Kyle Grey @kg4425

If you have ever heard, read or written the phrase “the patient is edematous but intravascular dry”, you have to check this review (doi.org/10.1186/s13054…) 👇 Fluid normally exchanges freely between the plasma and interstitial space and is returned to the “central circulation” primarily via the lymphatics. In disease states, such as sepsis, the return flow of fluid from the interstitial space to the plasma seems to be very slow, which promotes the well-known triad of "hypovolemia + hypoalbuminemia + peripheral edema" The authors discuss studies suggesting that there two key mechanisms contributing to this triad: (1) acute lowering of the interstitial pressure by inflammatory mediators such as TNFα, IL-1β, and IL-6 and, (2) nitric oxide-induced inhibition of the intrinsic lymphatic pumping As you know, fluid is filtered in the (pre-)capillary side and reabsorbed at the post-capillary end, right? Well, not really... According to the traditional model historically taught in introductory physiology and medical school (I still remember it...), in the precapillary (arteriolar) end, the high capillary hydrostatic pressure exceeds plasma oncotic pressure, causing net filtration of fluid out of the vessel into the interstitial space. In the post-capillary (venular) end, the hydrostatic pressure drops below plasma oncotic pressure, creating a net pressure gradient that causes reabsorption of ~90% of the filtered fluid back into the vessels. The remaining ~10% was thought to be drained by the lymphatic system According to the modern model (established via the discovery of the endothelial glycocalyx), in most tissues under normal, steady-state conditions, there is no sustained venular reabsorption. The endothelial glycocalyx layer acts as the primary semi-permeable filter. The effective oncotic gradient exists between the plasma and the subglycocalyx space, rather than the main interstitial fluid Under normal blood pressure, capillary hydrostatic pressure exceeds the effective opposing oncotic pressure across the entire length of continuous capillaries and post-capillary venules. Consequently, virtually all fluid filtered at the capillary level is picked up by the lymphatics, which then route the fluid through lymph nodes and return it to the venous system via the lymphatic ducts. Some exceptions exist in specialized vascular beds designed for continuous fluid absorption, such as the intestinal mucosa and renal peritubular capillaries. Also direct vascular reabsorption may occur temporarily during acute, severe drops in capillary hydrostatic pressure (e.g., severe hypovolemic shock or hemorrhage) to preserve plasma volume #foamed #foamcc #physiology

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@drkeithsiau Hypokalemic Periodic Paralysis (Andersen-Tawil)

@GUC_Info Power outage in Woodmoor

This was Hollywood scale academic fraud. Patients with a disabling condition (ANCA+ vasculitis) were treated with an ineffective drug, in the name of profit. Serious jail time is not only deserved but necessary to deter others.

Anish Koka, MD @anish_koka

4 months ago

On June 30, 2026, the NEJM retracted the clinical trial that got a drug approved by the FDA, triggering a $3.7B acquisition by Amgen. The reason: the primary endpoint data was manipulated. Here's how it happened, how it came to light, and who paid the price. 🧵

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Physiology first. 👉 Dilutional anemia (plasma expands more than RBC mass), physiologic Hb 10.5-11 👉 Hypercoagulable: ⬆️ VII, VIII, X, vWF, fibrinogen; ⬇️ protein S 👉 VTE risk 5x in pregnancy, ~20x postpartum

Hyper-subspecialization is all fun and games. Until the weekend. Suddenly the left pinkie specialist is covering general surgery.

What is this triad?

Alright, so now that we can confirm Bungie leadership was indeed involved in every step of deciding to end Destiny, I’ve got some unfiltered thoughts. -The content vault was the sole destroyer of all positive momentum and sentiment for the game when players now had to spend money on new expansions every year or two with an inherent fear that content would be vaulted anyways. “Pay for access” is the death of player investment and the DCV highlighted itself as the most destructive decision ever made in any game to-date. -Destiny 3 should’ve been green-lit immediately after the Witch Queen, Lightfall, and Final Shape reveals in 2020 and 2021. It would’ve been the perfect lead-in for concluding Destiny 2. They knew the saga was concluding with Final Shape and the game was becoming too bloated. Had they decided to do so, they could’ve announced Destiny 3’s release at this very moment 5-6yrs later. It also would’ve been the perfect bargaining chip to PlayStation for the acquisition by showing longevity of an established and secure IP with a clear title release forthcoming. -I can guarantee a very large base of players will decide to avoid this “new journey” in Bungie if it isn’t Destiny 3. This demographic of players over the last 10yrs are Destiny fans who spent the last decade exclusively in Destiny - even bringing their kids to enjoy. For sure, you’ll have many who will try whatever comes next, but if it isn’t Destiny, you’re going to have a very large gap. -Marathon’s “strong foundation” is grossly over-exaggerated. Don’t get me wrong, it’s a very good game that plays unbelievably well and perfectly emanates the identity of Bungie, but its retention concerns are so evident that to deny its existence is damaging. An extremely large portion of marathon players migrated from Destiny and are the core audience to consider here. To Shut down their original game with no plan in sight while saying “we have this instead” will not produce positive results. If marathon wants to succeed beyond its extraction mode, it needs a world built like Destiny, told like Destiny, and world-shaped from the marathon lore that’s been build since the 1990’s. -If Destiny 3 is not in development and they have no plans to continue the franchise, sell the rights to another reputable studio who believes in the IP and will keep it alive. Destiny is arguably the best looter shooter that defined a literal genre and to abandon development of one of the biggest established IP’s in history is a terrible business decision. -All of this stems from terrible decision making from the top-down. The game went from creating one of the greatest gaming worlds and stories ever made over the last decade to dollar signs and spreadsheets first. Game success comes from building a full experience that players cannot help but be immersed in. Blaming “industry shifts” for a game struggling is code for “we aren’t getting it right on our end because we’re making the wrong decisions at the wrong time.” The players haven’t changed; the reason for developing a game did. I’m angry. I’m frustrated. I’m sad. I’m hurt. I’m lost. Destiny was home for over 10yrs. I’ll see y’all in the tower.

Basically the whole D2 Sandbox team is gone, myself included. The good news is if you liked the way Destiny felt to shoot and play, there’s going to be a lot of great designers in the market looking to help other games step it up.

x.com/i/article/2067…

I'm a cardiologist. I prescribe cholesterol-lowering drugs every single day. They save lives. That science is settled and I will never tell you otherwise. But I'm going to say something that will make a lot of my colleagues uncomfortable — because someone needs to say it, and your doctor probably won't. Too many physicians make you feel crazy when you bring up statin side effects. You walk into your appointment and say "my muscles ache constantly" — and you're told it's in your head. You say "I'm exhausted all the time" — and you're told it's your age. You say "my sex drive disappeared" — and you get an awkward silence followed by a subject change. You say "I don't feel like myself anymore" — and you're told the benefits outweigh the risks, take the pill, stop reading the internet. I've watched it happen in my own field for twenty years. The conversation gets shut down. The patient gets dismissed. And then they do the one thing we should be most afraid of — they stop the medication entirely, without telling us, and lose the cardiovascular protection that's keeping them alive. That is the real cost of not being honest. Not the side effects themselves — the silence that drives patients away from treatment. In my practice, I see statin-related complications in at least 25% of my patients. Muscle pain. Fatigue that doesn't resolve with sleep. Reduced sexual drive. Brain fog. Cramping. Joint stiffness. Weakness that makes exercise — the very thing we tell them to do — feel impossible. Some of these improve with CoQ10 supplementation and optimizing vitamin D. Many do not. I wrote about the diabetes risk of statins in a New York Times op-ed in 2012. The backlash from the cardiology establishment was immediate. I was told I was undermining trust in a life-saving drug class. Fourteen years later, every major guideline acknowledges the risk I warned about. It's in the prescribing information. The physicians who attacked me for saying it now teach it to their residents. The truth doesn't care about professional comfort. It never has. Now a paper published this week in Science Advances has finally explained the mechanism behind statin myopathy — and the finding validates what millions of patients have been telling their doctors for years. Researchers discovered that statins activate the NLRP3 inflammasome in muscle cells — triggering an inflammatory cascade that causes muscle cell death, activates atrophy pathways, and disrupts muscle metabolism. This is entirely independent of the drug's cholesterol-lowering effect. The muscle damage isn't caused by lowering cholesterol. It's caused by a completely separate pharmacological action through a different pathway. The critical implication: the side effect can potentially be separated from the benefit. Blocking NLRP3 or restoring isoprenoids prevented muscle cell death without interfering with cholesterol reduction. Future therapies could preserve the cardiovascular protection while eliminating the muscle toxicity. Even more striking — the researchers found that background systemic inflammation significantly lowered the statin dose needed to trigger muscle damage. Patients with chronic inflammation, gut dysbiosis, or metabolic syndrome may be experiencing myopathy at doses their doctors consider "too low to cause problems." They're not imagining it. Their inflammatory state is priming the pathway. The muscle pain was never in their heads. It was in their NLRP3 inflammasome. And we finally have the molecular proof. Here's what I actually do in my practice — because I refuse to choose between protecting the heart and respecting the patient. Whenever possible, I avoid statins as my first-line approach for eligible patients by using alternatives that lower LDL through entirely different mechanisms with no muscle toxicity: PCSK9 inhibitors — Repatha and Praluent. Injections every 2-4 weeks that dramatically lower LDL without touching muscle tissue. No myopathy. No fatigue. No brain fog. For patients who can access them, these are transformative. Inclisiran — Leqvio. An siRNA injection I administer twice a year in my office. It silences the PCSK9 gene in the liver. Two shots a year. LDL drops roughly 50%. No muscle side effects. No daily pills. Now approved as first-line monotherapy. This is the future of lipid management and I use it aggressively. When statins ARE clinically necessary — and sometimes they are, especially post-heart attack or in combination therapy — I choose hydrophilic statins like rosuvastatin or pravastatin. These do not easily cross the blood-brain barrier. The cognitive complaints — the fog, the memory issues, the feeling of "not being yourself" — are substantially less common with these formulations because the drug stays out of the central nervous system. I never prescribe a statin without CoQ10. 100-300mg daily. Statins deplete the cellular energy molecule your muscles and heart depend on. Replenishing it reduces muscle symptoms in many patients. It should be standard practice. The fact that it isn't is a failure of our field. I check vitamin D and optimize it aggressively. Low vitamin D — which is epidemic — worsens muscle symptoms independently and compounds whatever the statin is doing. Target 50-80 ng/mL, not the bare minimum of 30. Bempedoic acid — Nexletol — for patients who can't tolerate any statin. Works upstream in the cholesterol pathway and is not active in muscle tissue. Specifically designed to avoid myopathy. Ezetimibe added to a lower statin dose. Cut the statin intensity, add ezetimibe to maintain the LDL reduction, and halve the muscle exposure. There is no excuse in 2026 for telling a patient "just deal with the muscle pain." The toolbox is deep. The alternatives exist. The only barrier is a physician's willingness to listen and adapt. I want to speak directly to every patient who has been dismissed. Your muscle pain is real. Your fatigue is real. Your cognitive changes are real. Your loss of drive — in every sense of the word — is real. A paper in Science Advances just proved the mechanism. You were never crazy. You were experiencing a documented inflammatory response in your muscle tissue that your doctor didn't have the science to explain — until this week. And I want to speak directly to my colleagues. We have to be honest. Not just about the benefits — which are enormous and undeniable — but about the side effects, the mechanism, and the alternatives. Patients who feel heard stay on treatment. Patients who feel dismissed stop their medications in silence — and die from the heart attacks we could have prevented if we'd simply been willing to have an honest conversation and switch the approach. The cardiologist who tells you statins are flawless is not protecting you. The wellness influencer who tells you statins are poison is not protecting you either. The truth lives in the middle — where it always has. Statins save lives. The side effects are real. The mechanism is now proven. The alternatives exist. And you deserve a doctor who holds all four of those truths at the same time. Both things can be true. They always could. Now we have the science to prove it.

Furosemide spiked 💉 with Albumin 👍🏼 or 👎🏼 #Nephpearls m.ajcc.aacnjournals.org/content/21/4/2…

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Aprocitentan in Patients With CKD and Resistant Hypertension ca. 2026 #Nephpearls ✅ Well tolerated ✅ Efficiently lowered BP, particularly nighttime ambulatory BP ✅ Markedly reduced urine albumin-to-creatinine ratio (UACR) in participants with CKD and resistant hypertension 👉 pubmed.ncbi.nlm.nih.gov/41363010/

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Harrison Barnes has been rocking #UNC team-issued Jordan 40s in the NBA Finals. The Black Falcon is still the highest-rated recruit to commit to the Tar Heels in the modern recruiting era (since 2000). Has made $221.1 million in career contract earnings. Legend.

Hypocomplementemia in glomerular diseases #Nephpearls #ECNeph Testing for complement activation is an essential early step in the evaluation of glomerular disease, whether limited to the kidney or part of a systemic syndrome In clinical practice, it is most common to measure the serum levels of complement components C3 and C4. C3 levels can be decreased by complement activation through any of the three pathways (classical, alternative, or lectin), whereas low C4 levels are generally indicative of activation through the classical pathway Thus, a finding of hypocomplementemia of C3, C4, or both can provide early clues as to the pathogenic mechanism at play and help hone in on the diagnosis. shop.lww.com/Handbook-of-Gl…

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BREAKING: Matt Able is withdrawing from the NBA Draft and headed to UNC. Story: on3.com/teams/north-ca…

Things that didn’t exist last time the Knicks were in the NBA finals: iPhone Facebook Instagram YouTube 𝕏 Tesla SpaceX Bitcoin Gmail Amazon Prime Google Maps Netflix streaming Android ChatGPT WhatsApp TikTok Snapchat Xbox Pinterest LinkedIn iPad Uber Airbnb Reddit Spotify Zoom

He's completely incompetent, even apart from being deranged.

Ben Meiselas @meiselasb

5 months ago

You are seeing in real time why Trump companies went bankrupt so many times. Set aside your politics. This guy is incapable of making a deal or meaningful decision and it follows the same cycle. Big flashy announcement (Epic Fury). Adversity hits (Hormuz closed). Defraud

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@mkizziah Thats simple 🔆t test 👉For quantitative data 👉Compare means b/w two groups 👉small sample size 🔆Chi Square test 👉For qualitative data 👉Compare proportions b/w two groups Ref-ilstu. edu #FOAMed #MedTwitter #MedEd

🚰 Hemodialysis is no longer just about diffusion. 💡 The future is convective. #Hemodiafiltration (#HDF) combines diffusion + convection to achieve superior clearance of middle molecules and protein-bound toxins. 📚 Trials like • ESHOL Trial • CONTRAST Trial • CONVINCE Trial suggest better survival and cardiovascular outcomes with high-volume HDF. 🎯 Target convection volume: ➡️ ≥ 23 L/session Why nephrologists are increasingly embracing HDF: ✅ Better middle molecule clearance ✅ Improved hemodynamic tolerance ✅ Better phosphate control ✅ Reduced inflammation ✅ Potential survival benefit “More than filtration. It’s better purification. It’s better care.” #GSR #BuddingNephros #Nephrology #Dialysis #KidneyDisease #CKD #NephTwitter #MedTwitter #HDF