Acute kidney injury Flashcards
Define acute kidney injury (used to be called acute renal failure)
Acute decline in renal function (decreased GFR), leading to a rise in serum creatinine (≥26.5 micromol/L) and/or a fall in urine output
Acute kidney injury can be staged into 3 stages (AKI 1/2/3)
How much has the serum creatinine rised by compared to baseline in each stage
AKI 1 - 1.5-2.99 times (rise of 50–99% from baseline within 7 days)
AKI 2 - 2-2.99 times (100–199% creatinine rise from baseline within 7 days)
AKI 3 - >3 times (200% or more creatinine rise from baseline within 7 days) - NEED RRT
Immediate dangerous consequences of AKI (hint: AEIOU)
Acidosis Electrolyte imbalance Intoxication - from toxins Overload - from fluid Uraemia complications
3 types of AKI
Pre-renal
Intra-renal
Post-renal
Pre-renal AKI refers to damage due to
Kidney hypoperfusion –> decreased GFR –> accumulation of toxins in blood
Blood urea nitrogen to creatinine ratio
5-20 : 1 (much more urea than creatinine in blood because a lot of urea reabsorbed whereas most creatinine excreted)
Causes of pre-renal AKI (4)
Absolute fluid loss
- dehydration
- haemorrhage
- vomiting/diarhhoea
Relative fluid loss
- hypotension/septic shock
- congestive cardiac failure
Renal artery stenosis/embolus
Liver failure
Renal (intrinsic) AKI refers to damage …
within the renal parenchyma
Post-renal AKI refers to damage …
due to obstruction of urine outflow tract (i.e. ureter)
All types of AKI exhibit decreased GFR which stimulates what system
RAAS to increase Na+ and water retention and therefore urea follows which increases the blood urea nitrogen ratio to creatinine
Causes of renal (intrinsic) AKI (5)
Glomerulonephritis, e.g. crescentic (rapidly progressive) GN
Tubular injury, e.g. acute tubular necrosis (usually from ischaemia)
Nephrotoxins - e.g. drugs (NSAIDs, aminoglycosides), radiocontrast
Interstitial injury, e.g. acute interstitial nephritis (due to allergic reaction to drugs)
Multiple myeloma (blood cancer)
Causes of post-renal AKI (3)
Compression
- of ureter, e.g. intra-abdo tumours
- of urethra - e.g. BPH
Obstruction within lumen
-calculi within ureter, bladder or urethra
Most common type of AKI is
pre-renal, i.e. hypoperfusion of kidneys
If pre-renal AKI sustains, it will go on to cause what
renal AKI - as persistent hypoperfusion will result in ischaemia of the tubules –> acute tubular necrosis because not enough oxygen and nutrients
What is azotaemia
High nitrogen containing compounds in urine
Acute tubular necrosis is a cause of renal (intrinsic) AKI - what is usually the cause of this
Sustained hypoperfusion (in pr-renal AKI) leading to ischaemia of tubules
Aminoglycosides (a type of antibiotic) are nephrotoxic - give an example
gentamicin
Investigations of AKI (6; 1 is radiological)
Serum creatinine U+Es Urine dipstick/other urinalysis FBC - may show anaemia Venous blood gas - indicates metabolic acidosis from anion gap
Renal USS
Questions to ask to confirm AKI history (4)
PMH of diabetes, hypertension, liver disease, congestive heart failure
Family history of congenital/systemic diseases like DM
Any nephrotoxic medication
Symptoms of uraemia
Symptoms (7) /signs (3) of AKI (most common is pre-renal AKI)
Symptoms
- oliguria
- symptoms of azotaemia (high nitrogenous compounds in blood) - confusion, lethargy, fatigue, anorexia, nausea/vomiting
- orthopnoea
Signs
- tachycardia
- hypotension (suggests pre-renal AKI)
- dry mucous membranes, skin turgor loss
Risk factors of AKI (6)
Age >65 CKD DM Malignant hypertension Congestive heart failure Nephrotoxins - aminoglycosides, NSAIDs, radiocontrast
Principles of management of AKI (STOP ACRONYM)
Suspect sepsis and treat
Toxins - stop/avoid nephrotoxic drugs
Optimise BP - IV fluids if dehydrated, diuretics if overhdyrated, stop antihypertensives if on them
Prevent harm - treat complications, review U+Es daily, review medication
Supportive management of AKI (3)
Fluid balance
- IV fluids if hypovolaemic
- restrict fluids if hypervolaemic
Optimise BP
- IV fluids or vasopressors
- stop antihypertensives
Stop nephrotoxic drugs - NSAIDs, aminoglycosides
1st line treatment of renal (intrinsic) AKI
Treat the underlying condition with SPECIFIC THERAPY, e.g. glomerulonephritis (often steroids, other immunosuppressants), acute tubular necrosis, interstitial injury
+ supportive measures (in other flashcard)
1st line treatment of post-renal AKI
+ then
Catheterisation - to relieve urinary retention
Relief of obstruction
-e.g. if stone then ureteral stent or lithotripsy
Dialysis is indicated in AKI if patient has… (think AEIOU complications of AKI)
severe metabolic Acidosis
hyperkalaemia (Electrolyte) refractory to medication
volume Overload unresponsive to diuretics - i.e. pull oedema
Uraemia (severe) –> pericarditis
Severe electrolyte imbalance of what cation occurs in AKI
K+ –> hyperkalaemia
ECG changes of hyperkalaemia (3)
Tall tented T waves
Broad QRS
Flat p waves
Hyperkalaemia has a high risk of going on to cause
arrhythmias - ventricular fibrillation –> cardiac arrest
Acute treatment of hyperkalaemia secondary to AKI (2)
Stabilise myocardium with IV calcium gluconate
Shift K+ back into cells with
- insulin + glucose infusion
- or salbutamol
Biochemical investigations of renal disorders (5)
U+Es - high K+, high urea Serum creatinine - increased FBC: +/- low RBCs, +/- leukocytes (infection) Urine dipstick Urine culture
1st line treatment of pre-renal AKI
+ then
Volume expansion and/or blood transfusion
Vasopressor if severe hypotension
COMMONEST CAUSE OF ACUTE KIDNEY INJURY
ACUTE TUBULAR NECROSIS (due to sustained hypoperfusion of kidneys)
