Week 3 Acute Kidney Injury Flashcards
(32 cards)
Which of these is a definition for AKI?
- Increase in serum creatinine by > 26.5
μmols/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
All of them
What are the definitions of AKI?
- Increase in serum creatinine by > 26.5
μmols/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
How are the three stages of AKI defined?
Is AKI a diagnosis or a syndrome?
Syndrome.
Underlying cause is the diagnosis
Does AKI mean the kidney is actually injured?
No it’s more just a syndrome which presents as poor kidney function but could be they aren’t getting enough blood or there is a blockage after in the ureta etc.
Three main categories of AKI?
- PRE-RENAL
reduced real or ‘effective’ blood volume - RENAL
glomerulus, tubules and interstitium - POST-RENAL
obstruction – multiple levels (e.g. ureter,
bladder etc)
Give example of blockages that typically cause AKI and blockages that typically don’t
Doesn’t cause AKI:
- Unilateral blockage of a ureta - kidney stones, tumour, extrinsic
- Unilateral renal artery stenosis
Does cause AKI:
- Bilateral renal artery stenosis/ ureta bloackage
- Renal artery stenosis/ ureta bloackage of solitary kidney
- Bladder lesions (tumour)
- Prostate - hypertrophy or cancer
- Myeloma
Rule: In a blockage both kidneys need to be blocked, if one is normal it will often compensate
Non-obstructive pre renal causes of AKI?
- Hypovolaemia e.g. bleeding, 3rd space fluid
losses, over-enthusiastic diuretic therapy! - Hypotension e.g. sepsis, cardiogenic shock, liver
failure - Reduced renal blood supply secondary to severe
renovascular disease (±ACEI), dissection of the
abdominal aorta etc
Even though AKI doesn’t nessesarily mean the kidney is damaged, what is still important to note?
Those who get AKI while in hostpital have a much prognosis, and never really return to normal kidney function. It’s a strong marker of mortality.
What is myeloma and how does it relate to AKI?
A myeloma is a type of cancer that originates in plasma cells.
These abnormal cells can also produce defective antibodies (called M proteins or paraproteins), which can clump together and cause an intrarenal blockage.
All patients with AKI get screened for this.
Two ways to image AKI
Urogram - contrast followed by CT or X-ray - specialist
Ultrasound - something most junior doctors would do
In both you are looking for a build up of fluid in the kidney (hydronephrosis) and dialated calyces
What must you always do for any patient with AKI?
All patients with significant acute kidney injury MUST have an ultrasound scan to exclude or demonstrate obstruction to the
renal tract
Three intrarenal areas that cause AKI
- Tubulointerstitium (tubules and the bit ‘in
between’) - Glomerular disease
- Blood vessels
Causes of Acute tubular injury (ATI)
– Tubular toxins, eg NSAIDs, gentamicin, cisplatinum,
– Severe prolonged hypotension (sepsis, MI)
– Renal hypoperfusion e.g. elderly patient on ACEI,
diuretic who has D&V
What does oliguria mean?
Oliguria means abnormally low urine output.
What is acute allergic interstitial nephritis?
What does it mean for treatment if there is eosinophilic
infiltration (rash)
Usually a reaction to drugs
e.g. PPIs, (omeprazole)
antibiotics, diuretics, NSAIDs
If aneosinophilic usually responds well to steroids. If there is eosinophilic infiltration it sometimes responds to steroids.
What is rapidly progressive glomerulonephritis (RPGN). What is a histological hallmark?
Rapidly progressive glomerulonephritis (RPGN) has an immune
aetiology & is histologically characterised by ‘glomerular crescents’
What are all these examples of?
- Goodpasture’s syndrome: anti-GBM Ab
- Wegener’s granulomatosis: PR3 Ab
- Microscopic polyarteritis (MPA): MPO Ab
- SLE: Anti-nuclear Ab (ANA), anti-dsDNA Abs
Rapidly progressive glomerulonephritis (RPGN)
Hint: RPG -> game -> good wins shrew mate
Vascular causes of intrarenal AKI
Haemolytic uraemic syndrome (HUS)
* E coli related (E coli O157)
* Familial cases (genetic aetiology)
What is Haemolytic uraemic syndrome (HUS)
Glomerular microvascular thrombosis
What are these investigations for:
- Urine dipstick – simple BUT important (is blood or
protein present) - Urine culture
- Renal Ultrasound - if obstructed then decompress
- Renal biopsy
- Angiography ± intervention
AKI
General treatment of AKI
- Optimise fluid balance and circulation
- Stop exacerbating factors e.g. nephrotoxic drugs
(check drug charts) - Appropriate prescribing (check BNF, discuss
with pharmacist) e.g. opiates accumulate in AKI - Supportive treatment e.g. dialysis, nutrition
Specific treatments for AKI causes:
- Obstruction
- Sepsis
- RPGN e.g. SLE
- Goodpasture’s syndrome
- Compartment syndrome
- Obstruction - drain renal tract (e.g. catheter,
nephrostomies) - Sepsis - effective antibiotics
- RPGN e.g. SLE - immunosuppression
- Goodpasture’s syndrome - Plasma exchange
- Compartment syndrome - fasciotomy
Why is bleeding contraindicated for dialysis?
Anticoagulation is required
