Great day-by-day recaps of #KidneyWk from the #NephJC team—perfect if you missed a session. Begin here 👉🏻 www.nephjc.com/news/2025/11...

Great day-by-day recaps of #KidneyWk from the #NephJC team—perfect if you missed a session. Begin here 👉🏻 www.nephjc.com/news/kidneyw...

Analysis of AKI-related mortality (43 countries, 1996–2021): ⬆️ in high-income nations (esp. older adults & women) and ⬇️ in LMICs. Drivers: HIC aging/comorbidity; LMIC younger pops + better infection control/access. Projection: gradual global rise to 2050. #KidneyWk25 #AKI

Great day-by-day recaps of #KidneyWk from the #NephJC team—perfect if you missed a session. Begin here 👉🏻 www.nephjc.com/news/kidneyw...

If you read only one obit of James Watson, read this one www.statnews.com/2025/11/07/j... (From the late Sharon Begley, for @statnews.com )

AI in Healthcare @asakhuja.bsky.social gave an excellent overview of what this entails, the opportunities and its limitations youtu.be/0qOaoGncKHw?... #NephGR #NephSky

Amazing #KidneyWk run

Why add thymus to a xenokidney (thymokidney)? → Induce central tolerance (new T cells see donor as self), cut T-cell rejection/DSA, enable lower IS (→ fewer infections/tox), and reduce chronic injury → longer graft life (early data). #KidneyWk #Xenotransplantation

Xenotransplant kidneys 👉🏻 ethics at #KidneyWk: Human 👩🏻 : autonomy/informed consent, unknown long-term risks, fair access, privacy. Animal 🐖 : robust welfare & 3Rs, limits on edits/breeding, humane endpoints, independent oversight. #Bioethics #Xenotransplantation

Xenokidneys at #KidneyWk: Trials are starting, but key hurdles remain—Rejection (AMR/TMA; anti-CD40 + C5 help, not cure). Technical (thrombosis; ureter/size). Infection (tight PCMV/PERV surveillance). Scale-up: DPF herds, standardized crossmatch, multicenter EXPAND trial.

#JustDoItSunday 🏃🏻‍♂️ #Run4Kidneys 🫘 ready for last day of #KidneyWk 2025 #850Challenge 🎗️

After AKI, don’t forget cardioprotective meds 💊 Observational data show restarting ACEi/ARB within 3–6 months is linked to lower mortality, while SGLT2i & statins also reduce death/CKD progression. Reintroduce when indicated, monitor K+ & kidney function. #AKI #KidneyWk

Post-AKI meds: • Dose smart: residual+dialysis CL, use TDM; PK/PD—vanc AUC/MIC>400; AG Cmax≈10×MIC; β-lactams time>MIC. • SGLT2i: ↓ CKD prog (aHR 0.72), ↓ recurrent AKI (0.75), ↓ mortality (0.63). • RAASi restart ≤6 mo → ↓ mortality (0.85). #AKI #KidneyWk

Starting HD? Don’t rush to 🛑loop diuretics. Medicare cohort (n=11,297): continuing loops ↓ hospitalizations (IRR 0.93), ↓ intradialytic hypotension (IRR 0.95) &↓ interdialytic weight gain; no mortality difference at 1 yr. If still making urine, consider continuing. #KidneyWk

AKI-D pearls: •Gentle UF & individualized Rx-minimize dialytrauma •⬇️frequency/intensity as recovery starts •Prevent IDH: 🆒 dialysate + slower UF •Consider tolerating pre-HD SBP 🆙 to 180 mmHg before starting antihypertensives to avoid recurrent AKI & aid ❤️‍🩹#KidneyWk

Blocking AKI: Nrf2 activation; senolytics/senomorphics (rapamycin, resveratrol, SGLT2i); mitochondrial protectors (NAD+); Klotho/SIRT1. Post-AKI care: assess vascular function + biological aging markers. #AKI #KidneyWk

AKI-D isn’t “ESRD lite.” Patients face ↑ disability, ↓HRQoL, CKD after “recovery,” and high CV events (Lee 2018). Outpatient HD still lacks ID flags, order sets, recovery monitoring, and dedicated teams. Time for AKI-D–specific pathways. #KidneyWk

AKI-D recovery is shaped by layers beyond the kidney: • Patient—older age, female, minority status, CKD/proteinuria, HF/CVD • Meds—nephrotoxins • Dialysis—↑UF/UFR, longer sessions, IDH • SDOH—neighborhood poverty, dual-eligibility (Babroudi et al., JASN 2024) #KidneyWk

LIBERATE-D RCT in AKI-D (n=218) — conservative dialysis (only when metabolic/clinical triggers) vs conventional 3x/wk. Kidney recovery at discharge: 64% vs 50% (ARR 13.8%). Adjusted OR NS → needs larger trial. #KidneyWk

Take-home from #KidneyWk💡 💧 Balanced crystalloids: modest survival benefit. 💉 IV bicarbonate: no survival advantage in severe acidosis overall. ⚠️ But in KDIGO stage 2–3 AKI + acidosis, may delay or reduce KRT need. The story of bicarb continues… #AKI #CriticalCare

BICARICU-2 insights 🔍 Event rates lower than expected, 15% crossover (controls got bicarb, 50% KRT). KRT reduction remains provocative—true renal protection or just buying time? Still not powered for MAKE-90. More data coming from MOSAICC & SODa-BIC! #KidneyWk

BICARICU-2: 627 adults with KDIGO stage 2–3 AKI + metabolic acidosis (pH≤7.2, HCO3≤20, SOFA≥4) in 43 French ICUs randomized to 4.2% NaHCO₃ (target pH≥7.30) vs usual care. Primary: 90-day mortality; key secondary: KRT, MAKE-90, organ failure. #KidneyWk

BICAR-ICU 389 adults with severe acidemia randomized to 4.2% IV bicarb vs usual care. Overall primary outcome neutral, but in AKI stage 2–3 bicarb ↓ composite events, mortality, organ failure & KRT use (52%→35%). More alkalosis, hyperNa, hypoCa. #KidneyWk

Treat acute metabolic acidosis? Bicarb may improve hemodynamics, arrhythmias, cellular energetics & immune function…but at the cost of intracellular acidosis, hypoK/hypoCa/alkalosis and Na⁺/volume load. Love this balanced view from Kraut & Madias at #KidneyWk

Amazing #KidneyWk 🏃🏻‍♀️ 🏃🏻‍♂️ Thank you, @kidneyboy.bsky.social and @nephjc.bsky.social for organizing it. @kdigo.org runners #Run4Kidneys 🫘 #850Challenge. Now we’re ready for day three of #KidneyWk !

Mixed or modest? Across SPLIT, SMART, BaSICS, PLUS & FLUID the signal is consistent: balanced crystalloids have ≈90% probability of a survival benefit in the critically ill. Effect modest, costs small. Prefer balanced (esp. sepsis/DKA); consider saline in TBI. #KidneyWk

PLUS RCT (NEJM 2022) 🇦🇺🇳🇿—53 ICUs, n=5,037: Plasma-Lyte 148 vs 0.9% saline for ICU resuscitation. 90-day mortality 21.8% vs 22.0% (OR 0.99); new RRT 12.7% vs 12.9%; max ↑SCr 0.41 vs 0.41 mg/dL. Bottom line: no difference. #KidneyWk

BaSICS 🇧🇷 75 ICUs(n=11,052). Plasma-Lyte 🆚 0.9% saline (fast vs slow). 90-day mortality 26.4% vs 27.2% (HR 0.97) → no overall difference; AKI/RRT/SOFA 🟰. Post-hoc: if pre-enrollment💧were balanced, mortality likely ↓ (92% overall; 96% sepsis). TBI signal harm. #KidneyWk

Balanced crystalloids beat saline in real-world care: • ICU (SMART): MAKE30 14.3% vs 15.4% (p=0.04) • ED (SALT-ED): 4.7% vs 5.6% (p=0.01) Also ↓ hyperchloremia & low HCO₃⁻. Default to balanced fluids. (NEJM 2018 SMART Trial) #ICU #AKI #KidneyWk

Normal saline isn’t “normal.” It reproducibly raises chloride and worsens acidemia vs balanced crystalloids. Observational/early studies link saline to ↑AKI, ↑RRT, ↑LOS, transfusions, ↑mortality. Choose balanced fluids first. (Young 2014; Shaw 2012; Yunos JAMA 2012) #KidneyWk

Dialysis in AKI = stability vs speed. In septic shock/poor EF/brain swelling—and if CRRT isn’t available—consider PD or PIRRT/SLED for better hemodynamic/ICP stability. IHD gives the fastest solute/fluids correction but ↑ osmolar shifts. (Ostermann, Blood Purif 2016) #KidneyWk

Invasive: CVP: simple trends, poor for fluid responsiveness. PAC: full hemodynamics but invasive; static pressures not predictive. TPTD: CO/GEDV/EVLW—useful but invasive. PWCA: continuous dynamic indices; limits with arrhythmias/vaso-tone. #KidneyWk

Non-invasive: Exam/CXR/BNP → poor for venous congestion. Lung+IVC US better; VExUS best—predicts AKI/HF events & guides decongestion. BIA/BIVA trend TBW/edema but can’t split intravascular vs interstitial; ↓accuracy in obesity. #KidneyWk

POCUS for volume/venous congestion = IVC + lungs + VExUS (not IVC alone). A-lines or small, collapsible IVC →give fluids. B-lines or plethoric IVC →diurese/dialyze. Don’t miss mimics (vasoplegia, PE, tamponade, pneumothorax). Grade congestion with VExUS. #POCUS #VExUS #KidneyWk

Fluid overload: recognize it at the bedside—rapid weight gain, pitting edema, crackles, ↑JVP, ascites. Labs can help; BNP/proBNP are most specific, many others are dilutional. Follow trends (not single values) and correlate with history, exam & imaging. #KidneyWk

Shock care: diagnose early & target physiology. Use multimodal endpoints (CRT, urine, mentation; lactate; MAP/ScvO₂/v-a CO₂ gap). Give fluids dynamically—stop when non-responsive. Aim guideline MAP. Start vasoactives early, matched to physiology. #KidneyWk

Sepsis resuscitation: start vasopressors earlier (w/ fluid restriction) vs fluids-first. CLOVERS: restrictive strategy (vasopressors first) did not lower 90d mortality vs liberal fluids. NE first; MAP 65; peripheral start ok; add vasopressin if needed. #KidneyWk #Sepsis #CLOVERS

HFpEF has a string kidney imprint. Cardio-renal loop → impaired renal function → salt/water retention → stiff LV. Single-cell ML prioritizes cardiomyocytes (CM1–3) as most perturbed; fibroblast FAP↑ & collagen remodeling (↑COL3A1) distinguish HFpEF from HFrEF. #KidneyWk

Adaptive/injured proximal tubule (aPT) organizes fibrotic niches—immune + Fib/MyoFib neighbors on 2-hop maps. “Factor 2” captures this niche, and its serum protein signature predicts incident CKD (UK Biobank). #CKD #KidneyWk

Mac–fibroblast axis in fibrosis: spatial mapping shows SPP1+ macrophages co-localize with myofibroblasts (Kuppe et al., Nature ’22). CXCL4 loss blunts Spp1-Mac expansion after IRI (Hoeft & Schaefer, Cell Rep ’23). CXCL4→SPP1+ Macs = targetable. #KidneyWk #Fibrosis

Mac–fibroblast axis in fibrosis: spatial mapping shows SPP1+ macrophages co-localize with myofibroblasts (Kuppe et al., Nature ’22). CXCL4 loss blunts Spp1-Mac expansion after IRI (Hoeft & Schaefer, Cell Rep ’23). CXCL4→SPP1+ Macs = targetable. #KidneyWk #Fibrosis

Fibrosis may start at the microvasculature: pericyte/Fib1-2 cells detach from capillaries → myofibroblasts. In IRI, distance rises 3.6→13.1 µm. ADAMTS12 is implicated—an early target to stop rarefaction & scar. #KidneyWk #Fibrosis

Rise and run, #KidneyRunners! 🌞🏃🏻 Day 2 at #KidneyWk 👉🏻 the warm-up for tomorrow’s #NephJC run is on. #Run4Kidneys 🫘 #850Challenge

Biomarker-driven AKI subphenotypes illuminate biology & prognosis—and reveal who benefits (or is harmed) by therapy. Keys: reproducible clusters across datasets, sCr persistence > magnitude, trial enrichment, gene–environment focus, and prospective validation. #KidneyWk #AKI

Subphenotyping can change answers. In CLOVERS: SP2 (“leaky endothelium”) had lower mortality with early vasopressors (restrictive fluids), while SP1 favored fluids. EUPHRATES/TIGRIS: endotoxin 0.6–0.9 subgroup signaled benefit → smarter, targeted trials. #KidneyWk #Sepsis #AKI

Biomarker-based AKI subphenotyping: ASSESS-AKI (n=748) clusters into SP1 cardiorenal injury, SP2 benign, SP3 AKI-on-CKD, SP4 sepsis. LCA with Ang2/Ang1 + sTNFR1 separates “leaky” vs “healthy” endothelium—enabling trial enrichment & targeted therapy. #KidneyWk #AKI

Creatinine trajectory ≠ noise it’s a subphenotype. Persistent AKI = highest risk: ↑ short-term mortality/AKD & long-term mortality/KRT; relapse tends to do better than persistence. Patients with relapse/persistence need follow-up & trials targeting trajectories. #KidneyWk #AKI

SA-AKI isn’t one disease. Precision moves from subphenotypes → endotypes → treatable traits. Key drivers: inflammation, microcirculatory dysfunction, metabolic reprogramming. Trials must match therapy to biology—sometimes multiple targets. #KidneyWk #AKI #Sepsis

AI’s promise in nephrology: leverage EHR + bedside data to spot early signals, predict risk, and shift care from detection → prevention. Evidence: up to 48h earlier AKI prediction, AUC >0.90—capturing complex patterns we can’t see. #KidneyWk #AKI

Outpatient CT contrast protocol Outpatient CT: an EHR e-alert (eGFR<45) with 1-click prophylaxis + lab follow-up improved process measures (timely SCr checks, standardized fluids) and streamlined care for post-contrast AKI risk. Workflow > warning alone. #AKI #KidneyWk