ACUTE RENAL FAILURE


DEFINITION
Med school / CCrISP notes.

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AETIOLOGY
See oliguria.
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BIOLOGICAL BEHAVIOUR

Pre-renal:

See oliguria notes

Renal:
Structural kidney injury is hallmark of AKI
Glomerular, tubular or interstitial damage leads to nephron dysfunction
- may be primary or due to prolonged ischaemia (ATN).

Ischaemic injuries follow three phases:

i) initiation phase - see
oliguria notes
- cellular injury is often proximal tubules; though distal nephron injury also occurs
- distal nephron can become obstructed by debris; principal site for apoptotic cell death.
--> inability to concentrate urine; failure to excrete concentrated urine, even in presence of oliguria is seen; low osmolality <300 mOsm/kg.

ii) maintenance phase
GFR stabilises and uraemic complications arise
- usually lasts 1-2 weeks

iii)  recovery phase
- kidney behaves as in CRF
- because only a proportion of the nephron mass has recovered, each nephron has a much higher daily solute load to excrete.
--> conserving Na+, K+, HCO3-, and H20 is therefore difficult.
- major water and eletrolyte losses are unusual however with good management,
--> except in post-renal diuresis, where large losses may occur.
- by 6mo, the kidney will be at ~85-90% of premorbid function.
--> some will not recover, progressing to CRF

Contrast nephropathy may be contributory
- if

Post-renal:
Urinary retention
--> progressive rise in intraluminal pressure
--> compression and thinning of renal parenchyma.
- must be bilateral obstruction to cause ARF, eg bladder neck or urethral blockage
 
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MANIFESTATIONS

Symptoms
Systemic
Anorexia, nausea, vomiting, occasionally diarrhoea, muscle cramps
Encephalopathy (late).
Volume overload.

Pre-renal
See oliguria notes

Renal
Oliguria in 50%.
Features of underlying cause.

Post-renal
Anuria is most often due to obstruction.
Features of underlying cause.

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INVESTIGATIONS

As per clinical suspicion
- and see also oliguria notes for invest

Urine
Heavy proteinuria or haematuria with casts suggests a primary renal insult

Plasma urea and creatinine
Normally these are excreted at steady state
- related to production rate, ADH release, metabolism rate and adequacy of renal function.
Urea is a less reliable measure than creatinine
- creatinine is produced at a more constant rate (unless rhabdomyolysis)
- and is not concentrated in the renal medulla.

Imaging
USS
Obstruction
must be ruled out immediately in the anuric pt
- and in 24 hours in all other pts with renal impairment.
- this will also give info about the kidney sizes.
XR
Plain abdo XR may detect renal calculi, but USS usually gives more information
CT scanning
Gives best anatomical detail
- and if contrast can be used adds info about renl function
--> remember all contrass are nephrotexic, particularly if ECF depleted or DM
Angiography & Radionuclide studies
Useful for blood flow / specific valvular lesions (and perhaps treatment of such)

Histology
Only done in normal-sized kidneys to diagnose acute cause.
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MANAGEMENT

See also oliguria notes
- there is crossover.

The 5 Rules of Renal Failure (CCrISP)
1. Kidneys need adequate perfusion
2. Perfusion depends on adequate BP
3. A surgical pt with low urine output usually requires more fluid.
4. Absolute anuria is most often due to urinary tract obstruction.
5. Poor urine output is not due to frusemide deficiency.

Principles of Management
i) Assist & correct resp / circulatory deficit
ii) Manage immediate life-threatening complications
iii) Exclude obstruction to the urinary tract
iv) Carefully diagnose and treat underlying cause
v) Summon help from a specialist.

Pre-renal
See oliguria

Renal
Treat underlying cause
Maintain fluid and electrolyte balance
- weigh patients and check electrolytes daily.
- avoid hypotonic IV fluids.
Maintain adequate nutrition
- while restricting fluid and sodium intake where required.
Treat hypertension with an ACE inhibitor (note below).
Modify drug regimen to take renal impairment into account.
Pulmonary oedema is best treated with morphine and oxygen
HDU care with renal physician input
- may use diuretics if deemed to have adequate preload and making some urine; little benefit if not responses and may be nephrotoxic themselves if oliguric.
- don't alter course but may help manage volume and nutitrion.
Ultimately, renal replacement therapy may be indicated
- e.g. hypervolemia and metabolic acidosis.
- e.g. intermitent hemodyalisis or constant ; filtration.
rhabdomyolysis
high CK, urine myoglobin, which degrades into free radicles and metabolites toxic to kidney.
enforced alkaline diureses e.g. mannitol needed to clear
ICU with aggressive hydration and monitoring

Post-renal

Relieve obstruction
- drainage of an infected obstructed urinary tract is a medical emergency.
--> urethral or suprapubic catheterisation
--> antibiotic cover is essential but often forgotten.
Post-obstruction diuresis may follow
- requiring fluid replacement: measure and replace (?0.75:1)
 
Treating Hyperkalaemia
Requires immediate treatment to prevent life-threatening dysrhythmia and cardiac arrest.
- the rate of rise is more important than absolute levels
Longstanding hyperkalaemia is less dangerous than a recent rise.
A rise to a level greater than 6.0 mmol/L shoulc cause concern
All iatrogenic causes should be stopped.
- this includes ACEi, and other K+ sparing diuretics.
If ECG signs are present, administer IV calcium
- followed by glucose with / without insulin, sodium bicarb and salbutamol IV under ECG monitoring.
- note no K+ is actually removed by doing this, it is simply moved intracellularly.
Ion-exchange resins should be avoided unless there is no alternative
- they are slow, and unpleasant for everybody.
- and orally they are potent constipating agents.
RRT will be needed if these are insufficient

Renal Replacement Therapy
Indicated if:
- uncontrolled hyperkalaemia
- severe salt and water overload, usually with pulmonary oedema
- uraemia (to prevent encephalopathy); a level of 35mmol/L unresponsive to other therapy is an absolute indication
- acidosis
RRT is discontinued once renal function improves to allow aadequate clearance of nitrogenous waste products.

Dialysis

Process by which small-molecular-weight solute equilibrates between a blood compartment and a dialysate compartment separated by a semipermeable membrane.
- solute moves across its concentration gradient.
- dialysate contains normal solute in appropriate concentrations to maintain normal blood concentrations, eg Na, Ca, Mg, Cl-.

Haemofiltration

Plasma water is driven under pressure through a semipermeable membrane in a large volume.
- like what happens in a glomerulus.
Water and solute are then replaced from a separate source and filtrate is discarded.
Allows higher clearance of small-molecular-weight substances
- and may be less stressful on the circulation of the critically ill.

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