Acute Kidney Injury Flashcards
What happens to creatinine at the kidney?
It is freely filtered by the glomerulus, but not reabsorbed or metabolised by kidney
What are some medications that cause an increase in serum creatinine?
Trimethoprim and cimetidine – they both inhibit tubular secretion
Creatine powder – will cause elevated creatinine and normal urea.
What are some causes of elevated urea/creatinine ratio?
Pre-renal hypovolaemia
Poor muscle bulk
Elevated BUN with GI bleeding, steroids and protein loading
What are the stages of acute kidney injury?
There are stages 1, 2 and 3 for acute kidney injury
Stage 1: elevated serum Cr of more than 26.4 OR > 150- 200% OR Less than 0.5mL/kg/hr for > 6 hours
Stage 2: Elevated serum Cr by 200-300% OR Less than 0.5mL/kg/hr for >12 hours
Stage 3: Elevated serum Cr of >300% or serum Cr >354 with elevated of >44 OR Less than 0.3mL/kg/hr for 24 hours or anuria for 24 hours
Just look at the picture coming up to refresh some of the reasons the kidney is so vulnerable.
Read: the medulla gets shafted!
“Please explain” some of the pathophysiology behind AKI.
Vasoconstriction is the problem with AKI. The biggest problem is the vasoconstriction!
In pre-renal AKI, what are the findings in the urine?
What is the FeNa?
The urinalysis should demonstrate normal urine with no cells or protein and there should be high urine osmolarity
The FeNa excretion should be low (<1%)
How do we diffentiate intrinsic (renal) AKI?
Interestingly it is categorised by anatomy.
Particularly we look at:
tubular
interstitial
glomerular
vascular
What is the mechanism of acute tubular necrosis?
This is due to prolonged ischaemia, due to a direct injury.
Classically it is self limiting and recovery is over 7 - 21 days
What are causes of interstitial nephritis?
Beta-lactams - all penicillins
Diuretics
Other antibiotics - sulfonamides, vanc, rifampicin, indinavir
NSAIDs - brufen
rarely infections and malignancies
What are the findings that would support an interstitial nephritis?
Firstly, decreased renal function
sometimes fever
leucocytosis
eosinophils in the urine
urinary WBC
Don’t treat with steroids. Stop offending agent
What are the findings of glomerular renal disease?
History important
blood tests may be important
active urinary sediment (haematuria)
renal biopsy usually required
What is the minimum number of red cell casts to diagnose GN?
What do normal red cells in the urine mean?
Just a single is needed.
Normal red cells suggests bleeding from the collecting system
What does the urinalysis look like in ATN?
What about myoglobinuria?
ATN is associated with granular muddy brown casts. Tubular cells or casts supports the diagnosis of ATN
Myoglobinuria has reddish brown or cola-coloured urine. The trick is a positive urine dip for haeme, and no RBC in the microscopic exam
What does the presence of WBC casts mean?
The presence of eosinophils suggests what?
This usually means pyelonephritis or acute interstitial nephritis.
well, sometimes it suggests interstitial nephritis. but these can also be seen in UTI and GN, and atheroembolic disease
What is the role of fractional excretion of sodium?
It is the most accurate test to differentiate prerenal and acute parenchymal.
How do we calculate the FeNa%?
UNa x PCr
—————————————– x 100
PNa x UCr
Are there any other conditions that make the interpretation of FeNa difficult?
Yes. While <1% is for prerenal and > 2% for parenchymal disease, the <1% is also seen with post-ischaemic ATN, ATN on top of CKD
AKI due to contrast, haem pigment, acute GN or vasculitis can also cause this
Con-current diuretic therapy also makes interpretation difficult.
What does the liver make cholesterol in setting of high albumin loss?
Not really sure. D’Intini reckons it is a substitute for albumin in the acopic liver.
Nasal infection for a month, and the College wants to test if you can figure out how to differentiate postinfectious GN and Wegener’s.
So, complement levels are low in postinfectious GN.
They are normal or high in Wegener’s
Which are the different conditions assocaited with low vs normal or high levels of complement?
This table is important to learn!
Evaluation of the renal parenchyma by ultrasound is important and useful.
It can provide some information about the kidney itself. A nice normal kidney with vascular cortex, versus the echogenic changes of damaged kidney.
When does contrast induced nephropathy occur? How much does the creatinine need to change to be defined as stage I AKI?
It occurs day 2 - 5 and it needs to move by 24 micromol/L to be classified as stage I
lots of risk factors.
withhold nephrotoxics
NAC doesn’t really help.
optimise the volume prior!
Sodibic is contraversial, but maybe will
What is the treatment of septic AKI complicated by hypotension (after having been adequately filled)?
Vasopressors (adr, NAdr)
