Page created on December 15, 2018. Last updated on November 23, 2019 at 18:13
In uraemia is central nervous system involvement frequent, especially when GFR is below 15 mL/min, as it is in end-stage renal failure. This condition is called uraemic encephalopathy. Important symptoms include:
- Fatigue
- Seizures
- Confusion
- Decreased cognitive function
- Coma (in severe untreated cases)
As you can see is coma only a small part of uraemic encephalopathy. It therefore doesn’t make sense to use the phrase “uraemic coma”. Almost nobody has used that phrase in medical journals since the 1980s, and because of dialysis isn’t coma common anyway.
Important factors for this development include:
- Anaemic and cytotoxic hypoxia of brain
- Acidosis -> hyperventilation -> hypocapnia -> cerebral vasoconstriction -> Lower brain perfusion
- Enzyme inhibition by uraemic toxins
- Hyperkalaemia
- Hypocalcaemia
- Due to decreased vitamin D production by the kidney and hyperphosphataemia
- Increased intracellular calcium
- Due to high PTH due to decreaed renal elimination of it
- Hyperosmolarity due to azotaemia. Fine-structure of proteins become altered.
- Neurotransmitter abnormalities
- Urea inhibits monoamine oxidase, which breaks down catecholamines and serotonin
- Glutamine levels are increased (other sources say that it’s decreased, so 🤷♂️)
Hola,
Why do you think that the increased IC calcium levels are due to PTH and not due to the increased permeability as well as decreased Na/K ATPase?
Hey
From this source: https://emedicine.medscape.com/article/239191-overview#a5
Anyway, I’m sure those details are not important. The book doesn’t even care why IC calcium is elevated.
the increase in IC calcium is due to high PTH , cause high PTH is always associated with renal failure as well as uremia . check the blue book page 506
Hey!
It already says in the topic that the increased IC calcium is because of PTH, so I don’t really understand your comment?