All I
Pre renal Renal
Is Post renal
d d
Due to variations Acute Tubular Due to mechanical
of d kidney Necrosis ATN due obstruction of urinary
perfusion Sepsis to chronic renal outflow lymphoma
hypovalaemia hypoperfusion or tumour prostate
haemorrhage glomerulonephritis hyperplasia T
urinary infection
Pathophysiology
A Pre renal Results from impaired kidney perfusion
leading to 4 Nat H2O absorption There is activation
re
of RAAS Angiotensin II a
potent vasoconstrictor
Aldosterone release promoting Nat H2O reabsorption in
the collecting duct Low blood volume is also a stimulus
to the hypothalamus to promote ADH release
B Renal Acute Tubular Necrosis ATN due to prolonged
ischaemia yielding direct microvascular endothelial injury
and tubular ischaemia Nephrotoxins e.g NSAIDs
ionated contrast or
aminoglycoside Abx
, C Post renal Obstruction results in T intra tubular
pressure yielding tubular ischaemia and
atrophy
Key diagnostic factors
Hypotension or hypovalaemia due to sepsis haemorrhage
vomiting diarrhoea I often in older pts poor oral intake
Assess volume status
by
Cap refill Pulse BP axillae membranes
Dry
Reduced urine production Oliguria confirms an AKI
diagnosis if output co Sml kg hr for at least 6 hrs
often AKI pts are not oliguria
NB Anuria is more indicative of an obstructive cause
Investigations
Urea Creatinine Shows an
acutely T serum
creatinine T serum Potassium met acidosis
I perfusion I glomerular pressure d glomerular
filtration d Creatine clearance T Serum Creatinine
To diagnose Aki
by Creatinine if
A Tin serum creatinine of 126 within 48 hrs Of
A Tin serum creatinine to 21.5 baseline
NB False tin Creatinine
e.g recent trimethoprim
False d in Creatinine
e.g pregnancy
Pre renal Renal
Is Post renal
d d
Due to variations Acute Tubular Due to mechanical
of d kidney Necrosis ATN due obstruction of urinary
perfusion Sepsis to chronic renal outflow lymphoma
hypovalaemia hypoperfusion or tumour prostate
haemorrhage glomerulonephritis hyperplasia T
urinary infection
Pathophysiology
A Pre renal Results from impaired kidney perfusion
leading to 4 Nat H2O absorption There is activation
re
of RAAS Angiotensin II a
potent vasoconstrictor
Aldosterone release promoting Nat H2O reabsorption in
the collecting duct Low blood volume is also a stimulus
to the hypothalamus to promote ADH release
B Renal Acute Tubular Necrosis ATN due to prolonged
ischaemia yielding direct microvascular endothelial injury
and tubular ischaemia Nephrotoxins e.g NSAIDs
ionated contrast or
aminoglycoside Abx
, C Post renal Obstruction results in T intra tubular
pressure yielding tubular ischaemia and
atrophy
Key diagnostic factors
Hypotension or hypovalaemia due to sepsis haemorrhage
vomiting diarrhoea I often in older pts poor oral intake
Assess volume status
by
Cap refill Pulse BP axillae membranes
Dry
Reduced urine production Oliguria confirms an AKI
diagnosis if output co Sml kg hr for at least 6 hrs
often AKI pts are not oliguria
NB Anuria is more indicative of an obstructive cause
Investigations
Urea Creatinine Shows an
acutely T serum
creatinine T serum Potassium met acidosis
I perfusion I glomerular pressure d glomerular
filtration d Creatine clearance T Serum Creatinine
To diagnose Aki
by Creatinine if
A Tin serum creatinine of 126 within 48 hrs Of
A Tin serum creatinine to 21.5 baseline
NB False tin Creatinine
e.g recent trimethoprim
False d in Creatinine
e.g pregnancy
