AKI Flashcards
Define AKI
An abrupt (<48hrs) reduction in kidney function defined as:
- An absolute increase in serum creatinine by >26.4µmol/l or by > 50%
- OR a reduction in UO to < 0.5ml/kg/h for >6hrs
How is AKI staged ?
Using KDIGO
Serum creatinine is used in practice as urine output is not measured well
- Stage 1 AKI - Serum Cr Increase >26µmol/L or Increase > 1.5-1.9 x reference Cr
- Stage 2 AKI - Increase > 2 to 2.9 x reference SCr
- Stage 3 AKI - Increase > 3 x reference SCr or increase to > 354µmol/L or need for RRT
What are the 3 main categories for AKI ?
- Pre-renal - anything that reduces the blood supply to the kidney
- Renal - these are intrinsic renal causes
- Post-renal - anything obstructive
What are the pre-renal causes of AKI ?
Essentially renal hypoperfusion
This can be caused by:
- Haemorrhage
- Volume depletion (e.g. D&V, burns)
- Shock - e.g. sepsis, anaphylaxis
- NSAIDs / COX-2, ACEi / ARBs
Outline the pathophysiology of AKI
- Hypoperfusion - due to volume depletion, sepsis etc
- Causes decreased intravascular volume
- In response to this ADH and aldosterone is secreted
- This results in Na+ and water retention
- Therefore oliguria (reduced urine output)
- AKI insuses
Describe the mechanism by which ACEi can caused reduced GFR ?
- ACEi inhibit Angiotensin II
- Angiotensin controls mediates vasoconstriction of the afferent arterioles so if this is inhibited there will be vasodilatation of the arterioles
- This will reduce the pressure in the afferent arteriole coming to the glomerular capillary which will result in a smaller NET pressure difference ==> reduced GFR
How can ACEi’s cause AKI ?
- Due to lowering the GFR if a patient becomes unwell with vomiting or diarrhoea, or they have bilateral renal artery stenosis reducing the perfusion of the kidneys
- Then they run the risk of causing a major decrease in GFR which can result in AKI
When should ACEi be stopped then ?
If someone on them is unwell with diarrhoea/vomiting, or dehydrated
What is the other class of drug which can cause hypoperfusion to the kidneys so should be stopped during the times ACEi’s would be stopped ?
- NSAID’s
- They are COX2 inhibitors
What does untreated pre-renal AKI lead to ?
Acute tubular necrosis - a condition involving the death of tubular epithelial cells that form the renal tubules of the kidneys
What are the causes of acute tubular necrosis ?
- sepsis and severe dehydration
- rhabdomyolysis and drug toxicity
What is the treatment of pre-renal and renal AKI ?
- Fluid Challenge for hypovolaemia (so give saline solution)
- If they still have low BP then could give vasopressors – e.g. adrenaline, dopamine, noradrenaline
- Treat underlying cause
- If patient uraemia, severe metabolic acidosis, hyperkalaemia refractory to medical management, or volume overload unresponsive to diuretics the do dialysis
What is the general mechanism of renal AKI ?
Diseases causing inflammation or damage to cells causing AKI
What are the different structures within the kidney which can be damaged to result in renal AKI ?
- Blood vessels
- Glomerular disease
- Interstitial Injury
- Tubular Injury
So building on what structures could be damaged in the kidney to cause renal AKI, what are the specific causes of renal AKI ?
- Vascular - vasculitis, renovascular disease
- Glomerular - GN
- Interstitial Nephritis - usually due to drugs
- Tubular Injury - Ischaemia—prolonged renal hypoperfusion, Drugs (gentamicin), Contrast, Rhabdomyolysis