Renal Failure

Question 1

What are the stages of kidney injury?

Answer 1

RIFLE- need to know baseline renal function

RISK
INJURY
FAILURE
LOSS
END-STAGE

The further down, the worse the outcomes

Question 2

What UO defines OLIGURIA:

Answer 2

Essentially HALF NORMAL
400ml/day or <20ml/hr

ie. Kids: <0.5ml/kg/hr
ie. Infants: <1ml/kg/hr

Question 3

What UO defines ANURIA:

Answer 3

<100ml/day

Paeds: none

Question 4

PRErenal causes of AKI:

Answer 4

Hypoxia
Hypovolaemia
Hypotension
Oedema states (eg. CCF)
Vascular insufficiency:
STRUCTURAL
–> Renal artery stenosis/ clot
–> Renal vein clot
–> Hepatorenal syndrome
–> Dissection
AUTOREGULATION
–> NSAIDS, ACE, ARB.

Question 5

RENAL causes of AKI:

Answer 5

—-GLOMERULAR—-
Primary GN:
- IgA, foc/seg, membr, min change (nephrotic)
Secondary GN:
Nephritic: Post strep, IgA, vasculitis (TTP, HUS), endocarditis, Goodpastures
Nephrotic: SLE, HIV, HepB/C

—-TUBULOINTERSTITIAL—-
Acute tubular necrosis
ISCHAEMIC:
- Prolonged pre-renal insult
TOXIC
EXOG: Contrast, NSAIDs, Aminoglycosides, Ethylene glycol, Snake bite
ENDOG: Myoglobin, Haemoglobin, Uric acid, Bence-Jones proteins
STASIS: eg. obstruction by casts/ crystals

ATIN
- Pyelo
- Immune drug reaction
–> NSAIDs, Blactams, phenytoin, sulphonamides etc.

Question 6

Urea/Cr ratio. How to interpret:

Answer 6

Urea/ (Cr/1000)

>100 = Pre-renal
40 - 100 = Normal or post-renal
<40 = Renal

Question 7

Nephritic Syndrome:

Answer 7

Haematuria- casts, dysmorphic
Hypertension- Na/H20 retention
Oliguria
Mild proteinuria

______
Post-strep
IgA
Vasculitis (TTP, HUS)
Goodpasture
Endocarditis

Question 8

Nephrotic Syndrome:

Answer 8

Proteinuria- frothy, hypoalbuminaemia
Oedema
Hyperlipidaemia
+/- haematuria

____
Most primary GN
HIV/HepB/C
Malign.

Question 9

What is Goodpasture Syndrome?

Answer 9

Immune/ hypersensitivity.

Anti-GBM anitbodies –> autommune vasculitis of:
- Lungs: alveolar haemorrhage
- Kidneys: acute GN (nephritic)

Question 10

How can NSAIDS cause AKI?

Answer 10

Many different possibilities:

Prerenal
- Impaired autoreg
Renal:
- ATN (toxic)
- AITN (immune)

Question 11

Clinical features of Rhabdo:

Answer 11

Muscle pain only in 50%
Weakness only if severe

Hypovolaemia from fluid retention in injured muscles

Elevated CK 5x or more
HyPERK, HyPERuric, HyPERohosphat
HyPOcalcaemia
Metabolic acidosis

Myoglobinuria
–> ‘Tea’, red/brown
–> + for ‘blood’ on dipstick (but no RCC on cyto)
–> Pigmented casts
–> Causes toxic ATN –> renal failure

Question 12

What is renal tubular acidosis:

Question 13

General management of AKI:

Answer 13

Correct fluid status
Maintain renal perfusion
Avoid nephrotoxics
Dose reduce meds PRN
Maintain urine output/ clearance
Seek + treat cause
Ongoing monitoring/ supportive
________

Fluid challenge with 0.9% saline
If unresponsive to filling, maintain MAP >65 with NA/adren.
Frusemide
- bolus if overloaded.
- maintain UO >0.5ml/hr if oliguric
IDC, fluid chart
Fluid restrict to insensible (500ml) + overt measurable losses only.

Tx HTN usual ways. Aim patient’s usual BP.

ECG/ telem
Tx HyperK usual ways (if manifest, or if >6.5). Stop aldosterone/spirono/ACE etc.
HyperNa (hypotonics), Symptomatic HypoNa (dialysis)
Acidosis: NaBic, dialysis.
Others usually nil specific

RRT PRN

Question 14

Indications for renal replacement therapy in AKI/ acute renal failure:

Answer 14

Refractory:

Oliguria or anuria
Urea >35 or encephalopathy
Cr > 400
K >6.5 or rapidly rising
Na <100 or >160
pH <7.1
Refractory APO
Dialyzable tox

Question 15

Types of renal replacement therapy:

Answer 15

Haemodialysis
Peritoneal dialysis
–> Uses concentration gradient

Haemofiltration
–> Uses a pressure gradient
–> Blood is ‘pushed’ through the system + solutes ‘squeezed’ out

Haemodiafiltration

‘Continuous’ (eg. ICU) vs ‘intermittent’ RRT