Acute Kidney Injury Flashcards
definition
abrupt reduction in renal function (over a period of less than 48 hours) defined as
- absolute increase in creatinine above 26.4micromol/litre
OR
- increase in creatinine by 50% or more
OR
- reduction in urine output
the term acute kidney injury can only be used when
adequate fluid resuscitation has been attempted and an obstruction has been ruled out
KDIGO STAGING CLASSIFICATION stage 1
- increase in creatinine above 26micromol/litre or increase in creatine above 1.5-1.9x reference creatinine
- urine output less than 0.5ml/kg/hour for more than 6 consecutive hours
KDIGO STAGING CLASSIFICATION stage 2
- increases in creatinine above 2 to 2.9x reference value
- urine output less than 0.5ml/kg/hour for more than 12 consecutive hours
KDIGO STAGING CLASSIFICATION stage 3
- increase in creatinine greater than 3x reference value
- urine output less than 0.3ml/kg/hour for 24 hours or 12 hours for aneuria
Risk factors for acute kidney injury in the patient
- older age
- previous AKI
- chronic kidney disease
- diabetes
- heart failure
- liver disease
- PVD
Exposure risk factors for acute kidney injury
- hypotension
- hypovolaemia
- sepsis
- deteriorating NEWS
- recent contrast
- exposure to certain nephrotoxic medications
causes of AKI are divided into 3
- pre- renal causes (functional)
- renal causes (structural)
- post-renal causes (obstructive)
pre-renal acute kidney injury caused by
decreased blood flow to the kidneys
pre-renal AKI can be due to
- absolute loss of body fluid
- relative loss of fluid
- renal hypoperfusion
absolute loss of body fluid caused by
fluid actually leaving the body caused by haemorrhage, diarrhoea and vomiting or burns
relative loss of body fluid caused by
total amount of fluid within the body stays the same
- distributive shock= fluid moves from within blood vessels into the tissues
- cariogenic shock= seen in congestive heart failure where there is impaired pumping of the heart so blood pools in the venous side
renal hypo perfusion is caused by
problem localised to the renal artery
- renal artery stenosis
- hepato-renal syndrome
- NSAIDS, cox-2 inhibitors, ACE inhibitors and ARBS
in all of the causes of pre-renal AKI
there is reduced blood flowing to the glomerulus therefore, there is a reduction in glomerular filtration rate therefore, reduced amount of creatinine and urea get filtered which causes azotemia and also causes oliguria §
oliguria
less than 0.5mls/kg/hour of urine is produced
normal urine output
0.5mls/kg/hour which amounts to 30mls/ hour in a 60kg person
less blood getting filtered through the kidney also activates what
the RAAS system which causes the release of aldosterone by the adrenal cortext which causes the kidneys to re-asbord sodium and water which causes the re-absorption of even more urea
the re-absorption of sodium and water means that
less sodium is excited and because less water is excreted urine becomes very concentrated
in pre-renal AKI urine osmolarity
is greater than 500mosmol/kg most of which is urea which is why the urine smells so strongly
ACE inhibitors reduce production of what
angiotensin II
function of angiotensin II
mediates arterial vasoconstriction which increased glomerular filtration rate
ACE inhibits can cause
a fall in glomerular filtration rate by causing efferent arteriolar vasodilation therefore, someone on an ACE inhibitor should stop it if they get diarrhoea or vomiting
untreated pre-renal AKI will cause
acute tubular necrosis
acute tubular necrosis
hypo perfusion to the renal tubular cells causes ischaemia, infraction and necrosis of the cells
common causes of acute tubular necrosis
sepsis, severe dehydration, rhabdomyolysis and drug toxicity
acute tubular necrosis is the most common cause of what
acute kidney injury in hospital
treatment of pre-renal AKI
- Assess for hydration= blood pressure, heart rate, urine output, JVP, capillary refill time, oedema
If hypovolaemia= crystalloid fluids (0.9% NaCl) give 500mls and repeat as required or colloid (gelofusin) - if you have given 1 litre and still no improvement get help!!
renal AKI is caused by
an damage to the glomerulus, tubules or intersitium
tubular causes
- most common cause is acute tubular necrosis
acute tubular necrosis commonly occurs
because of a pre-renal AKI and can also be caused by nephrotoxins
nephrotoxins include
amino glycoside (gentamicin), lead, myoglobin released in rhabdomyolysis, ethylene-glycol (anti-freeze), radio-contrast dye, uric acid
uric acid is a
waste product that can build up during chemotherapy called tumour lysis syndrome
whatver the cause of acute tubular necrosis when the cell die off
they slough off and block the renal tubule increasing the pressure within the tubules, so fluid is trying to flow from the high pressure glomerulus into the high pressure glomerulus which just does not work therefore, glomerular filtration rate falls causing azotema and oliguria
necrotic tubular cells cannot participate in what
re-absoprtion or secretion which cause potassium to build up causing hyperkalaemia and a build up of hydrogen ions causing a metabolic acidosis
acute tubular necrosis causes a
brown granular cast
if the underlying cause of the acute tubular necrosis is addressed then
people can recover because the tubular cells can regenerate over the course of a few weeks
what is another cause of renal AKI
GLOMERULONEPHRITIS
glomerulonephritis is often caused by
antigen-antibody complexes deposition in the glomerular tissue which activates the complement system which attracts macrophages and neutrophils which then release lysosomal enzymes causing inflammation and damage to the podocytes which causes proteinuria and haematuria because large molecules can enter the filtrate
also the fluid leakage in glomerulonephritis causes a
reduction in the pressure difference which drives filtration of small molecules causing a reduction in GFR causing oliguria and more fluid remains in the blood causing oedema and hypertension
in glomerulonephritis the inability to excrete nitrogenous waste products causes
azotemia
another cause of renal AKI is
acute interstitial nephritis
acute interstitial nephritis
inflammation of the interstitial over the course of a few days-weeks
this inflammation is caused by the infiltration of immune cells (neutrophils and eosinophils)
acute interstitial nephritis is typically caused by
NSAIDS, penicillins and diuretics
early symptoms of acute interstitial nephritis
oliguria and eosinophiluria and fever and a rash
symptoms of acute interstitial nephritis
usually resolve is the medication is stopped but if not it will cause renal papillary necrosis which causes haematuria and loin pain
initial investigations for AKI
- Us+Es= Na, K, urea and creatinine
- FBCS and coagulation screen
- urinalysis
- ultrasound
- immunology= ANA, ANCA and GBM
- protein electorpheres and bens jones protein if there is a suspicion of myeloma
indications for renal biopsy
- urgent indications= suspected rapidly progressive GN, positive immunology and AKI
- semi-urgent indications= unexplained AKI requiring diagnosis, rule out obstruction and volume depletion
before renal biopsy you must ensure
it is safe to carry out
- normal clotting, normotensive and no hydronephrosis
post-renal AKI
caused by obstruction of outflow from the kidneys
post- renal AKI caused by
- external compression of the ureters (intra-abdominal tumour of urethra (benign prostatic hyperplasia)
- internal blockage (kidney stones, strictures, cancer)
if only 1 ureter is obstructed
called a unilateral obstruction and if the other kidney is functioning normally then kidney function is normal preserved
if both ureters are obstructed or the uretrha is obstructed
called a bilateral obstruction and this causes post-renal AKI
whatever the cause of obstruction it will cause
backlog of fluid into the kidney into the renal tubules causing an increase in pressure within the renal tubules therefore, reducing the glomerular filtration rate
reduction in GFR means
less creatinine and urea will get filtered causing azotemia and also causes oliguria
high pressure within the renal tubule initially increase the
re-absorpton of sodium, water and urea
but over time the increased pressure within the renal tubules causes
the epithelial cells within the tubules to get damaged which are the cells responsible for re-absorpton so less sodium and urea get re-absorebed
management of post-renal AKI
catheter and if this fails a nephrostomy
life-threatening complications of AKI
- HYPERKALAEMIA
- FLUID OVERLOAD
- SEVERE METABOLIC ACIDOSIS (PH LESS THAN 7.15)
- uraemia pericardial effusion
- server uraemia (urea greater than 40)
normal potassium is between
3.5-5
hyperkalaemia
potassium greater than 5.5
life-threatening hyperkalaemia
potassium greater than 6.5
hyperkalaemia causes
muscle weakness and cardiac arrhythmias
ECG changes in hyperkalaemia
K=6-7= Peaked T waves K= 7-8= flatted p waves, prolonged PR interval, depressed ST segment and peaked T wave K= 8-9= atrial standtil, prolonged QRS duration K= greater than 9= sine-wave pattern
management of hyperkalaemai
- cardiac monitoring and IV access
- 10ml 10% calcium glutinate (OVER 2-3 minutes)
- Insulin (10 units act rapid) with 50mls 50% dextrose (over 30 minutes)
- salbutamol nebulised (over 90 minutes)
calcium gluconate
does not actually affect potassium levels but it reduces the excitability of cardiomyoctes reducing the risk of ventricular fibrillation
insulin
facilitates the uptake of glucose into cell causing intra-cellular shift in potassium
salbutamol
promotes cellular uptake of potassium
drugs causing hyperkalaemia
spironolactone, ramipril, atenolol and amiloride (potassium sparing diuretic)
indication for urgent haemodialysis
- hyperkalaemia (any potassium greater than 7 or greater than 6.5 with no repose to medical management)
- severe acidosis pH less than 7.15
- fluid overload
- urea great than 40 or pericardial rub or effusion
