Abdul Mannan: Paradox of Bleeding and Clotting in Uremic Coagulopathy
Abdul Mannan, Consultant Haematologist, Director Haemophilia Centre and Haematology Lab Lead at Betsi Cadwaladr University Health Board, shared a post on LinkedIn:
“Your dialysis patient is bleeding from their gut.
But their clotting tests look normal.
Sound familiar?
This is uremic coagulopathy, and most people still don’t fully understand what’s going wrong at the platelet level.
Here’s what’s actually happening:
- Excess urea generates cyanate, which carbamylates the αIIbβ3 integrin on platelets.
The fibrinogen-binding site gets structurally altered. Platelet aggregation fails at the final step.
- GPIb receptors on platelets get proteolysed, reducing von Willebrand factor adhesion.
The platelet never properly sticks to the damaged vessel wall in the first place.
- Nitric oxide and prostacyclin levels are both elevated in uraemia. Both independently inhibit platelet activation. It’s a double hit.
- Anaemia makes it worse. Below a haematocrit of 25%, red blood cells can’t physically push platelets to the vessel wall (margination).
No margination, no effective primary haemostasis.
Now here’s the part that keeps me up at night.
The same uraemic toxins that cause bleeding also drive a prothrombotic state.
- Indoxyl sulfate triggers eryptosis, exposing phosphatidylserine on red blood cell membranes.
- These surfaces act as a scaffold for coagulation factor assembly and thrombin generation.
The result?
These patients bleed from their gut, clot off their fistula and stroke.
Both. At the same time.
This is why managing bleeding in a dialysis patient isn’t just about giving desmopressin and hoping for the best.
The pathophysiology is layered, and the treatment has to match it.”
More posts from Abdul Mannan on Hemostasis Today.
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