Renal replacement therapy Flashcards
What is renal replacement therapy
it is life-supporting treatment for renal failure
this can involve dialysis
transplanation
What is the function of the kidneys
Filtration & excretion
* Balances electrolytes
* Balances fluid
* Acid-base balance
BP regulation
Regulation of RBC production (EPO is produced here)
Vitamin D activation
When is RRT necessary?
- Stage 5 CKD (requires long term life sustaining therapy)
- Acute kidney injury (can potentially be revesed)
- Failure to perfom filtration (can oead to life threatneing consequnces)
RRT is temporary life sustaining therapy for AKI)
What are the causes of needing emergency RRT
- Hyperkalaemia
- Severe pulmonary oedema
- Severe acidosis
- Severe uraemia (pericarditis, seizures)
- Ingestion of poisons (ethylene glycol)
first three are due to resistant to treatment
What does RRT replace
Filtraion and excerition
- it can do regulate electorlytes in a safw way
- regulate fluid balance
- acid base balance
What can’t RRT replace
- can’t replace BP regulations
- regulates RBC (no EPO)
- can’t activate vitamin D
transplanation will address all these things
only gets GFR to 15ml/min
RRT: Dialysis
What is dialyis>
Removing solutes in a liquid using a semi peremabele membranes
What are the two membranes that are used in dialysis
- Synthetic (Polysulfone)
- Biological (Peritoneum)
with syntehtic you can alter the size of pores, and do rapid clearance or slow
How do partclies move across a membrane
- Diffusion
- ultrafiltraion
- convection (solute drag, small solutes move acorss with fluid)
- osmosis
Haemodialysis
What is Haemodialysis?
- Intermittent (so about 4 hours, 3x a week)
- its outside the body (extracorporeal)
- can be done in hospital or at home (some will do it home)
- forces used are diffusion and ultrafiltraion)
blood removed, filtred,
Haemodialysis
Haemodialysis structure describe it
there’s a dialisier (has many fibrils, that increase surface area)
there is a fluid where a solutes can move into
Haemodialysis
Haemodialysis employs a countercurrent gradint
what does that mean
So, blood travels on one side of dialysis
membrane
Fluid travels on other side of
dialysis membrane
you can change membrane pore size, high flux dialysers have larger pores which have enhanced middle molecule clerance
Haemodialysis
What do we need practially do to Haemodialysis?
Patient
* Access to blood
* Dialyser
* Dialysis machine
* Ultra-pure water
* Dialysis nurse
Haemodialysis
In an acute setting, how do we get access to blood
Temporary dialysis catheter/Vascath
catheter needs to be wide of enough, need a large enough vein
need distance, so blod doesnt mix
In an chronic setting, how do we get access to blood
Dialysis
catheter/tunnelled line (tunnels under skin, to stop infection -> which may lead to sepsis)
Arterio-venous fistula/graft
What is the difference between AV fistula v AV graft
AV fistula: connection between artery and vein (so the vein enlarges, so you can put needles in, because the vein is now more stable)
AV graft: grafts can clot
What is meant by ultrapure water
it’s water that is free from
- Chlorine
- Heavy metals
- XS Mg/Ca
- Endotoxins
- Bacteria
Peritoneal dialysis
What is Peritoneal dialysis
- Continuous therapy
- inside body (corporeal)
- Semi-permeable membrane (in the Peritoneum)
- usually done at home
- uses diffusion, osmosis and convection
Why are there limits when it comes to the peritoneal membrane
because membrane pores can be variable
What happens in peritoneal dialysis
- put fluid in allow it to dwell
- solution comes out, conaims solutes that contrains excess, fluids, toxins, electorlytes etc
- the fluid we use in (glucose starches)
- we put in lacate to create a buffer
use excess glucose solution to get more water out
starches: used to keep water flowing in one direction, as glucose can equlibrate
How do we regulate acid base in dialysis
as h+ freely moves into tissues, you need to add an ALKALI to patient from the dialysis solution
Types of peritoneal dialysis
What are the types of peritoneal dialysis
Continuous Ambulatory PD
- involves manual exchnages (around 4x a day)
Automated PD
- this happens overnight, about 6-8 hours)
What do we consider when offering PD
- need to think about age, as fraility may mean the person is unable to do the dialysis (they may need someone to help them) -> need to think about vision and dexterity
- Previous abdominal surgery/Stomas (hard to access peritoenial)
- Polycystic kidneys
In the home
- need to think about water source being near the bedroom
- need to have regualr hand washing to prevent infections
- need to have somewhere to store the PD fluid
HD
What are the problems with haemodialysis
Need to think about access
* Risk of clotting
* Central venous stenosis
Infection –more likley in lines over AVF
* Bacteraemia
* Endocarditis
* Osteomyelitis/discitis
- Haemodynamic instability
- Can cause fatigue
What are the benefits of HD over PD
Short/ intermittent treatment time
It’s in a hospital
Defined fluid removal
What are the benefits of PD
Continuous/daily treatment
Less chance of haemodynamic instability
it’s at home
can have a more “liberal diet” potentily
Offers flexiblity for holidays
What are the disadvantges to HD
Access complications
Lifestyle disruption
Holidays
Stricter diet
Muscle cramps/Fatigue
Haemodynamic instability
What are the disadvanatges of PD
Access Peritonitis risk
Peritoneal sclerosis
Membrane failure risk
storage of kit at home
What are the problems with PD
PD tube dysfunction
* Constipation tube can be blocked
* Migration
* Occlusion e.g. fibrin
Infection
* Peritonitis abdominal pains
* Gram +ve > -ve bacteria
*Membrane failure
* Encapsulating Peritoneal Sclerosis (EPS)
- Encapsulating Peritoneal Sclerosis (EPS): can end up with adhesions, can cause obsurtcion and nurtional difficulties
problem with dialysis…
When you have haemodialysis what happens with CV risk
it increases due to
* Cardiac disease
* LVH due to hypertension, anaemia, fluid overload
* Calcification of arteries, lipid abnormalities
problem with dialysis
What are the other risks/problems with dialysis in general
-infections can happen
-does not correct anaemia
-does not correct bone disease
-can lead to malnutrion
Transplanation
Why is transplanation the treatment of chocie
mproved quality of life
* Improved survival
* Recovery of renal function(there’s now EPO and Vitamin D production)
Where do kidney transplant go
typically in right or left illiac fossa
ureter will be in the bladder, blood supply put in aorta
How are the donors for transplanation
Live Donor
* Deceased Donor (Cadaveric – brain/cardiac death) – “Waiting List
Assessing the transplant opp
what does transplanation depend on
Age-related comorbidity: Frailty Scoring
* Cardiovascular risk
Immunosuppression risk (need to think about maligancies)
Surgical factors:
* BMI >30
* Vascular anatomy & intra-abdominal space (PKD)
* Immunological factors
- if they have certain antibodies hard to find a sutible match
Complications of transplants
What are the early/medium term complications
- CV morbidity/mortality (period of risk)
- Infection (immunosupression load is higher)
- Rejection (first years)
Complications of transplantation
What are the long term complications of transplanation
Increased CVD risk
* Transplant-associated diabetes because of steriods
* Opportunistic infections / Viral reactivation
* Malignancy esp. non-melanoma skin cancer & virus associated e.g. PTLD
(EBV) -> can happen years later sometimes
How are donor and recipeent matched
Need to look at
must ve matched acorss Species
- Blood group antigens (ABO) – not always (possible to desensitize)
- need to matched acorss blood type antigens
HLA antigens
* Class I A/B
* Class II DR
cannot have pregormed HLA antibodies that are directed by the donor HLA type, quickly can attack the donor kidney
basically more tightly matched,
How do we match HLA antigens
do tissue typing (analysing HLA types)
How do people get pre-existing anti HLA antibodies
- Pregnancy
- transfusion
- previous transplant
*
Why do we immunosupress
- to reduce the ablity of t cells to fight the kidney (reduce ablity to fight infectiosn and cancer though)
- because 30-40% may still be rejected, but this can be treated
use a triple therapy
CNI (calcineurin inhibitors) e.g. Tacrolimus ( prescribed by BRAND NAME, OD/BD)
* Antiproliferative agents e.g. Mycophenolate (MMF), Azathioprine
* Corticosteroids – prednisolone
can also use Basiliximab – anti-CD25
Explain transplant immunology
- APC presents non self anigen to t cell
- t cell recpetor trigger
- co stimulation from t cell
- this releases calcineurin
- which transcibes nculeus of IL-2
- IL-2 gets secreted, acts on cells
- sends signals for proliferation
- proliferate cells that recognise that non self antigen
- which will lead to rejection
How do we stop the transplant immunology pathway
- Block calinurin being released by using Tac CyA
- steriods block transcription
- sirolimus blocks TOR pathway
- use antiproliferatiev agents
What risks do we need to consider when doing immunosupression
Leaves you at risk of Infection like
* CMV
* Fungi/oral thrush
* Pneumocystis
High dose steroids
* GI protection PPI
* Bone protection (becasue you get some bone thinning) -> so we need calcium supplementation
