Flashcards in Acute kidney injury Deck (62):
Is acute kidney injury common?
Mortality increases with increasing severity of AKI. T/F
Define acute kidney injury (AKI)
Rapid decrease in kidney function characterised by >26.4mmol rise in serum creatinine OR 50% increase creatinine from baseline OR reduction in urine output
When is AKI defined?
After fluid resuscitation
After obstruction is excluded
Define the stages of AKI
Stage 1 - creatinine rise >26 OR increase 1.5-1.9 reference creatinine
2-2.9 reference creatinine
3 reference creatinine OR increase to >354 OR need for renal replacement therapy
Is AKI usually based on urine production or creatinine? Why?
Because urine output is usually poorly measured on wards
AKI is a diagnosis. T/F
False - it's a description for which there will be an underlying cause
How can you categorise the causes of AKI?
What are some pre-renal causes of AKI?
- diarrhoea & vomiting
- cardiogenic shock
- hepatorenal syndrome
What is hepatorenal syndrome?
Kidney failure as a result of liver failure
Is pre-renal AKI reversible?
Volume depletion can be reversed and AKI can recover
How does angiotensin II affect the kidney?
Efferent arteriolar vasoconstriction and thus increased kidney BP (hydrostatic capillary pressure) and thus increased GFR
How does an ACE inhibitor affect the kidney?
Loss of angiotensin II vasoconstriction and thus no arteriolar constriction (i.e vasodilation) and thus reduced GFR
Why might a patient with diarrhoea and vomiting (i.e volume depletion) who is on an ACE inhibitor present with AKI? How is this prevented?
Reduced volume combined with vasodilation from effects of ACEi causes reduced GFR and hence AKI
Tell patients on ACEi/NSAID/Diuretic to stop drugs during periods of diarrhoea and vomiting
Explain the pathphysiology of AKI
Volume depletion -->
Decreased intravascular volume -->
RAAS system & ADH increase -->
Salt & water retention -->
What happens if pre-renal AKI is missed?
It can lead to acute tubular necrosis
What is acute tubular necrosis? What are the common causes?
Histological diagnosis of a type of AKI (commonest form)
How is pre-renal AKI treated?
Reversal/removal of precipitating factors
- Assess hydration
- Fluid challenge for hypovolaemia
How can you assess the hydration status of a patient?
What types of fluid challenge are indicated in AKI?
Over which level of fluids given, with no clinical improvement, should you seek help?
How are fluid challenges given?
Give fluid bolus, reassess, repeat as needed
Why should dextrose not be given in AKI? Why not hartmans?
It does not go into the intravascular volume
It contains potassium which is not ideal in AKI
What are some causes of renal AKI?
- ANCA associated small vessel - Wegner's, GPA
- lupus nephritis
- post infective
- infective endocarditis
Acute tubular necrosis
Acute interstitial nephritis
- TB infection
Diseases causing inflammation or damage to cells leading to AKI. Which category of AKI does this describe?
How can renal AKI be further subdivided?
What are the symptoms of AKI?
- Constitutional (anorexia, fatigue, etc)
- Nausea and vomiting
- Fluid overload (oedema, SOB)
What are the signs of AKI?
Fluid overload (oedema, hypertension, pulmonary oedema, effusion)
Uraemic (itch, pericarditis)
Which points of a history might point towards AKI?
Diarrhoea and vomiting
Recent contrast (angiogram, etc)
Which clinical results might point towards AKI?
Urinalysis (blood & protein)
Blood results (anaemia, eosinophilia, raised CK)
Why might sore throat point towards AKI?
Post strep glomerulonephritis
Why might haemoptysis point towards AKI?
What are the triple whammy drugs?
Does myeloma cause anaemia?
Haemorrhage can cause anaemia. T/F
Low calcium and high phosphate points to what?
Vitamin D deficiency perhaps from CKD
What might eosinophilia indicated?
Interstitial nephritis (main cause drugs)
How can compartment syndrome cause AKI?
How would you investigate an AKI?
FBC & coagulation screening
Protein elecrophoresis & bence jones proteinuria (>50 y/o)
Hyperkalaemia is a medical emergency. T/F
Haemolytic uraemic syndrome causes which biochemical derangement?
What might abnormal clotting indicate in relation to AKI?
Sepsis and disseminated intravascular clotting
Blood and protein in the urine indicate which category of AKI?
How is immunology useful in relation to AKI?
ANA (lupus nephritis)
What are the urgent and non-urgent indications for renal biopsy?
Urgent - suspected rapidly progressing GN OR positive immunology
Non-urgent - unexplained AKI
What are the contra-indications to renal biopsy?
Warfarin or aspirin
Hydronephrosis (i.e obstruction0
Is you've fluid resuscitated but blood pressure is still low then what is the next step?
Should nephrotoxic drugs be stopped? What else?
Yes & anti-nephrotics & avoid nephrotoxic/high potassium antibiotics (trimethoprim, gentamicin, co-tramoxazole)
What are the complications of AKI?
Severe acidosis (40)
What is the pathogenesis of post renal AKI? List the causes
Obstruction causing back pressure & hydronephrosis
How is post renal AKI treated?
What is hyperkalaemia associated with?
What is the normal range for potassium?
3.5-5 (>5.5 is hyperkalaemia --> 6.5 is life threatening)
How should hyperkalaemia be assessed once it has been biochemically noted?
Muscle weakness & tingling
How does hyperkalaemia look on an ECG?
Peaked T waves
Prolonged PR interval
Sine wave pattern
How is hyperkalaemia managed?
10ml 10% calcium gluconate
Insulin (actarapid) and dextrose
Calcium resonium (NOT in acute setting)
What are the indications for haemodialysys?
Hyperkalaemia >7 (or >6.5 and non-responsive to treatment)
Severe acidosis (40 + pericardial effusion/rub
How is acidosis treated?
What is the natural history of AKI?
Complete recovery (most)
Recover with progressive renal failure (5-10%)
No recovery (10-15%)
Risk factors for developing AKI?
Co-morbidity (heart failure, liver failure, etc)