MEDI7111 Lecture Notes - Lecture 13: European Synchrotron Radiation Facility, Metabolic Acidosis, Calcium Oxalate
Acute Kidney Injury
Epidemiology
Mild AKI (creatine ~150μmol/L) occurs in approximately 10% of all hospitalised patients. It
occurs in 5-20% of all critically ill patients and has a 70% male preference. AKI is
predominantly iatrogenic in aetiology and as such is highly preventable. Being aware of the
pharmacological renal toxins and the care taken to retain renal perfusion can help avoid AKI
in patients with potentially limited. However, the condition typically resolves completely
with no long term effects if the patient survives the acute injury.
Aetiology
Pre-renal causes (60-70%):
Pump problem
oCardiac failure
Circulating volume problem
oHypovolemia/shock
Renal hemodynamic problem
oOcclusion of the renal artery
Atheroma rupture and thrombotic occlusion
Tumour occlusion
oRenal vein thrombosis
oDrug effects on arterioles (NSAIDS and ACEIs)
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Acute tubular necrosis typically occurs in ischemic events as the tubules are particularly
susceptible to ischemia, as a result of the arrangement of blood vessels.
Renal causes (25-40%):
Blood stream infection
Acute glomerulonephritis
Toxins
Drugs
Rhabdomyolysis (crush injury/major trauma)
Haemolysis
Multiple myeloma
Post-renal causes (5-10%):
External obstruction
oProstatitis/BPH/prostate cancer
oCervical cancer
oRetroperitoneal fibrosis
Internal Obstruction
oRenal calculi
oUrothelial malignancy
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oBlood clots
oUreteric stricture
Clinical Features
AKI is defined as a precipitous and significant (>25-50%) decrease in GFR over a period of
hours to days with accompanying accumulation of nitrogenous wastes in the body with or
without a decrease in urine output.
Abrupt reduction in eGFR (not a useful predictor of recovery but does assist in
diagnosis)
Oliguria (occurs in 75% of patients)/anuria
Defects in secretory/re-absorptive functions of the kidney
oSeen on urea and electrolytes blood test
Significantly elevated serum creatinine
oIndicates GFR is below 50% of full function
oDue to the exponential relationship of serum creatinine and eGFR, small
changes in eGFR can be seen as large changes in serum creatinine when
kidney function is limited so this is not a reliable indicator of injury
Management
Take a thorough history (esp. drug history)
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Document Summary
Mild aki (creatine ~150 mol/l) occurs in approximately 10% of all hospitalised patients. It occurs in 5-20% of all critically ill patients and has a 70% male preference. Aki is predominantly iatrogenic in aetiology and as such is highly preventable. Being aware of the pharmacological renal toxins and the care taken to retain renal perfusion can help avoid aki in patients with potentially limited. However, the condition typically resolves completely with no long term effects if the patient survives the acute injury. Renal hemodynamic problem: occlusion of the renal artery. Tumour occlusion: renal vein thrombosis, drug effects on arterioles (nsaids and aceis) Acute tubular necrosis typically occurs in ischemic events as the tubules are particularly susceptible to ischemia, as a result of the arrangement of blood vessels. External obstruction: prostatitis/bph/prostate cancer, cervical cancer, retroperitoneal fibrosis. Internal obstruction: renal calculi, urothelial malignancy, blood clots, ureteric stricture.
