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Chronic Kidney Disease (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/1.73m 2 )

Stage 1



Stage 2


– 89

Stage 3


– 59

Stage 4


– 29

Stage 5




» Stage 0 – normal kidney function, normal GFR, and NO proteinuria


» Stage 1 – slightl y diminished kidney function with normal or high GFR; with kidney damage



kidney damage present eg. pathological abnormalities, proteinuria





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


hypertension and fluid overload

metabolic acidosis – due to kidney’s impaired ability to excrete H+; managed via NaHCO3

» may manifest itself as tachypnoea – respiratory co mpensation

anaemia – due to kidney’s impaired ability to secrete EPO

bone disease – due to kidney’s impaired ability to activate Vitamin D; related to Ca2+ absorption

electrolyte imbalance – most importantly hyperkalaemia!


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. DON’T miss rectal cancer if giving EPO to mask anaemia


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 PO 4 2 - – from decreased excretion

» increase in FGF 23 – to induce PO 4 2 wasting

» decrease in calcitriol (Vit D3) – direct result of FGF 23

» decrease in serum Ca 2+ – from decreased calcitriol

» increase in PTH – as a result of decreased serum Ca 2+

» increase in bone destruction – to restore serum Ca 2+

hence, aims of treatment include:

» reducing PO 4 2 - :

§ binding of PO 4 2 - to prevent absorption – eg. via Ca 2+ , Mg 2+ , Al 3+ taken with meals

§ long er dialysis sessions - PO 4 2 - removal is a time dependent event



» 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 la rge 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

§ ane urysmal 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 advanta ge 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 th e 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


» living donation vs. deceased donation

§ psychological assessmen t 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,


§ 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; u sually plasma exchange and IVIG

cell mediated – usually easier to manage

§ steroids – all the AE’s 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)