Acute Kidney Injury Flashcards
what does the kidney interstitium comprise of mainly in health
microvascular capilaries
what is the function of the mesangium in the glomerulus
structural support
definition of AKI
increase in serum creatinine of >26.5 umol/l in 48 hours
increase in serum creatine of 50% more than baseline within 7 days
urine volume <0.5ml/kg/hr for 6 hours
when would someone be started on dialysis for AKI
when they are AKIN stage 3
probably in ICU
types of AKI
pre renal
renal
post renal
pre renal causes of AKI
hypovolaemia (e.g. haemorrhage)
3rd space fluid loss (e.g. pancreatitis)
diuretics
hypotension (e.g. septic shock, liver failure)
reduced renal blood supply secondary to severe renovascular disease, aortic dissection
renal artery stenosis
post renal causes of AKI
prostate hypertrophy or cancer
bladder lesions or cancer
ureter calculi or tumour or compression from another tumour
does post renal AKI have to involve both kidneys or just one
both
or one if only one present
what is hydronephrosis
swelling of one or both kidneys that occurs when there is a blockage meaning the urine can’t drain
what must be done in all patients with significant AKI
an ultrasound scan to exclude or demonstrate obstruction to the renal tract
renal causes of AKI
acute tubular injury
renal ischaemia
acute tubular necrosis
interstitial nephritis
glomerulonephritis
and others
what is the commonest cause of AKI in hospitals
acute tubular injury
causes of acute tubular injury
toxins (e.g. gentamicin, NSAIDs, radio contrast dye)
severe prolonged hypotension
renal hypoperfusion
initial oliguria
what should be done for patients who have diarrhoea and vomiting and are on ACEi
ACEi should be stopped to avoid renal hypoperfusion which would cause AKI
what happens to urine output in acute tubular injury AKI
initially oliguria
then may be polyuric in recovery phase
which region of the kidney operates at a more hypoxic level
medulla
3+ protein and 4+ blood on a dipstick suggest what is the most likely cause
autoimmune
what histology marker is characteristic of rapidly progressive glomerulonerphritis
glomerular crescents
vascular cause of renal AKI
haemolytic uraemic syndrome
- e coli related
- genetic related
what can be seen in histology of haemolytic uraemic syndrome
glomerular microvascular thrombosis
what should you ask about in an AKI history
renal history (e.g. CKD, diabetes)
family history
urine volume
drug history (e.g. new drugs, nephrotic drugs - NSAIDs, ACEi, antibiotics)
systemic symptoms (e.g. diarrhoea, rash)
what clinical examination should be done for AKI
fluid status (JVP, postural BP)
check for evidence of infection
look for rashes
look for joint pathology
arterial bruits
palpate bladder
check drug chart
what does the anti-nuclear factor test for
SLE
what does the anti-neutrophil Ab test for
vasculitis
what does the anti-GBM Ab test for
Goodpasture’s syndrome
what investigation is important to do in AKI if there is hyperkalaemia
ECG
treatment prinicples of AKI
optimise fluid balance and circulation
stop exacerbating factors (e.g. drugs)
appropriate prescribing (e.g. lower doses)
supportive treatment as appropriate (e.g. dialysis, nutrition)
treatment of obstructive/post renal AKI
drain renal tract
treatment of sepsis
effective antibiotics
treatment of RPGN
immunosuppression
treatment of Goodpasture’s syndrome
plasma exchange
treatment of compartment syndrome
fasciotomy
when should you start dialysis
severe uraemia
- no prospect of immediate improvement
- uraemic encephalopathy or seizures
- uraemic pericarditis
hyperkalaemia unresponsive to medical treatment
fluid overload (esp. pulmonary oedema) resistant to treatment with diuretics/fluid restriction
severe acidosis
problems and complications of haemodialysis in AKI
pneumothorax
infection
bleeding
anticoagulation required which may be problematic in patients with bleeding
hypotension may be troublesome in some patients
