Acute kidney injury Flashcards
Define AKI
An abrupt deterioration in renal function, usually over hours - days
Usually reversible
What are the hallmarks of AKI?
Falling urine output + rising creatinine and urea
Discuss RIFLE classification of AKI
Describes AKI - uniform definition
Three severity levels:
R - risk (patient is at risk of kidney damage)
I - injury (kidneys have been inured)
F - failure (kidneys have failed)
Two outcomes:
L - loss (loss of funtion)
E - end stage renal disease (end stage renal disease has developed)
What are the stages of AKI outlined by RIFLE?
- R = stage 1 (a serum creatinine rise of >26.4micromol/L or a 1.5x increase in 48hrs)
- I = stage 2 (a 2-3x increase in serum creatinine)
- F = stage 3 (a >300% increase in serum creatinine equal to >354micromol/L)
What is normal serum creatinine?
Women: 53-115 umol/L (0.5-1.0mg/dL)
Men: 88-150umol/L (0.7-1.2mg/dL)
What level of creatinine might indicate renal
>1.2mg/dL / >115umol/L
Why do men have higher creatinine levels?
Higher muscle mass generally
What are causes for increased urea, other than altered renal function?
- Corticosteroid treatment
- Tetracycline treatment
- GI bleed (blood enters gut, it is high in protein and leads to production of urea)
Outline causes of high creatinine other than renal damage
- High muscle mass
- Red meat ingestion
- Muscle damage/ rhabdomyolysis
- Decreased tubular secretion due to durgs such as cimetidine or trimethoprim)
Discuss mortality rates associated with AKI
- Uncomplicated AKI 5-10%
- AKI complicating non-renal organ failure 50-70%
Outline some causes of AKI
- Rhabdomylolysis: crush injuries, myoglobin (nephrotoxin) released, resulting in acute tubular necrosis. Can also occur in haemolysis where haemoglobin is the nephrotoxin
- Acute cortical necrosis: renal hypoperfusion causes blood to be diverted to the medulla of the kidney meaning the cortex is hypoperfused and irreversible glomerular damage occurs (cortical necrosis)
- Contrast nephropathy: in patients with impaired renal function iodinated radiological contrast media can be nephrotoxic
What is creatinine?
- Indicator of renal health
- Breakdown product of creatine phosphtae in muscle, produced at a constant rate
- Removed from the blood purely by the kidneys
- High creatinine = low GFR
What is the most accurate way to measure GFR?
- Measuring clearance of exogenous filtration markers e.g. inulin, iothalamate or iohexol
* Rarely done because it is £££ and requires strict protocol
What are the stages of AKI
Stage 1: Rise in serum creatinine >26.5mmol/L or 150-200% of baseline
Stage 2: increase of creatinine 200-300% of baseline
Stage 3: >300% increase of baseline
What are the disadvantages of using serum creatinine to measure GFR?
- Many factors affect serum creatinine
- Rises in serum creatinine take 12-24hrs to rise following surgery
Outline pre- renal causes of AKI
- Reduced perfusion (hypovolemia or haemorrhage)
- Sepsis
- Third spacing of fluid (e.g. pancreatitis, fluids leak out into peritoneal cavity thus depleting vascular fluids)
- Heart failure
- Renovascular disease
- Patients with bilateral artery stenosis that have been started on ACEi, causes ATN
Outline renal causes of AKI
- ATN
- Glomerulonephritis
- Interstitial nephritis
Outline post-renal causes of AKI
- Mechanical obstruction
- Retroperitoneal fibrosis
- Lymphoma
- Tumour
- Enlarged prostate
- Stricture
- Ascending UTI
- Urinary retention
What is the most common form of AKI?
ATN due to prolonged ischaemia
Outline some causes of ATN
- ROS
- Compliment activation
- Drugs
- Endotoxins
- Radiocontrast media
*45% of cases of AKI are caused by ATN
History associated with pre-renal AKI
Haemorrhage, vomiting, diarrhoea, sweating
Hx of sepsis, burns, GI surgery or pancreatitis
Thirst, dizziness, tachycardia, oliguria, anuria
History associated with intrinsic/ renal AKI
Usually ATN caused by:
- Severe infection, nephrotoxic drugs, major surgery
- Hx of rash, haematuria or oedema with hypertension suggestive of nephritic syndrome
- Query recent drug use and medications
Patients most likel to present with post-renal AKI
- Men with prostate enlargement
- Hx of malignancy
Discuss physical examination findings of a patient with AKI
- Hypo/ hypertension
- Asterixis
- Fluid loss? Hypotension and signs of circulatory collapse
- Glomerular disease? Hypertension, oedema, proteinuria, microscopic haematuria
- Presence of rash/ pettechiae? suggestive of glomerulonephritis
- Abdominal bruit? Renovascular disease
- Prostatic disease? Abdo distension due to full bladder
What tests would be done if AKI was suspected?
- Metabolic profile
- FBC
Venous blood gases
- Urinalysis and culture
- Renal ultrasound
- Chest x-ray (pulmonary oedema/ cardiomegaly)
Subsequent: CT/ MRI to evaluate cases of obstruction, cytoscopy if urethral stenosis suspected
*Renal biopsies rarely carried out for AKI
How many litres of fluid are filtered by the kidney every day?
180L
2L of urine produced
Electrolyte disturbance in AKI
Acute kidney injury (AKI) is often associated with systemic complications including volume overload; electrolyte and acid-base disturbances, particularly hyponatremia, hyperkalemia and metabolic acidosis
Why might a patient not have a metabolic acidosis due to AKI?
Vomiting
How are pre, intra and post renal AKI diagnosed?
Pre renal: largerly a clinical diagnosis e.g. if a patient has had a big bleed etc
Can be tricky to differentiate between pre-renal and renal esp. as pre renal can cause ATN (renal)
Renal: assess how full the bladder is
How can we differentiate between pre-renal and renal AKI?
Pre-renal: RAAS is activated leading to sodium and water retention = higher urine osmolality (>500)
Intra-renal: water isnt retained as well so urine osmolality is generally lower (<500), ATN = cell casts in urine, renal tubular epithelial cells, glomerulonephritis will cause haematuria
