Urinary 12 - AKI Flashcards
List the 3 possible findings in AKI:
1) Increased serum Creatinine by > 26.5uM in 48hrs
2) Increased serum Creatinine by > 1.5x baseline within 7 days
3) Urine volume < 0.5 ml/kg/hr for 6 hrs
Define AKI:
Decline in GFR over days/weeks, upsetting ECF volume, electrolyte and acid-base homeostasis, and causing accumulation of nitrogenous waste products
The causes of AKI are split into which 3 categories?
1) Pre-Renal
2) Intrinsic Renal
3) Post-Renal
How do heart failure, sepsis, cirrhosis and anaphylaxis all cause AKI?
Decreased ECF volume = Decreased renal perfusion
How do NSAIDs, ACEi and AIIR antagonists cause AKI?
Impair renal autoregulation pathways = cannot increase renal perfusion
If pre-renal AKI is not rapidly treated, what will it develop into? Why?
ATN - Acute Tubular Necrosis
Inadequate perfusion = ischaemic cell damage
Drug OD = nephrotoxic cell damage
What are the 2 types of Acute Tubular Necrosis (ATN)?
1) Ischaemic
2) Nephrotoxic
What parts of the kidney is most susceptible to ischaemia?
Proximal tubule (part. S3 segment) Thick Ascending Limb of LoH (TAL)
Give 5 causes of nephrotoxic ATN (acute nephrotoxic necrosis):
1) Myoglobin
2) Poisons
3) Drugs
4) Bilirubin
5) Urate
Why may an elderly person develop nephrotoxic ATN after prolonged immobilisation?
Prolonged immobilisation causes rhabdomyolysis
Myoglobin is toxic to tubular cells, and may obstruct tubule = necrosis
Name 5 intrinsic renal diseases leading to AKI:
1) Acute Tubular Necrosis (ATN)
2) Glomerulonephritis - IgA nephropathy, SLE
3) Small vessel disease - Haemolytic anaemia
4) Acute Tubulo-Interstitial Nephritis - Infection/toxin-induced
5) Renal artery/vein occlusion
Describe post-renal causes of AKI:
1) Obstruction within lumen
2) Obstruction within wall
3) External compression
Must affect both kidneys
What serum findings are ALWAYS found in AKI?
Raised Creatinine
Raised Urea
What ECG changes are associated with raised serum K+?
- Tall T waves
- Small/absent P waves
- Increased P-R interval
What changes to ECF [K+] typically occurs in AKI?
Raised ECF [K+]
What signs of underperfusion can you check for externally?
- Cool peripheries
- Increased pulse
- Decreased BP/postural hypotension
- Decreased skin turgor
If dipstick test shows ^ proteinuria and ^ haematuria, what is the most likely cause of the AKI?
Glomerulonephritis (intrinsic renal)
Which investigations would be carried out if suspected glomerulonephritis, and what would the findings be?
Urinalysis: Proteinuria + Haematuria
Urine microscopy: RBC casts
Biopsy
List some risk factors for AKI:
- Increasing age
- Diabetes mellitus
- Cancer
- Trauma
- Sepsis
- Dehydration
Why is it important to restrict Na+ and water intake in AKI?
To reduce fluid retention and overload, as kidneys cannot adequately excrete fluid/toxins
Give some treatments for high [K+] in AKI:
- Restrict dietary K+
- Calcium gluconate
- IV Insulin + Dextrose
- Stop K+ sparing diuretics +/- ACEi / ARBs
What is the treatment of acidosis caused by AKI?
Sodium bicarbonate
In which situations may you perform dialysis on a patient with AKI?
- Presence of dialysable nephrotoxin
- Hyperkalaemia not responding to treatment
- Severe metabolic acidosis
- Fluid overload not responding to diuretics
- Signs of uraemia (^thirst, muscle cramps, confusion, anorexia, fatigue, nausea/vomiting, pruritis)
If hyperkalaemia or fluid overload in AKI is not responding to treatment, what could be considered?
Dialysis
If patient with AKI has the following symptoms:
Increased thirst, pruritus, confusion, anorexia, fatigue, muscle cramps…
What do you suspect and how will you treat it?
Uraemia
Dialysis
