Acute kidney injury Flashcards
List the functions of the kidneys
- Body fluid homeostasis – urine production
- Regulation of vascular tone – controls BP
- Excretory function – physiological waste e.g. urea, creatinine, drugs
- Electrolyte homeostasis -Na, K, Cl, Ca, Phos
- Acid-base balance –H+ and bicarbonate
- Endocrine function – production of erythropoietin; vitamin D metabolism and activation; renin
- Drug metabolism and disposal
What % of hospital admission patients develop AKI?
1 in 7 (some say 1 in 5)
Describe the traditional definition of AKI
• Rapid loss of glomerular filtration and tubular function over hours to days
• Retention of urea/creatinine
– Failure of homeostasis; even small increases in C are dangerous
What are some problems with the traditional definition of AKI?
– Lack of standardisation
– Absolute creatinine, changes in creatinine, urine output, need for dialysis
– Creatinine is insensitive and a late marker
– RRT hard endpoint but very late marker
– Wide spectrum of renal injury
Describe the current definition of AKI
• Increase in SCreatinine
– By ≥ 26.5 μmol/l (0.3 mg/dl ) within 48 hours; or
– To ≥ 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or
• Urine volume <0.5 ml/kg/h for 6 hours
Describe some immediately dangerous consequences of AKI
Acidosis – can cause cardiac arrest
Electrolyte imbalance - Hyperkalaemia can cause cardiac arrest
Intoxication - e.g. opiates can cause respiratory (and then cardiac) arrest
Overload - overload with fluid and pulmonary oedema can cause cardiac arrest
Uraemic complications
What are the 3 classes of aetiology for AKI?
- Pre-renal - Blood flow to kidney
- Renal (intrinsic) - Damage to renal parenchyma
- Post-renal - Obstruction to urine exit
List some pre-renal causes of AKI
Reduce effective circulation volume
– Volume depletion (haemorrhage/dehydration) - D&V
– Hypotension / shock – Sepsis is a major contributor in up to 50% cases of AKI
– Congestive cardiac failure / Liver failure
Arterial occlusion
Vasomotor
– NSAIDs/ACE inhibitors
List some intrinsic renal causes of AKI
Acute tubular necrosis (ATN) - Ischaemic
Toxin-related – Drugs (aminoglycosides / amphotericin / NSAID) – Radiocontrast – Rhabdomyolysis (Haem pigments – Snake venom / Heavy metals - Pb, Hg – Mushrooms etc
Acute interstitial nephritis (many causes including drugs (PPIs))
Acute Glomerulonephritis
Myeloma
Intra renal vascular obstruction
– Vasculitis
– Thrombotic microangiopathy
What type of cause is myeloma?
intrinsic renal
List some post-renal causes of AKI
Obstruction
– Intraluminal (calculus, clot, sloughed papilla)
– Intramural – within wall (malignancy, ureteric stricture, radiation fibrosis, prostate disease)
– Extramural – outside urinary system, compression (RPF, malignancy)
Why is the kidney susceptible to hypoperfusion?
Intrarenal heterogeneity of:
o Blood supply
o Oxygenation
o Metabolic demand
The cortex is richly perfused, whereas the medulla receives around 10-15% of renal blood flow
Medulla is hypoxic, yet metabolically active
Describe the course of acute ischaemic renal injury
Initiation
• Exposure to toxic/ischaemic insult
• Renal parenchymal injury evolving
• AKI potentially preventable
Maintenance
• Established parenchymal injury
• Usually maximally oliguric now
• Typical duration 1-2 weeks (up to several months)
Recovery
• Gradual increase in urine output
• Fall in serum creatinine (may lag behind diuresis)
If GFR recovers quicker than tubule resorptive capacity, excessive diuresis may result (eg post-obstructive natriuresis)
List an iatrogenic cause of AKI
Radiocontrast nephropathy (RCN)
- AKI following administration of iodinated contrast agent for imaging purposes
- Common contributor to hospital acquired AKI
- Usually transient renal dysfunction resolving after 72h
- May lead to permanent loss of function
List some risk factors for radiocontrast nephropathy
- Diabetes mellitus
- Renovascular disease
- Impaired renal function
- Paraprotein
- High volume of radiocontrast
- All of the above
