Acute kidney injury Flashcards
AKI : Definition
Acute kidney injury (AKI) is an acute decline in kidney function, leading to a rise in serum creatinine and/or a fall in urine output.
AKI : What are the different types
- Pre renal AKI : most common
- Intrarenal AKI
- Post Renal AKI
AKI : Pre-renal causes
AKI : Pre-renal causes
Lack of blood flow causing ischaemia - usually due tohypovolaemia or hypotension
1. Renal artery stenosis : reduced blood flow
2 . Hypovolaemia
* Diarrhoea/vomiting
* Haemorrhage, Burns, 3rd space losses in Pancreatitis
3 . Hypotension
* Sepsis : Systemic vasodilation
* Congestive HF : reduced perfusion 2nd to poor ejection fraction of the heart
AKI : Definition
AKI : Intrinsic AKI pathophysiology
intrinsic cellular damage to glomeruli, renal tubules or interstitium of the kidneys themselves.
AKI : Definition
AKI : Intrinsic causes
intrinsic cellular damage to glomeruli, renal tubules or interstitIum of the kidneys themselves.
1 .* Prolonged pre-kidney AKIthat progresses to overt cellular damage is the most common cause.*
2 . Nephrotoxins(e.g., iodinated contrast agents, NSAIDs, aminoglycoside antibiotics)
3 . Inflammation
* Glomerulonephritis
* Acute tubular necrosis ATN (most common)
* Acute interstitial nephritis
* Rhabdomyolysis
AKI : Postrenal AKI pathophysiology
- Obstruction to the urine coming from the kidneys.
- Kidney injury associated with obstruction results from increased intratubular pressure yielding tubular ischaemia and atrophy
AKI : Postrenal AKI causes
- Kidney stone
- External compression of the ureter
- Ascending urinary infection (including pyelonephritis)
- Benign prostatic hyperplasia,
- Urinary retention
AKI : Clinical features
Pre -renal AKI may present with
1.Dizziness and Orthostatic hypotension
2. Vomiting - suggestive of hypovolaemia
3. Thirst and signs of hypovolaemia
4. Reduced Urine output
- Anuria } 2nd to post renal urinary obstruction or very severe pre-renal cause
Post renal AKI may present with
5. LUT sx : urgency, frequency, or hesitancy are suggestive of a urinary tract obstruction.
- Prostatic hyperplasiais a common cause of obstructive AKI in older men
6. Haematuria } caused by UTI / Kidney stones or acute glomerularnephritis
7. Fever, rash, and/or arthralgia } small vessel vasculitis or interstitial nephritis
AKI : Classification - Stage 1
- Rise in serum creatinine of 26 within 48 hours
- (1.5x) 50% or greater rise in serum creatinine over past 7 days
- Fall in urine output <0.5ml/kg/hour for >6 hours in adults
AKI : Classification - Stage 2
- Increase in creatinine 2.0 - 2.9 x baseline
- Reduction in urine output < 0.5ml/kg/hr for > 12 hours
AKI : Classification - Stage 3
- Increase in creatinine >3.0 x baseline or >353
- Reduction in urine output < 0.3ml/kg/hour for >24 hours
AKI : Investigations
- Creatinine
* Acute rise required for dx } rises are delayed for 24 hours post AKI - Daily U+Es until AKI has resolved
- Urine dipstick
- Kidney US } if ?Post renal cause
AKI : Management
- Optimise volume status / BP
* IV fluid resuscitation - if good response, likely pre-renal AKI cause
* Assess volume status and ensure BP is adequate
* Fluid input/output } consider catheterisation - Avoid nephrotoxins
- Treat underlying cause e.g. Sepsis
AKI : Complications
- Hyper-kalaemia : 2nd to impaired excretion
- Metabolic acidosis : impaired excretion of H+ ions due to renal impairment and low eGFR, may also be 2nd to sepsis which increases lactic acid production
-
Pulmonary oedema
- Iatrogenic secondary to excess IV fluid
- Renal artery stenosis can cause flash pulmonary oedema
AKI : Nephrotoxins to stop
- NSAIDs } cause interstitial nephritis
- Aminoglycosides } } cause interstitial nephritis
- Ace inhibitors, Angiotensin receptor antagonist, Diuretics
- RAAS modifying agents reduce kidneys amity to adapt to reduction in perfusion in AKI } make it more difficult to maintain eGFR in hypovolaemia
4 . Metformin
5 . Lithium
6 . Digoxin
