Christoph Bammer 🩺 🎸

www.preprints.org/manuscript/2...

We can learn so much from @resiapretorius.bsky.social, @dbkell.bsky.social & team! A stunning preprint!

Das Gefühl, wenn in der Strategiebesprechung zum „Umgang mit COVID-19 im Krankenhaus“ die „Das-Internet-ist-für-uns-alle-Neuland“-Vibes förmlich greifbar sind.

Dafür gibt es aber einen griffigen Hashtag, den ich gerne zur Selbstreflexion anbieten möchte: #BrainHealthChallenge
3/3

Bell-Skala 30 - 40.
In Österreich.
2025.
Ich warte noch auf die Pointe.
Vielleicht findet man sie ja in der „Standortbestimmung der ÖGN zum postakuten Infektionssyndrom (PAIS)“?
Leider nein.
2/3

Ein Herr Professor, seines Zeichens Facharzt für Neurologie und Psychiatrie, mit einer beeindruckenden Karriere auch in Forschung und Lehre, schreibt in seinem PVA-Gutachten, dass die Erkrankung ME/CFS nicht existiert, da es sich um eine rein psychiatrische Störung handle.
1/3

Write a horror story using only three words

„…auf Sicht gesehen…“
(those who know)

Just imagine the possibilities, particularly for severely affected PAIS or ME patients, if combined with something like daratumumab, and all without the need for an extracorporeal procedure.

Someone really should be researching this.
4/4

How to Cure Autoimmune Glomerulonephritis and... : Journal of the American Society of Nephrology dium-glucose transporter 2 inhibitors are considered as “supportive care” and control of proteinuria, seems a primary treatment goal without reasoning the cause of proteinuria. We propose to refine these concepts based on the shared pathophysiology of these diseases: 1. Disease acuity as the primary determinant of therapy. Rapidly progressive GN, relapsing GN, and chronic GN require different priorities. Rapidly progressive GN depends on the level and nephrotoxicity of the involved antibodies and complement activation, and may require immediate complement inhibition and antibody removal from the circulation before a B cell-targeting therapy is initiated to control de novo autoantibody production. 2. Relapsing or chronically active disease need long-term control of immunological activity with a B cell-targeting monotherapy, in case of single autoreactive lymphocyte clones, e.g., in ANCA vasculitis or anti-nephrin/anti-PLA2R-nephrotic syndrome. In contrast, diseases with numerous autoantigens/clones, i.e., lupus nephritis or anti-phospholipid syndrome should benefit from combination therapies, similar to kidney transplantation. 3. All forms of GN and most relapsing podocytopathies lead to glomerulosclerosis and nephron loss, i.e., CKD. This implies CKD management following the latest KDIGO CKD risk matrix and treatment recommendations. In relapsing GN/podocytopathies, CKD care is the second treatment priority; in chronic GNs it becomes the first treatment priority in contrast to “supportive care”. In relapsing and chronic disease, proteinuria levels may represent either activity, CKD or both; hence, proteinuria alone does not inform treatment choices. This review aims to overcome existing hurdles by redefining treatment pritorities in GNs and podocytopathies based on the underlying autoimmune pathomechanisms to define immunotherapy and by implementing CKD care for conceptual clarity and better long-term outcomes. Autoimmune glomerulonephritis (GN) and podocytopathies are immune-mediated kidney diseases with different clinical presentations and histotypes. Traditionally, proteinuria and histotypes are used for prognosis prediction and hence define intensity of immunotherapy. Renin-angiotensin system and sodium-glucose transporter 2 inhibitors are considered as “supportive care” and control of proteinuria, seems a primary treatment goal without reasoning the cause of proteinuria. We propose to refine these concepts based on the shared pathophysiology of these diseases: 1. Disease acuity as the primary determinant of therapy. Rapidly progressive GN, relapsing GN, and chronic GN require different priorities. Rapidly progressive GN depends on the level and nephrotoxicity of the involved antibodies and complement activation, and may require immediate complement inhibition and antibody removal from the circulation before a B cell-targeting therapy is initiated to control de novo autoantibody production. 2. Relapsing or chronically active disease need long-term control of immunological activity with a B cell-targeting monotherapy, in case of single autoreactive lymphocyte clones, e.g., in ANCA vasculitis or anti-nephrin/anti-PLA2R-nephrotic syndrome. In contrast, diseases with numerous autoantigens/clones, i.e., lupus nephritis or anti-phospholipid syndrome should benefit from combination therapies, similar to kidney transplantation. 3. All forms of GN and most relapsing podocytopathies lead to glomerulosclerosis and nephron loss, i.e., CKD. This implies CKD management following the latest KDIGO CKD risk matrix and treatment recommendations. In relapsing GN/podocytopathies, CKD care is the second treatment priority; in chronic GNs it becomes the first treatment priority in contrast to “supportive care”. In relapsing and chronic disease, proteinuria levels may represent either activity, CKD or both; hence, proteinuria alone does not inform treatment choices. This review aims to overcome existing hurdles by redefining treatment pritorities in GNs and podocytopathies based on the underlying autoimmune pathomechanisms to define immunotherapy and by implementing CKD care for conceptual clarity and better long-term outcomes. Copyright © 2025 by the American Society of Nephrology...

The compound is gradually moving beyond its original use in transplantation medicine into the mainstream of nephrology, for example, as part of new treatment approaches for GBM-associated glomerulonephritides (journals.lww.com/jas...).
3/4

I’ve long wondered whether this enzyme might actually be superior to plasmapheresis, especially when combined with subsequent B-cell depletion, and whether it could hold therapeutic potential in treating #PAIS, including #ME/CFS.
2/4

Every now and then, I come across #Imlifidase again, an enzyme capable of cleaving circulating and bound IgG antibodies.
1/4

in Kombination mit Daratumumab und ganz ohne extrakorporales Verfahren.
Irgendjemand sollte da mal dran forschen.
4/4

How to Cure Autoimmune Glomerulonephritis and... : Journal of the American Society of Nephrology dium-glucose transporter 2 inhibitors are considered as “supportive care” and control of proteinuria, seems a primary treatment goal without reasoning the cause of proteinuria. We propose to refine these concepts based on the shared pathophysiology of these diseases: 1. Disease acuity as the primary determinant of therapy. Rapidly progressive GN, relapsing GN, and chronic GN require different priorities. Rapidly progressive GN depends on the level and nephrotoxicity of the involved antibodies and complement activation, and may require immediate complement inhibition and antibody removal from the circulation before a B cell-targeting therapy is initiated to control de novo autoantibody production. 2. Relapsing or chronically active disease need long-term control of immunological activity with a B cell-targeting monotherapy, in case of single autoreactive lymphocyte clones, e.g., in ANCA vasculitis or anti-nephrin/anti-PLA2R-nephrotic syndrome. In contrast, diseases with numerous autoantigens/clones, i.e., lupus nephritis or anti-phospholipid syndrome should benefit from combination therapies, similar to kidney transplantation. 3. All forms of GN and most relapsing podocytopathies lead to glomerulosclerosis and nephron loss, i.e., CKD. This implies CKD management following the latest KDIGO CKD risk matrix and treatment recommendations. In relapsing GN/podocytopathies, CKD care is the second treatment priority; in chronic GNs it becomes the first treatment priority in contrast to “supportive care”. In relapsing and chronic disease, proteinuria levels may represent either activity, CKD or both; hence, proteinuria alone does not inform treatment choices. This review aims to overcome existing hurdles by redefining treatment pritorities in GNs and podocytopathies based on the underlying autoimmune pathomechanisms to define immunotherapy and by implementing CKD care for conceptual clarity and better long-term outcomes. Autoimmune glomerulonephritis (GN) and podocytopathies are immune-mediated kidney diseases with different clinical presentations and histotypes. Traditionally, proteinuria and histotypes are used for prognosis prediction and hence define intensity of immunotherapy. Renin-angiotensin system and sodium-glucose transporter 2 inhibitors are considered as “supportive care” and control of proteinuria, seems a primary treatment goal without reasoning the cause of proteinuria. We propose to refine these concepts based on the shared pathophysiology of these diseases: 1. Disease acuity as the primary determinant of therapy. Rapidly progressive GN, relapsing GN, and chronic GN require different priorities. Rapidly progressive GN depends on the level and nephrotoxicity of the involved antibodies and complement activation, and may require immediate complement inhibition and antibody removal from the circulation before a B cell-targeting therapy is initiated to control de novo autoantibody production. 2. Relapsing or chronically active disease need long-term control of immunological activity with a B cell-targeting monotherapy, in case of single autoreactive lymphocyte clones, e.g., in ANCA vasculitis or anti-nephrin/anti-PLA2R-nephrotic syndrome. In contrast, diseases with numerous autoantigens/clones, i.e., lupus nephritis or anti-phospholipid syndrome should benefit from combination therapies, similar to kidney transplantation. 3. All forms of GN and most relapsing podocytopathies lead to glomerulosclerosis and nephron loss, i.e., CKD. This implies CKD management following the latest KDIGO CKD risk matrix and treatment recommendations. In relapsing GN/podocytopathies, CKD care is the second treatment priority; in chronic GNs it becomes the first treatment priority in contrast to “supportive care”. In relapsing and chronic disease, proteinuria levels may represent either activity, CKD or both; hence, proteinuria alone does not inform treatment choices. This review aims to overcome existing hurdles by redefining treatment pritorities in GNs and podocytopathies based on the underlying autoimmune pathomechanisms to define immunotherapy and by implementing CKD care for conceptual clarity and better long-term outcomes. Copyright © 2025 by the American Society of Nephrology...

bei neuen Behandlungskonzepten von z. B. GBM-assoziierten Glomerulonephritiden (journals.lww.com/jas...).
Nicht auszudenken, was u. U. alles möglich wäre (auch für PAIS- bzw. ME-Schwerbetroffene) z. B.
3/4

in Kombination mit anschließender B-Zell-Depletion, und ob es nicht einen therapeutischen Stellenwert haben könnte in der Therapie von #PAIS inkl. #ME/CFS.
Langsam kommt die Substanz nämlich auch aus der Transplantationsmedizin in den Mainstream der Nephrologie, bspw.
2/4

In gewissen Abständen stolpere ich immer wieder über #Imlifidase, ein Enzym, das zirkulierende und gebundene IgG-Antikörper spalten kann. Seit jeher frage ich mich, ob dieses Enzym der Plasmapherese nicht überlegen ist, v. a.
1/4

PEM-Erfassung fehlen.
Die Caveats bzgl. GET bei PEM müssten klarer formuliert werden.

P.S.: DOI führt (dzt. noch?) ins Leere.
6/6

Die Evidenz bzgl. „20 % Long-COVID = ME/CFS“ muss man mit einer Prise Salz nehmen; es ist nicht so einfach (nach welchen Kriterien und Follow-ups?).
Die hervorgehobene labordiagnost. Batterie ist diskutabel, essentielle Tests auf z. B. Orthostase, Handkraft und standard.
5/6

Einordnung seitens DGN müsste herausgestellt werden, dass diese psychosomatische und funktionelle Erkkrankungsmodelle überbetont und damit Falschbehandlung Tür und Tor öffnet.
4/6

VO₂peak ist ein funktioneller Biomarker für PEM, wissenschaftlich validiert; freilich aber kein "Labor-Biomarker".
ME/CFS ist keine neurolog. Erkrankung, diese Zuordnung ist administrativ (ICD), die Erkrankung ist neuroimmun-metabolisch und multisystemisch.
Bzgl.
3/6

ME/CFS ist keine Ausschlussdiagnose, auszuschließen sind Mimics oder andere Ursachen von Fatigue. Es bestehen klare Diagnosekriterien.
„Keine Biomarker“ stimmt so nicht.
2/6

Ein paar Gedanken zu Senoner D, Sebesta C. ME/CFS: Current Insights and Future Directions. Adv Can Res & Clinical Imag.
5(1): 2025. ACRCI.MS.ID.000602. DOI: 10.33552/ACRCI.2025.05.000602.
1/6

Ich persönlich verstehe ja nicht, was es in Bezug auf PAIS- und ME/CFS-Definition und Bedarfserhebung für Versorgung noch zu diskutieren gibt. Der Lackmustest ist klar und einfach: Wenn in einer Behandlungseinrichtung ME/CFS-Erkrankte adäquate Behandlung bekommen (auch zuhause), dann zählt
1/n

Die Unsichtbarkeit sei flächendeckend gegeben heißt es vom zuständigen Mysterium auf Anfrage. #SarcasticSunday
3/3

Berichten zu Folge befindet sich Wonderwoman bereits im Anflug in Ihrem unsichtbaren Flugzeug, um die unsichtbare Anlaufstelle mit ihren unsichtbaren, gut geschulten Ärzt•innen zu besichtigen.
2/3

Wonderwoman als Ärztin im Anflug, Festung Hohensalzburg im Hintergrund (sort of). Erstellt mit Grok.

Speaking of „fiktive Modellprojekte“: In einer österr. Stadt, deren Namen nicht genannt werden soll, ist, wie medial angekündigt, nun im Herbst der Betrieb der ersten ME/CFS-Anlaufstelle aufgenommen worden.
1/3

man ihnen erklärt, wie es den Betroffenen wirklich geht“, erklärt mir jüngst ein Mitglied der ZSK.
Die Schnittmenge dieser und jener Charaktere, die gern auf fiktive Modellprojekte verweisen, scheint relativ groß zu sein. 2/2

„…wird die Aussagekraft dieser Daten von einzelnen Partnern (in der Zielsteuerungskommission, Anm.) angezweifelt…“
Und wer sich nun fragt, wer diese „Partner“ denn sind: solche ohne medizinischen oder Public-Health-Background. „Denen fällt die Kinnlade herunter, wenn 1/2

public-health.meduniwien.ac.at/fileadmin/co...

Danke @kathrynhoffmann.bsky.social für die Initiative!

Cover: Pflegeanleitung

Der Anlass für ein zweites Gespräch mit @ninaweber.bsky.social:
die Frage, wie es Mila inzwischen geht, und die Veröffentlichung des Pflegeleitfadens mit @mecfs.at und @kathrynhoffmann.bsky.social von @meduniwien.ac.at.
public-health.meduniwien.ac.at/abteilungen/...

"Viele an ME/CFS Erkrankte haben keinerlei medizinische Betreuung"

@sabinehermisson.bsky.social im Interview mit @ninaweber.bsky.social im @spiegel.de

Angenommen, ich wäre gerade Minister für Gesundheit und Soziales.
Ich würde jetzt die Notbremse ziehen und ganz schnell flächendeckend seriöse Politik betreiben.
Vielleicht gleich mal bei der Kommunikation beginnen…