C. AKI Flashcards
what does the urinary system consist of
- 2 kidneys
- 2 ureters
- a single midline urinary bladder
- single urethra
what are the functions of the kidney
- regulating blood volume & blood pressure (RAAs system)
- regulating plasma concentration of ions (acids and bases)
- maintaining plasma pH
- conserving valuable nutrients like N-based: urea, NO (ie. through kidney)
- elimination of toxic/unwanted substances
- adjusting red blood cell count in response to oxygen
demand (EPO from bone marrow) - maintenance of calcium and phosphate balance (kidney activates vitamin D)
why is AKI important
- can progress to CKD which is irreversible
signs and symptoms of AKI
- may be asymptomatic (look at blood results)
- reduced urine output or anuria
- change in urine appearance
- change in urine smell
- swelling in ankles, legs or around the eyes
- fatigue or tiredness
- shortness of breath
- nausea and vomiting
- abdominal pain
- dehydration and thirst
- seizure or coma
- chest pain or pressure
- confusion or drowsiness
*need to assess whole patient
what stage do you have if you are in 2 categories
choose the worse one
what are the causes of pre-renal AKI (volume responsive AKI) - 80%
- caused by inadequate perfusion of kidneys
- hypovolaemia eg. trauma, dehydration
- loss of peripheral resistance eg. sepsis (slack blood vessels so decreased BP)
- reduced cardiac output eg. heart failure
- renovascular obstruction eg. thrombosis
how role do pharmacists play in preventing/managing pre-renal AKI
- ensure hydration
- manage sepsis by correct choice of antibiotics
- optimisation of heart failure medicines
- blood thinners/anti-platelets to prevent thrombosis
what are the causes of renal AKI (intrinsic AKI) - 10%
- caused by any factor that causes damage either to kidney itself of the surrounding vasculature (inherited disorders, toxins etc)
- Pre-glomerular - small arteries & arterioles e.g. wall disruption via malignant hypertension
- Glomerular – glomerular capillary network e.g. glomerulonephritis
- Post-glomerular - tubules & interstitium e.g. tubular necrosis
what are the causes of post-renal AKI (obstructive AKI) - 10%
- involves obstruction of urinary outflow anywhere along the renal tract beyond the opening of the collecting ducts
- Ureteric obstruction e.g. kidney stones
- Bladder outflow obstruction e.g. benign prostatic hyperplasia
what are the risk factors for AKI (baseline risks)
- advanced age
- DM (high blood sugar so more pressure on kidneys to filter it)
- CKD
- heart failure as heart can’t pump as much blood
- liver failure as decreased metabolism so more strain on kidneys
- arterial disease (cholesterol build up in arteries)
what are the risk factors for AKI (clinical conditions) - reversible
- sepsis
- hypotension/shock
- dehydration (most common, diuretics put you at risk)
- rhabdomyolysis (destruction of striated muscle cells, toxic to kidney, SE of statins)
- cardiac/vascular surgery (disturbs how much blood can be pumped)
complications of AKI
- oliguria or anuria and oedema
- hyperkalaemia
- uraemia
- hypertension
- acidosis
CKD
- hyperphosphatemia
- anaemia
- hypocalcaemia
*bottom 3 are CKD
major role in primary prevention of AKI
- recognise and assess high risk patients
- assess fluid status/balance
- obtain level of baseline renal function
role of clinical pharmacist in AKI prevention
- appropriately manage nephrotoxic drugs
- treat infections early
- optimise the patients blood pressure
what is the pharmacists role in AKI
- eliminate potential causes (e.g medicines with nephrotoxic potential)
- avoid inappropriate combinations of medicines (ie - multiple BP medicines, would 1 do?)
- ensure all medicines are clinically appropriate (due to renal function change)
- if a medicine must be used:
- Amend doses appropriate to renal function
- Monitor blood levels of drug wherever possible (lithium, phenytoin, short therapeutic window)
- Keep course as short as possible
- following discharge, advise patient and GP which medicines have been stopped and if any need to be restarted
what medicines can cause AKI
- NSAIDs/COX-II inhibitors
- Diuretics
- ACE inhibitors/ARBs
- Iodine-based contrast media
how do NSAIDs (aspirin, ibuprofen) cause AKI
- inhibit synthesis of prostaglandins (COX pathway)
- prostaglandins cause vasodilation of afferent arteriole
- hence NSAIDs cause vasoconstriction
- reduces renal blood flow and pressure in glomerular capillaries
- reduces GFR
- promotes fluid retention
information about prostaglandins
- PGI2, PGE1, PGE2 produced locally in kidney
- vasodilatory agents so increase renal blood flow and GFR
- released by dehydration, acute stress, SNS, angiotensin II
- oppose vasoconstriction of SNS/angiotensinII (ie prevent excessive reduction in GFR and renal blood flow which can lead to renal ischaemia)
when is NSAID use contraindicated
- renal ischaemia
- heamorrhagic shock
- elderly
how do ACE inhibitors/ARBs cause AKI
- cause widening of the efferent arteriole (decreased vasoconstriction), which slows the renal blood flow, BP and reduces GFR
- also get hyperkalaemia
- Angiotensin receptor blockers prevent vasoconstriction and aldosterone release and hence same effects
*of importance in renal vascular disease, particularly those with bilateral renal artery stenoses, with reduced renal perfusion
how do diuretics cause AKI
- cause increased or excessive production of urine
- hypovolaemia (loss of salt and water or a decrease in blood volume)
- thus reducing renal blood flow
how does iodine-contrast media cause AKI (taken for a scan, shows on screen)
- causes contrast-induced nephropathy which is associated with a sharp decrease in kidney function over 48-72 hours
- indicated by an increase in serum creatinine
medicine sick day rules with AKI
- unwell with:
vomiting or diarrhoea - dehydration (unless minor)
fevers, sweats, shaking - STOP taking these medicines and restart when well (after 24-48 hours or eating and drinking normally)
- if in doubt contact pharmacist, GP or nurse
- ACEIs (end in ‘pril’): lisinopril, perindopril, ramipril
- ARBs (end in ‘sartan’):
losartan, candesartan, valsartan - NSAIDs: (anti-inflam painkillers): ibuprofen, naproxen, diclofenac
- diuretics: furosemide, spironolactone, indapamide, bendroflumethiazide
- metformin (for diabetes)
how would ACEI/ARB medication be affected by renal function
- accumulate
- lipid-lowering agents e.g. fibrates, statins
- increased risk of rhabdomyolysis (toxic products)
- stop if AKI due to rhabdomyolysis
- otherwise, continue therapy but monitor
- stop if patient develops unexplained / persistent muscle
how would NSAID medication be affected by renal function
- accumulate so avoid SR/XL preparations
- increase in CNS side effects: drowsiness, confusion, respiratory depression
- reduce dose and use short-acting where possible
- use opiates with minimal renal excretion e.g. fentanyl, oxycodone, hydromorphone
how would diuretic medication be affected by renal function
- accumulate
- hypokalaemia, hypocalcaemia, hypomagnesaemia, hyponatraemia, hyperuricaemia
- tinnitus & deafness (usually with high doses and rapid IV administration)
- overdiuresis leading to hypoperfusion of the kidneys can cause or exacerbate AKI
- loop diuretics (furosemide & bumetanide) preferred as thiazides less effective if GFR < 25ml/min
- however thiazides can potentiate the effects of loop diuretics
- higher doses may be needed to achieve a diuresis in patients with fluid overload
- monitor and adjust dose as necessary
- potassium-sparing diuretics: if hypoperfusion of the kidneys, avoid
how would metformin medication be affected by kidney function
- renally excreted so avoid if GFR < 30ml/min
- lactic acidosis - damage to vascular system and can end up in hypoglycaemia as can’t excrete metformin well
what resource is used on wards for calculating kidney function
THINK kidney medicines optimisation tool
what are the 2 main equations for calculating renal impairment
- Cockcroft and Gault (normally used due to variability)
- eGFR (MDRD)
why is F lower for females in Cockcroft and Gault
- F = location of fat/muscle
- women store fat more densely on hips/breasts
what is creatinine
- product of muscle breakdown
- depend how much muscle you have
- entirely secreted by kidneys
- 24 hour lag in secretion
how do you calculate amputees renal function
- what % of weight has been lost
- consider in weight part of equation
how do you calculate transgenders renal function
- if on hormone treatment for 6 months or longer then kidneys will act as gender that you are transitioning to
- if less than that then original gender
- if won’t disclose – calculate by both methods and discuss with consultant for plan
what are the problems when calculating renal impairment
- may all have same Cr levels but doesn’t taken into consider weight/muscle mass
- if frail, have little muscle mass and hence will need a reduction in dose
- if a muscle builder, will have higher turnover of muscle and hence will need a increase in dose
- if overweight, the excess weight doesn’t contribute to Cr but equation thinks so, so may need to use IBW
what weight should we use with Cockcroft and Gault
- ABW = Actual Body Weight (what you weigh)
- IBW = Ideal Body Weight (what you “should weigh”)
- DDW = Dose Determining Weight (IBW + a bit)
- For obese patients, using ABW will over-estimate renal function potentially resulting in an overdose
- No official guidelines on what to do, go by what place you work at recommends
- A lot of places use a DDW
what are the limitations with Cockcroft and Gault
- extensive oedema (doesn’t contribute to Cr)
- rapidly changing renal function
- pregnant women (diff formula)
- children (diff formula)
- increased creatine consumption (supplements)
- extremes of body mass
- extremes of age
what are the limitations with eGFR
- very poor or good renal function
- rapidly changing renal function
- pregnant women
- children
- increased creatine consumption
- extremes of body mass
- age >75
- doesn’t take into account patients size
or weight (it standardises weight)
when should you avoid nephrotoxic drugs
- AKI
- CKD 4-5
- kidney transplants
- ESRD: the damage is already done – drug choice is less important (but must still consider patient, side-effects, accumulation)
what is the main source used in drug dosing in renal impairment
renal drug handbook (allows for more risk)
