AKI Flashcards
causes of AKI?
PRERENAL: decreased blood flow
- absolute loss of fluid: diarrhoea, vomiting, blood loss, severe burns
- relative loss of fluid: CHF, distributive shock
- renal artery stenosis
INTRARENAL: damage to tubules, glomerululus or interstitium
- acute tubular necrosis
- glomerulonephritis
- acute interstitial nephritis
- rhabdomyolysis
- tumour lysis syndrome
POSTRENAL: obstruction to outflow
- blockage: kidney stones
- external compression of ureter: BPH, intra-abdominal tumours
what patients are at increased risk of AKI
history of AKI
CKD
other organ failure/ chronic disease e.g. HF, liver disease, DM
use of nephrotoxic drugs
iodinated contrast in past week
65 or over
cognitive impairment > reduced fluid intake
what is done for patients at risk of AKI who are undergoing an investigation requiring contrast
IV fluids to reduce risk
ACEIs and ARBS temporarily withheld
the kidneys are primarily responsible for ___ balance and maintaining ___
fluid
homeostasis
how is AKI detected?
decreased UO
electrolyte disturbance
fluid overload
symptoms of AKI?
oliguria (<0.5ml/kg/hr)
pulmonary and peripheral oedema
arrhythmias (changes in potassium and acid-base balance)
uraemia (pericarditis, encephalopathy)
what is included in ‘urea and electrolytes’
urea
creatinine
potassium
sodium
criteria for diagnosing AKI?
rise in creatinine of ≥26mmol/L in 48 hours
≥50% rise in serum creatinine known/ presumed in past 7 days
oliguria for >6 hours in adults (8 in children)
All patients with AKI should have ____ (Ix)
What patients should have renal US?
urinalysis
no identifiable cause/ at risk of urinary tract obstruction
management of AKI?
mainly supportive
- careful fluid balance
- med review
which medications should be stopped in AKI as they may worsen renal function?
NSAIDS (except aspirin at cardioprotective dose- 75mg OD) Aminoglycosides ACEI ARBS Diuretics
these are NAAAD good
which medications may have to be stopped in AKI due to increased risk of toxicity? (but don’t usually worsen AKI themselves)
metformin
lithium
digoxin
which of the following should be stopped in AKI and why
- paracetamol
- ARBs
- diuretics
- statins
- aspirin 75mg OD
- metformin
- aminoglycosides
ARBS, aminoglycosides and diuretics should be stopped as they may worsen renal function
Metformin should be stopped due to increased risk of toxicity
T/F: loop diuretics are recommended in AKI to boost urine output
False
can, however, be used in those who experience significant fluid overload
T/F: low dose dopamine is recommended in AKI to boost renal perfusion
False
in AKI, hyperkalaemia requires prompt treatment to avoid ____
arrhythmias
which can be life threatening
treatment of hyperkalaemia?
stabilise cardiac membrane: IV calcium gluconate
Shift in potassium from extracellular to intracellular: insulin/ dextrose infusion + neb salbutamol
Removal of potassium from body: calcium resonium, loop diuretics, dialysis
when is renal replacement therapy e.g. haemodialysis indicated in AKI?
pt not responding to medical treatment of complications e.g. hyperkalaemia, pulmonary oedema, acidosis, uraemia
what is azotemia?
&&&&&&&&&&&
occurs in AKI
what is tumour lysis syndrome and what kind of AKI is it associated with?
cancer treatment > increased uric acid (waste product from dead cancer cells) > nephrotoxic > ATN > intrarenal AKI
what is azotemia?
aka uraemia
high levels of nitrogen containing compounds in the blood (creatinine, urea)
occurs in AKI due to reduced GFR
what cause of AKI presents with oliguria, eosinophilia, fever, rash
acute interstitial nephritis
causes of acute interstitial nephritis?
type I or IV hypersensitivity (infiltration of immune cells (neutrophils, oesinophils)> inflammation)
typically caused by medications e.g. NSAIDs, penicillin, diuretics
presence of “muddy brown casts” in urinalysis is pathognomonic for what underlying cause of AKI?
acute tubular necrosis (dead cells build up in tubules then excreted out as dead, brown cylinders)
cause of ATN?
ischaemia (often caused by a prerenal AKI)
nephrotoxins: aminoglycosides, heavy metals, myoglobun, radiocontrast, uric acid
most common cause of AKI?
ATN
cause of ATN?
ischaemia (often caused by a prerenal AKI)
nephrotoxins: aminoglycosides, heavy metals, myoglobun, radiocontrast, uric acid
T/F: acute tubular necrosis is reversible
true- usually takes 7-10 days for full recovery
T/F: acute tubular necrosis is reversible
true- usually takes 7-10 days for full recovery
pre-renal uraemia vs acute tubular necrosis
1) urine sodium
2) urine osmolality
3) response to fluid challenge
4) serum urea: creatinine ratio
PRU 1) low 2) high 3) good 4) increased ATN 1) high 2) low 3) poor 4) normal
(prerenal: kidneys hold on to sodium to preserve volume)
how to differentiate between acute and chronic renal failure
renal USS best (most pts have bilateral small kidneys)
Hypocalcaemia also suggests chronic- lack of vitamin D
exceptions to the rule that CRF patients have bilateral small kidneys?
ADPKD
Diabetic nephropathy
Amyloidosis
HIV-associated nephropathy
ADPKD
1) gene mutations?
2) screening investigation for relatives?
3) management?
1) PDK1 (polycystin-1): 85% of cases. PKD2 (polycystin-2): 15% of cases.
2) abdominal USS
3) tolvaptan (if CKD 2 or 3/ rapidly progressive)
features of ADPKD
hypertension recurrent UTIs abdo pain renal stones haematuria CKD
extra-renal manifestations of ADPKD?
liver cysts (most common)
berry aneurysm
cardiovascular: mitral valve prolapse, mitral/tricupspid incompetence, aortic root dilation, aortic dissection
