Lecture 19-AKI Flashcards
What is AKI?
Abrupt decline in actual GFR
What can override compensatory responses in mild hypoperfusion?
NSAIDs and ACE-I
What are the causes of pre-renal AKI?
- hypovolaemia
- cardiac failure
- systemic vasodilation
- pre-glomerular vasoconstriction
- post-glomerular vasodilation
What causes acute tubular necrosis (ATN)?
Ischaemia, nephrotoxins, sepsis
Why is ATN a misnomer?
Not actually tubular necrosis but the cells are damaged and cannot be immediately reversed
Which part of the nephron is damaged in ATN and which part is spared and why?
PCT is damaged by ischaemia and DCT preserved as O2 demands are lower
What are some endogenous nephrotoxins that damage epithelial cells lining tubules?
Myoglobin, urate and bilirubin
When is ATN more likely to occur?
Reduced kidney perfusion and nephrotoxin exposure
What is rhabdomyolysis?
Due to muscle necrosis and release of myoglobin which is toxic to tubule cells and can cause obstruction
What colour is urine in a patient with rhabdomyolysis?
Coca-cola coloured
What are renal causes of AKI?
- thrombotic microangiopathy
- acute interstitial nephritis
What causes thrombotic microangiopathy?
Endothelial damage -> platelet thrombi -> partial obstruction of small arteries -> destruction of RBCs
What causes acute interstitial nephritis?
- toxins such as antibiotics, NSAIDs and PPIs
- infections
What is post-renal failure also known as?
Obstructive AKI
What does obstruction of kidneys with continuous urine production cause?
Increased intraluminal pressure -> dilation of renal pelvis due to hydronephrosis -> reduced renal function
What can cause post-renal failure?
Problems:
- within lumen: stones, clots, tumours
- within wall: stricture
- pressure from outside: enlarged prostate, tumour
How is AKI diagnosed?
- raised urea and creatinine in the blood
- may have metabolic acidosis, hyperkalaemia, hyponatraemia, hypocalcaemia
What can cause hyperkalaemia?
- excess intake
- movement out of cells due to acidosis, hypertonicity, tissue damage
- reduced urine loss
- drugs: RAAS inhibitors, NSAIDs, ENaC blockers
Which investigations are used to confirm a diagnosis of AKI?
- urinalysis: blood and protein
- urine microscopy: culture urine if dipstick positive
- ultrasound
- chest x-ray for fluid overload
- kidney biopsy
How is AKI managed?
- manage volume overload: restrict dietary Na and water
- treat hyperkalaemia
- dialyse if metabolic acidosis where HCO3- cannot be given, if fluid overload or if signs of uraemia
How is hyperkalaemia treated?
- calcium gluconate
- decreased dietary K+
- stop K+ sparing diuretics
- dextrose and insulin
What is the outcome of uncomplicated ATN?
Most patients recover within 2-3 weeks if no superimposed insults but hypotension on dialysis -> ischaemic lesions
How can AKI be prevented?
- avoid nephrotoxins
- detect early
- hydration
What are the risk factors for AKI?
- increased age
- CKD
- dehydration
- nephrotoxins
- radio-iodinated contrast in the last week
