Editing Acute renal failure


'''Sudden reduction in renal function resulting in the accumulation of nitrogenous wastes.'''

== '''Principles of renal failure in surgical patient:''' ==

* The kidneys cannot function without adequate perfusion
* Renal perfusion is dependent on adequate blood pressure
* A surgical patient with poor urine output usually requires more fluid
* Absolute anuria is usually due to urinary tract obstruction
* Poor urine output in a surgical patient is not initially treated with diuretics

== '''Aetiology''' ==

* '''Pre-renal (75%) - can lead to ATN in hours.''' The kidney is structurally and functionally intact, but blood flow and GFR are reduced.
** Sepsis
** Hypovolaemia
** Low cardiac output
* '''Renal (20%) - involves parenchymal damage'''
** Acute tubular necrosis - commonest
** Renal ischaemia - hypoxia, hypo-perfusion
** Medications
*** Nsaids, ACE inhibitors
*** Note trimethoprim can cause a 30% rise in creatinine, without necessarily reflecting kidney injury, due to competitive inhibition of creatinine metabolism
** Iodinated contrast media
*** Can occur within 48 hours of administration
*** Pre-hydration
*** ?NAC
*** Systematic reviews now saying this may not really exist
** Interstitial nephritis
** Hepatorenal syndrome
** Abdominal compartment syndrome
* '''Post-renal (5%) - obstruction and back-pressure'''
** Bilateral ureteric obstruction
** Bladder outlet obstruction

== Pathophysiology: ==

* GFR can be estimated from serum creatinine, BMI and gender
**
* Pre-renal injuries:
** Systemic hypoperfusion leads to increased sympathetic neural tone and release of renin and ADH
** Leads to arteriolar vasoconstriction primarily in the renal, splanchnic and musculocutaneous circulations to preserve blood flow to the heart and brain
** Renal vasoconstriction leads to reduced blood flow and GFR
* Acute tubular necrosis
** Occurs in the setting of prolonged or severe ischaemia
** Renal tubular cells are more vulnerable than the cortex due to their position deep in the medulla
** May lead to necrosis, with denuding of the epithelium and occlusion of the tubular lumen by casts and cell debris
* Urine output
** Normal urine output is 0.5-2mL/kg/hr
** Oliguria is <0.5mL/kg/hr
** Anuria is <100mL/day (approx 0.1mL/kg/hr)

== Diagnosis and classification: ==

* Oliguric (<400mL/ day or <17mL/hr)
* Non-oliguric (>2L/day)
* '''After you have excluded post-renal causes, and undertaken adequate fluid resuscitation, you can diagnose and classify as AKI based on:'''
** 'Acute Kidney Injury Network' classification is most useful according to CCrISP - one of:

* Three stages of AKI:

== Approach to workup/investigation: ==

* Sudden onset post-op complete anuria is post-renal UNTIL PROVEN OTHERWISE
** Catheter kinks
** Surgical damage to urinary tract
** Probably needs an USS straight away if nothing obvious found
* Initial investigations:
** Dipstick/MCS/osmolarity
*** Marked proteinuria or microscopic haematuria with casts suggests a primary renal insult
*** Casts
**** ATN: pigmented coarse granular casts and renal tubular epithelial cells
**** Glomerulonephritis: proteinuria, haematuria, red cell casts
**** Pyelonephritis: White and red cell casts
** USS
*** As above - mandatory in anuric patient
*** The acutely injured kidney will be echo bright due to oedema, but normal size
*** CKD likely shows a small (<9cm) kidney with echo-bright parenchyma
** Bloods to consider
*** FBE/UEC/CMP
*** LFT (hepatorenal)
*** CK (rhabdomyolysis - dark brown urine that tests positive for myoglobin)
*** CRP
*** VBG/ABG (for lactate and overall physiology)

* Establish aetiology:
** Is it pre-renal? And do we need to restore volume?
** Differentiating prerenal from renal
*** Prerenal will be a/w dehydration - consider whether large losses are occurring elsewhere
*** BUN > 20
*** Brown urine? Myoglobinuria?
*** In ATN, expect low osmolar urine with high sodium and low urea/creatinine, because the concentrating ability is impaired. In pre-renal AKI, the concentrating ability is retained, so you tend to get high osmolarity and high urea/creatinine. See full table below.
** If prerenal - is it hypovolaemia or heart failure?
*** If hypovolaemic - give fluids
*** If heart failure - give diuretics
* Management:
** IDC?
** Avoid nephrotoxics - aminoglycosides, NSAIDs, ACE inhibitors, opioids, beta blockers
** Alter dose of renally excreted meds
** Careful fluid balance - restore perfusion as much as possible by first restoring euvolaemia, then an accurate maintenance fluid rate
** Check electrolytes - essentially check indications for dialysis
** Check for complications below
** Maintain sats >94%

== '''Complications''' ==

* '''Hyperkalaemia'''
** See separate topic
**
* '''Pulmonary oedema'''
** Sit patient upright
** Stop all infusions
** High flow oxygen
** Monitor saturations
** ?IV diamorphone 2.5 mg
** ?IV GTN infusion if SBP > 100
** ?IV frusemide
** ?ICU
* '''Indications for dialysis:'''
** Absolute:
*** Refractory hyperkalaemia (>6mmol/L)
*** Refractory pulmonary oedema and fluid overload
*** Uraemic encephalopathy
** Relative:
*** Acidosis (pH < 7.2)
*** Uraemia
**** Threshold relates to the rapidity of rise as well as the absolute urea level and presence of symptoms
**** Rise above 35mmol/L unresponsive to other therapies is usually an absolute indication
*** Pericarditis
*** Toxin removal

[[Category:Renal]]
[[Category:Intern education]]