Acute kidney injury Flashcards
Concept of AKI
What is acute kidney injury
Sudden deterioration in kidney function
What is timing for AKI
Timing
Can be Hours / days / weeks
so it has to be less than three months
What can hapeen in AKI
Mild drop in renal function to complete loss of kidney function (kidney failure)
May result in failure to maintain, fluid, electrolyte and acid base balance
use to called acute renal failure
Identification
How to stage AKI
- RIFLE Criteria – 2004
- Risk – Injury – Failure – Loss – ESRD
Kidney Disease Improving Global Outcomes (KDIGO) Group Clinical
Practice Guideline - 2012
Identification
what are the stages of AKI
Stage 1: mild increase in creatnine
stage 2: doubling of creatjnine
stage 3: more than double ot if the creatnine goes to 357 (you may need dialysis)
if urine output decreases, tells you something is up with the kidneys
once creatnine goes to stage 3, you start to experience the loss of kidney function
can also use urine output, harder to do, may not be accurate,
How common is AKI
very common
I in 5 emergency admissions into hospital have or develop
AKI
we have incidence of AKI increasing, because of increase of detection, increasing elderly population
costs about 1% of NHS budget (1 billion
What are the consequences of AKI
there is a high mortality rate
16.6% increase mortality for stage 1
there are 100,00 deaths associated with AKI
What other conditions cause mortality when you have AKI
sepsis
True or False
AKI can cause CKD
Patients with AKI are more likely to develop stage 5 renal disease
Patients with AKI and CKD are even more likely to develop stage 5 renal disease
CKD links to AKI
true or false
CKD and protienuria do not increase risk of AKI
False
it does
Risk factors
What are the risk factors of AKI
Do history ones
Age > 65 years
Having a history of
* Chronic Kidney Disease
* Diabetes
* Heart failure
* Liver disease
* if you rely on others for fluid intake
Risk factors
What are the risk factors of AKI
things that could be in a hospital that affect BP
-sepsis
-hypotension
-hypovolaemia
-dehydration
-reduced fluid intake
Risk factors
What drugs can increase risk of AKI
- Diuretics
- ACE inhibitors / ARBs
- BP medication
- Metformin
- NSAIDs (pain relief, reduce inflammation)
- gentamicin (used to treat bacterial infections)
- acyclovir (used to treat herpes infections)
- contrast
Causes
How do we classify causes of AKI
PRE-renal: perfusion failure
INTRINSIC: intrinsic disease of kidney
POST renal: obstruction of urinary system
Pre renal causes
What are the pre renal causes
perfusion
- Hypovolaemia
- Hypotension
- Renal artery occlusion
- heart failure, liver failure (hypervolaemic states)
- Drugs
- -ones that reduce BP, circulating volume (direuetics) or renal blood flow
- E.g. dehydration, gastrointestinal losses, haemorrhage, burns
- E.g. sepsis
- E.g. ACE inhibitors, NSAIDs, diuretics, anti-hypertensives
Causes (PRE)
What dilates the afferent aterioles in kidney
ANP
Prostoglandins
increases GFR
Pre renal causes
What can vasoconstrict the afferent ateriole
NSAIDs
think about nsaids block prostoglandins, which means you vasocinstrict
which as a result decreases GFR
Pre Renal causes
What vasoconstricts the efferent ateriole?
ANP
Angiotensin 2
noradrenaline
vasoconstricting increases GFR (think hose pipe analogy)
if you stand at the end of hosepipe, then you back up the fluid
PRE renal causes
What vasodilates efferent ateriole
ACE 1
lose ablity to vasocnsotirct, which decreases GFR
Renal autoregulation
What is the blood pressure in the autoregulation zone of kidneys
around 80 to 180 mmHg
Pre renal
what happens when blod volume decreaes
your perfusin reduces
because unable to autoregulate, to vasdoilate/constrict afferent or efferent enough
PRE renal
What is the treatment of perfusion failure
keep the tissue perfusion
-replacing fluids (blood, IV fluid)
-restorin
- giving blod pressure support (giving inotropic drugs)
- restoring aterial patency (means something about blockages)
stop the use of
- NSAIDS
- or blocking the RAAS system
POST renal
what are the causes of post renal causes
usually obstruction
- Benign prostatic hypertrophy
- Tumours
- Fibrosis
- Stones (would need to be biltaeral which is quite rare
Tumours: Intrinsic e.g. bladder, ureter
Extrinsic e.g. prostate, cervix
Treatment (POST renal)
How would you treat obsrutcuon
Nephromstomy
Bladder cathereter
urinary stent
INTRINSIC renal causes
What are the ‘renal’ causes
Tubules
Acute Tubular Necrosis (consequence prolonged pre renal perfusion problems)
Acute interstitial nephritis
sarcodsis, and TB
Drugs (NSAIDS, ABs)
infection (HIV, hepatitis B/C, Post streptococcal, Endocarditis, Covid)
Systemic diseases like (vasculitis, Lupus, Myeloma)
Glomerulonephritis
can be reversible
may need dialysis until kidneys restore function
AIN:
caused by drugs, set of an allergic reaction of kidney (eoisonphlils etc), because of inflmamtio causes tubular damage -> treat with steriods
INTRINSIC renal causes
What is the difference between nephrotic vs nephrictic
Onset: Nephrotic (insidious), nephritic (abrupt)
Odema: Nephrotic (lots), nephritic (some)
BP: Nephrotic (normal), nephritic (raised)
Serum albumin: Nephrotic (raised), nephritic (normal)
Haematuria: Nephrotic (can be there), nephritic (its there)
Nephrotic: where there is loss of filtraion barrierm leak proteins, lose proteins from blood
Nephritis: more inflmmation, rapid reduction in urine output and kidney function), blood in urine
INTRINSIC renal causes
What can cause death in AKI
AKI patients dont usually die from AKI there’s usally other reasons
Infection, cancer, cardiovascular disease
What are the complications of AKI
Hyperkalaemia
Acidosis
Pulmonary oedema
can be managed, using dialysus, pottassium loweing drugs etc
Natural history of AKI
What are the differenet histories
- Can make a full recovery
- Can go from AKI to CKD
- Acute on chronic kidney disease
- Can go from AKI to end stage renal disease
Prevention
How do we prevent AKI
we need to identify those at risk of AKI early
* Patient related risk factors (age, co-morbidies)
* Admission related risk factors (sepsis, infections)
* Intervention / treatment related risk factors (are they gettings ABs like gentimycin, NSAIDs etc)
Asssess
How do we monitor AKI
Urine output
Input / Output
Weights
Mangement
How do we manage AKIs
- Starts with identification and recognition of AKI risk (or indeed AKI)
- Fluid balance
- Fluid intervention (Oral and IV)
- Exclude obstruction (sorted with catherter)
- Urine Dipstick
- Treatment of underlying problems
- Stopping nephrotoxic drugs and context specific nephrotoxic drugs (like NSAIDs if not needed)
- Ongoing monitoring and treatment adjustment
- Ongoing monitoring and fluid intervention adjustment
- Referral
What are the indictaions for dialysis
Fluid overload (not sorted by diuretics)
* Hyperkalaemia (not sorted by perfusion)
* Severe metabolic acidosis
* Severe uraemia
-removal of poisons of toxins (can give antidotes, and use dialysis to remove toxins)
