acute kidney injury W3 Flashcards
name for structural support in glomerulus?
mesangium
definition of acute kidney injury?
increase in serum creatinine by >26.5μmols/L in 48 hours or,
increase in serum creatinine by >1.5x baseline creatinine within last 7 days or,
urine volume <0.5ml/kg/hr for 6 hours
staging system for AKI: AKIN 1?
(SCr = serum creatinine)
increase in SCr > 26.5 μmol/L in 48 hrs or
SCr > 1.5-1.9 fold over baseline SCr
staging system for AKI: AKIN 2?
increase in SCr > 2-2.9 fold over baseline SCr
staging system for AKI: AKIN 3?
increase in SCr > 3 fold over baseline SCr or
increase in SCr >394 μmol/L or
started on dialysis
adverse renal outcomes that severe AKI is independently associated with?
increase incidence of chronic kidney disease
increased incidence of end-stage renal disease
what is AKI
a syndrome (not a formal diagnosis)
so need to think about the underlying cause
differential diagnosis of AKI?
pre-renal (reduced real/effective blood volume)
renal (glomerulus, tubules, interstitium)
post-renal (obstruction - multiple levels, eg ureter, bladder etc)
pre-renal causes of AKI?
hypovolaemia eg bleeding, 3rd space fluid losses, excessive diuretic therapy
hypotension eg sepsis, cardiogenic shock, liver failure
reduced renal blood supply secondary to severe renovascular disease (+/- ACEi), dissection of abdominal aorta etc
post-renal causes of AKI?
note - need obstruction of all kidneys to result in AKI
causes:
prostate - hypertrophy, cancer
bladder lesions - tumour
ureter - calculi, tumour, extrinsic compression (retroperitoneal fibrosis, tumour)
what is myeloma in the kidney?
intrarenal obstruction. B cell neoplasm, makes many of one antibody, precipitates in kidney and all tubules blocked up.
how is obstruction diagnosed? when must this be done?
imaging (often ultrasound - cheap and portable)
must be done within 24 hours in all patients with significant acute kidney injury to exclude/demonstrate obstruction.
renal causes of AKI?
acute tubular injury (ATI) - most common
Tubulointerstitium
Glomerular disease
Blood vessels
causes of ATI?
tubular toxins (gentamicin, cisplatinum (chemo), NSAIDs)
severe prolonged hypotension (sepsis, MI)
renal hypoperfusion (eg elderly patient on ACEi/diuretic who has D&V)
initial oliguria then may exhibit polyuric recovery phase
what causes 50% of all acute renal failure?
renal ischaemia
where does renal ischaemia mainly affect the kidney? what does this cause?
outer medulla. causes cells to fall apart!
treatment?
none
tubulointerstitial causes?
acute allergic interstitial nephritis:
drug related eg PPIs (omeprazole), antibiotics, diuretics, NSAIDs
may have an eosinophilia (no rash)
often respond well to steroids
glomerular causes of AKI?
rapidly progressive glomerulonephritis (RPGN): immune aetiology and characterised by ‘glomerular crescents’
examples of cresentic RPGN?
Goodpasture’s syndrome
Wegener’s granulomatosis
Microscopic polyarteritis
SLE: anti-nuclear Ab
goodpasture’s syndrome features?
antibody binds to basement membrane.
microscopic polyarteritis staining pattern?
‘perinuclear’ pattern
Wegeners granulomatosis staining pattern?
‘cytoplasmic’ pattern
vascular causes of AKI?
haemolytic uraemic syndrome (HUS)
E coli related
familial cases
haemolytic uraemic syndrome - affect on glomeruli?
glomerular microvascular thrombosis
features of AKI history?
renal history (pre-existing renal disease, diabetes, family history)
urine volume
drug history (new drugs, nephrotoxic drugs)
systemic symptoms - diarrhoea, rashes etc
features of clinical examination in AKI?
fluid status - dehydrated? (JVP, postural BP)
evidence of infection?
rash, joint pathology
arterial bruits? (underlying renovascular disease)
palpable bladder (obstruction)
check drug chart!
investigations in AKI?
urine dipstick (important! - blood, protein)
urine culture
renal ultrasound
renal biopsy
angiography
blood tests for AKI?
FBC, blood film, clotting screen
biochemistry (Ca2+, PO4^2-, LFTs and albumin)
creatinine kinase (rhabdomyolysis)
blood cultures
virology and serology (eg hep B, ASOT)
features of urine with rhabdomyolysis
dark colour - cocacola!
immunological tests?
IgGs and serum electrophoresis (myeloma)
complement levels (SLE, post strep GN)
autoantibodies
general treatment of AKI?
optimise fluid balance and circulation
stop exacerbating factors eg nephrotoxic drugs
appropriate prescribing
supportive treatment eg dialysis, nutrition
specific treatment of AKI?
obstruction - drain renal tract
sepsis - antibiotics
RPGN (eg SLE) - immunosuppression
Goodpasture’s syndrome - plasma exchange
compartment syndrome - fasciotomy
institution of dialysis?
severe uraemia:
-no prospect of immediate improvement
-uraemic encephalopathy or seizures
-uraemic pericarditis
hyperkalaemia unresponsive to medical treatment (>6.5)
fluid overload (especially PO), resistant to diuretics/fluid restriction
severe acidosis (results in myocardial depression and hypotension)
how is dialysis carried out?
intermittent haemodialysis
continuous haemodialysis
