8 yrs, early predictor of ↑ GFR . 📍Mayo Imaging Classification → htTKV + age classify rapid progressors (1C-1E) with faster GFR decline. 📍Imaging Texture → Features like entropy improve prediction of CKD stage 3 📍Cyst Segmentation → Biomarkers like TCV and CPSA predict disease progression. 📍PKD Genotype → PKD1/PKD2 variants impact disease severity and KF onset. 📍Serum Bicarbonate → Lower levels predict faster progression. 📍Copeptin → ↑ levels linked to ADPKD progression and response to tolvaptan. 📍Serum Uric Acid → ↑ levels predict faster TKV growth and KF onset. Urinary Inflammatory Markers → 📍Biomarkers like MCP-1, KIM-1 predict damage and progression. 📍Urine Metabolites → PKM2 and cAMP tied to progression. 📍Tubular Secretion Markers → Impaired secretion linked to fibrosis and progression. 📍Urine-to-Plasma Urea Ratio → Predicts urine concentrating defects and faster progression. 📍Asymptomatic Pyuria → Linked with earlier KF and faster ↑ eGFR.

Summary of Autosomal dominant polycystic kidney disease (ADPKD) part1 #nephSAP 🧵