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Chronic

Kidney Disease (Renal Failure)


STAGES OF RENAL FAILURE

there are 5 stages of renal failure classification based on glomerular filtration rate
all individuals with GFR < 60 for 3 months classified as having chronic kidney disease


5 Stages of Renal Failure

CKD Stage
GFR Level (ml/min/1.73m2)

Stage 1
90

Stage 2
60 89


Stage 3
30 59

Stage 4
15 29

Stage 5
<15

NB:
Stage 0 normal kidney function, normal GFR, and NO proteinuria
Stage 1 slightly diminished kidney function with normal or high GFR; with kidney damage
kidney damage present eg. pathological abnormalities, proteinuria

MEDICATIONS

avoid NSAIDs prostaglandins normally cause dilation of the afferent arteriole; NSAIDs will constrict
ACE inhibitors used to control blood pressure
other medications can be used too, but evidence suggests that ACEI may be better
NB: will initially decrease individual glomerular filtration rate and increase creatinine initially
approx. 20-30% decrease in GFR hence contraindicated in Stage 4 renal failure patients

COMPLICATIONS OF CKD

hypertension and fluid overload


metabolic acidosis due to kidneys impaired ability to excrete H+; managed via NaHCO3
may manifest itself as tachypnoea respiratory compensation
anaemia due to kidneys impaired ability to secrete EPO
bone disease due to kidneys impaired ability to activate Vitamin D; related to Ca2+ absorption
electrolyte imbalance most importantly hyperkalaemia!

ANAEMIA

blood transfusions not popular in potential transplant patients due to risk of sensitisation - EPO used now
aim for Hb approx. 110 slightly lower than normal to avoid risk of CVS events if Hb too high
BUT anaemic patients must be reviewed for an anaemic workup prior to receiving EPO
eg. DONT miss rectal cancer if giving EPO to mask anaemia

BONE DISEASE

Vitamin D pathway:
inactive vitamin D synthesised in the skin (from cholesterol and UV light)
partial activation of Vitamin D to D2 in the liver

complete activation of Vitamin D to D3 in the kidney


physiological response in bone disease:
increase in PO42- from decreased excretion
increase in FGF23 to induce PO42 wasting
decrease in calcitriol (Vit D3) direct result of FGF23
decrease in serum Ca2+ from decreased calcitriol
increase in PTH as a result of decreased serum Ca2+
increase in bone destruction to restore serum Ca2+
hence, aims of treatment include:
reducing PO42- :
binding of PO42- to prevent absorption eg. via Ca2+, Mg2+, Al3+ taken with meals
longer dialysis sessions - PO42- removal is a time dependent event

RENAL REPLACEMENT THERAPY

overview:
start discussion when eGFR decreasing < 20, and renal function is irreversible
options renal transplant, haemodialysis, peritoneal dialysis

haemodialysis usually 3 days/week for ~5hrs per session
ideally through an AV fistula which can take 4-6 weeks to mature
takes time for vein wall to thicken and remodelling to occur
if haemodialysis is necessary immediately vas cath inserted into large vein (eg. internal jugular)
permacath (partially buried under skin) is better if dialysis not necessarily immediately
haemodialysis cannot substitute a real kidney, and mortality is still quite high
side effects:
cold vasodilation and inflammatory process
cramps fluid shifts
fluctuating blood pressure fluid shifts
lethargy especially towards the end of the session
access complications:
infection increased risk of bacteraemia
blockage clot or stenosis
aneurysmal fistulas - ?risk of rupture

peritoneal dialysis uses the lining of the peritoneal cavity as a membrane for dialysis
insertion of a catheter into peritoneal cavity at least 1-2 weeks prior (Tenckhoff catheter)
daily process but has the advantage of being able to be done at HOME
fluid is a medium for infection though sugar filled warm fluid
peritonitis usually enteric flora, skin (Staph. aureus); and can lead to acceleration of peritoneal
membrane life span
has a limited life span as the membrane can become exhausted
regular aperients necessary constipation can cause catheter malfunction
usually considered in young patients 3-4years of peritoneal dialysis before haemodialysis or renal
transplant

transplantation:
living donation vs. deceased donation
psychological assessment of the donor necessary with living donor
paired kidney exchanges are possible

blood group must be matched in cadaveric transplants, but not so much in living
immunosuppression:
tacrolimus calcineurin inhibitor
mycophenalate anti-metabolite
steroids
IL-2 inhibitors
complications:

surgical complications vessel breakdown, bleeding, ureteric leakage, wound infection, pneumonia,
UTI
immunosuppression leading to infections (all types of infections, but in particular)
CMV reactivation OR CMV+ to CMV - patient; can cause diarrhoea, low WCC
PCP ?prophylaxis Bactrim
rejection AB mediated vs. cell-mediated
AB-mediated harder to treat; usually plasma exchange and IVIG
cell mediated usually easier to manage
steroids all the AEs related to long term steroid use
cancer skin cancer risk increases with immunosuppression; routing skin surveillance necessary
usually SCC, but can also be BCC
lymphoma also possible (thought to be EBV mediated)

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