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
