Acute Kidney Injury Flashcards

1
Q

What happens to creatinine at the kidney?

A

It is freely filtered by the glomerulus, but not reabsorbed or metabolised by kidney

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2
Q

What are some medications that cause an increase in serum creatinine?

A

Trimethoprim and cimetidine – they both inhibit tubular secretion

Creatine powder – will cause elevated creatinine and normal urea.

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3
Q

What are some causes of elevated urea/creatinine ratio?

A

Pre-renal hypovolaemia

Poor muscle bulk

Elevated BUN with GI bleeding, steroids and protein loading

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4
Q

What are the stages of acute kidney injury?

A

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

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5
Q

Just look at the picture coming up to refresh some of the reasons the kidney is so vulnerable.

A

Read: the medulla gets shafted!

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6
Q

“Please explain” some of the pathophysiology behind AKI.

A

Vasoconstriction is the problem with AKI. The biggest problem is the vasoconstriction!

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7
Q

In pre-renal AKI, what are the findings in the urine?

What is the FeNa?

A

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%)

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8
Q

How do we diffentiate intrinsic (renal) AKI?

A

Interestingly it is categorised by anatomy.

Particularly we look at:

tubular

interstitial

glomerular

vascular

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9
Q

What is the mechanism of acute tubular necrosis?

A

This is due to prolonged ischaemia, due to a direct injury.

Classically it is self limiting and recovery is over 7 - 21 days

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10
Q

What are causes of interstitial nephritis?

A

Beta-lactams - all penicillins

Diuretics

Other antibiotics - sulfonamides, vanc, rifampicin, indinavir

NSAIDs - brufen

rarely infections and malignancies

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11
Q

What are the findings that would support an interstitial nephritis?

A

Firstly, decreased renal function

sometimes fever

leucocytosis

eosinophils in the urine

urinary WBC

Don’t treat with steroids. Stop offending agent

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12
Q

What are the findings of glomerular renal disease?

A

History important

blood tests may be important

active urinary sediment (haematuria)

renal biopsy usually required

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13
Q

What is the minimum number of red cell casts to diagnose GN?

What do normal red cells in the urine mean?

A

Just a single is needed.

Normal red cells suggests bleeding from the collecting system

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14
Q

What does the urinalysis look like in ATN?

What about myoglobinuria?

A

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

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15
Q

What does the presence of WBC casts mean?

The presence of eosinophils suggests what?

A

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

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16
Q

What is the role of fractional excretion of sodium?

A

It is the most accurate test to differentiate prerenal and acute parenchymal.

17
Q

How do we calculate the FeNa%?

A

UNa x PCr

—————————————– x 100

PNa x UCr

18
Q

Are there any other conditions that make the interpretation of FeNa difficult?

A

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.

19
Q

What does the liver make cholesterol in setting of high albumin loss?

A

Not really sure. D’Intini reckons it is a substitute for albumin in the acopic liver.

20
Q

Nasal infection for a month, and the College wants to test if you can figure out how to differentiate postinfectious GN and Wegener’s.

A

So, complement levels are low in postinfectious GN.

They are normal or high in Wegener’s

21
Q

Which are the different conditions assocaited with low vs normal or high levels of complement?

A

This table is important to learn!

22
Q

Evaluation of the renal parenchyma by ultrasound is important and useful.

A

It can provide some information about the kidney itself. A nice normal kidney with vascular cortex, versus the echogenic changes of damaged kidney.

23
Q

When does contrast induced nephropathy occur? How much does the creatinine need to change to be defined as stage I AKI?

A

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

24
Q

What is the treatment of septic AKI complicated by hypotension (after having been adequately filled)?

A

Vasopressors (adr, NAdr)

25
Q

How does one treat pulmonary haemorrhage?

A

Plasma exchange

26
Q
A