Flashcards in Urinary 12 - AKI Deck (25):
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
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?
2) Intrinsic 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)?
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):
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?
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
List some risk factors for AKI:
- Increasing age
- Diabetes mellitus
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?
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?