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Definitions

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Oliguria: Decreased urine output values

Uraemia: Raised level of urea in the blood

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Azotaemia: Raised level of nitrogenous compounds in the blood

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NSAIDs: Non-steroidal anti-inflammatory drugs

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Intrinsic: Originating due to factors caused within the body

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Benign: No harmful effects

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Malignant: Dangerous/harmful effects

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Hypoperfusion: Sudden reduction to blood flow to the kidneys

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GFR: Glomerular Filtration Rate

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Eosinophiluria: Eosinophils in the urine

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Haematuria: Blood in the urine











Useful equations
Creatinine clearance: (U x V)/P mL/min
U = Urine creatinine conc
...
umol/L
** urine collection is the main source of error in calculating creatinine
concentration/remember to calculate flow rate per minute – usually expressed in 24 hrs (aka
1440 minutes) (V/1440 = V mL/min)
Estimated GFR (eGFR aka Cockcroft-Gault equation): ((140 – AGE in years) x WEIGHT in
kg)/plasma creatinine umol/L = X mL/min
eGFR is invalid for people who are pregnant, >18yo, or extremes in body mass
(anorexia/obesity)
Underweight BMI = <18
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5 - 24
...
The aetiology of AKI is prerenal/intrinsic/post-renal
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Normal physiology of the kidneys
In normal physiology, the function of the kidneys is to remove waste, produce hormones and
control extracellular fluid volume and composition
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Filtrate (waste), which is initially filtered by
small arterioles called glomeruli within the kidneys, travels to the renal tubules
...
Filtrate is turned into urine and
excreted
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How the condition affects normal physiology
PRE-RENAL AKI
With pre-renal AKI, the cause of the kidney injury occurs before the kidneys, relating to the
renal artery or renal vein
...
Decreased renal blood flow can be caused by a
variety of circulatory insufficiencies such as absolute loss of body fluid caused by
dehydration, vomiting, severe burns and major haemorrhage or relative fluid loss caused by
septicaemia, low cardiac output (i
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congestive heart failure – pooling of blood in venous
side of heart – which reduces blood fluid volume) and hypotension
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Tubular function in pre-renal AKI is preserved despite the renal hypoperfusion (sudden
reduction in blood flow)

INTRINSIC AKI
Intrinsic AKI is caused by intrinsic damage to the kidneys, including damage to the tubules,
glomeruli or interstitium (space between the tubules)
...
Causes include acute tubular necrosis (ATN), renal
diseases such as acute interstitial nephritis, and intrarenal obstruction
...
ATN occurs when the epithelial cells that line the tubules necros (die), this
can be caused by ischemia (lack of blood flow to the cells); this lack of blood flow can be
originally caused by pre-renal AKI (pre-renal AKI results in decreased blood flow to the
kidneys)
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Nephrotoxins: Another cause of ATN is due to the presence of nephrotoxins, which can
damage epithelial tubular cells
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Uric
acid can build up when cancer cells undergo targeted treatments such as chemotherapy
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Regardless of cause, when epithelial tubular cells necros they move inward and block the
tubule, creating a higher ‘pressure level’ within the tubule
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As a result
of this pressure increase the fluid filtered across from one area to another is lower, lowering
the glomerular filtration rate (GFR)
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If the underlying issue causing ATN is addressed, patients can recover due to the ability of
tubular epithelial cells to regenerate in a matter of weeks
Interstitium: Acute Interstitial Nephritis (AIN)
AIN is inflammation of the interstitium caused by an influx of immune cells (neutrophils and
eosinophils)
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Early symptoms include oliguria and eosinophiluria,
general symptoms include fever and rash
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RPN can
cause haematuria and flank pain
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POST-RENAL AKI
Post-renal AKI is caused by an obstruction to the outflow from the kidneys in the ureters,
blocking the flow of urine
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The impact of kidney outflow can also be caused by a blockage within
the ureter, including kidney stones
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In normal physiology filtered fluid
moves from high pressure arterioles to low pressure renal tubule
...
Due to the decrease in blood filtered per min, less water
compounds i
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urea and creatinine are filtered out of the blood, leading to azotaemia (high
levels of nitrogen compounds in the blood) and oliguria (low levels of urine)
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The high pressure within the tubular systems forces more
reabsorption of sodium, water and urea, but not creatinine because little to no creatinine
gets reabsorbed
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Hypertension (high blood pressure): The most common cause of CKD
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The thickening of the artery walls results in a
narrow lumen and thus less blood and oxygen get delivered to the kidney, resulting in
ischaemic injury to the nephron’s glomerulus
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TGFB1 among other growth factors cause regression of mesangial cells to a previous immature

stem cell state called mesangioblasts
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Glomerulosclerosis reduces the
nephrons’ ability to filter blood, leading to CKD
Diabetes: Second most common cause of CKD
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The process of glycation
causes an efferent arteriole to become stiff and narrower (known as hyaline arteriosclerosis)
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The kidneys
response to this high-pressure state, supportive mesangial cells secrete excess extracellular
matrix (glomerulosclerosis) which expand the glomerulus
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Other causes include: pyelonephritis, renovascular disease and polycystic kidneys

Compare RIFLE and KDIGO
There are differing NICE guidelines to detect AKI
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RIFLE staging (risk, injury, failure, loss of function, end stage renal disease
[ESRD]) is used to classify AKI based on serum creatinine and urine output
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KDIGO covers
both RIFLE and AKIN, taking into account changes in creatinine in 48 hours or a
decrease in GFR over 7 days
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Categories include GFR category and ACR (Albumin:Creatinine ratio)
category, which range from G1 to G5 and A1 to A3 respectively
Compared to KDIGO, RIFLE can be used to diagnose AKI independently, and is
used so in the most frequency
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Another positive is that the uniform definition for AKI is defined in
stages 1 to 3, which is assessed by serum creatinine and urine output, that same
factors that RIFLE uses to diagnose AKI

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