12.7.1: Acute kidney injury Flashcards
What timeframe does an acute kidney injury occur over?
Hours to days (rather than weeks to months)
True/false: ‘acute on chronic’ kidney disease is possible.
True
* This describes an acute injury suffered in addition to pre-existing chronic renal disease.
* The injury may or may not be related to the cause of pre-existing disease.
How can we subdivide acute kidney injury based on location and cause?
- Haemodynamic i.e. pre-renal azotaemia
- Intrinsic renal
- Post-renal e.g. urethral obstruction
What might cause a haemodynamic AKI?
Anything that affects renal blood flow OR causes systemic hypotension
Common causes:
* Hypovolaemia
* Anaesthesia
* Use of NSAIDs
Explain how NSAIDs could cause a haemodynamic AKI
- NSAIDs cause prostaglandin inhibition
- Prostaglandins are very important in maintaining afferent renal blood flow
- NSAID overdose may lead to haemodynamic AKI; some patients are very susceptible even at normal doses
True/false: if we address the underlying cause of a pre-renal azotaemia early enough, we might be able to resolve it.
True
* There is some suggestion that haemodynamic AKI isn’t a true AKI, it is simply reduced renal blood flow. Usually we can restore renal perfusion using IV fluids.
* If we do not correct this early enough, intrinsic renal damage occurs: there is renal ischaemia and hypoxia.
What could cause intrinsic renal AKI?
- True renal damage is most commonly ischaemic/hypoxic or toxic in nature.
- Primary renal disease and infectious causes may also be implicated
What could cause ischaemic (intrinsic renal) AKI?
- Hypovolaemia; distributive/obstructive/cardiogenic shock
- Deep prolonged anaesthesia, especially where BP is not monitored ± there has been bleeding
- Thrombosis/DIC
- Hyperviscosity/polycythaemia
- NSAIDs
Polycythaemia
Abnormally high concentration of circulating red bloods cells.
Polycythaemia vera: bone marrow neoplasm that leads to over-production of erythrocytes.
Provide examples of primary renal disease that could lead to intrinsic renal AKI
- Infectious causes: urinary tract infection/pyelonephritis; Lepto
- Immune-mediated: glomerulonephritis, SLE
- Neoplasia e.g. lymphoma
Which organisms are most commonly implicated in UTIs?
a) gram-positive cocci
b) protozoal organisms
c) gram-negatives/ E. coli
d) gram-positive rods e.g. corynebacterium
c) gram-negatives/E. coli
Provide examples of secondary disease that could lead to intrinsic renal AKI
- Infectious cause e.g. FIP, Leishmania
- Malignant hypertension - prolonged 180mmHg systolic will cause pressure damage to kidneys
- Sepsis - due to endothelial glycocalyx damage, vascular leak, and microcirculatory disruption
- Hepatorenal syndrome in cirrhosis (rare)
Provide examples of nephrotoxins that could lead to intrinsic renal AKI
- NSAIDs
- Ethylene glycol
- Lillies (cats)
- Vitamin D toxicity (in psoriasis cream, harmful if ingested)
- Aminoglycoside antibiotics
What are the 4 phases of intrinsic AKI?
- Asymptomatic - towards the end of this phase, azotaemia begins to develop + urine output drops
- Hypoxia and inflammation responses propagate renal damage, particularly in the proximal tubule and the loop of Henle (these are highly metabolically active cells)
- This phase lasts up to 3 weeks. Urine output may be increased or decreased.
- Recovery phase: can last weeks-months; only happens if the kidneys haven’t completely died. Sodium may be lost and there is severe polyuria -> this can result in hypovolaemia, causing recurrent damage through hypoxia.
What happens if backflow pressure = GFR? e.g. with a urinary obstruction
- If backflow pressure = same as pressure in glomerulus, GFR becomes 0.
- Kidneys then die.
- This is why it is important to address urinary obstructions.
Describe how a post-renal AKI could develop/what could cause this
- Urinary obstruction e.g. ureteral damage post-spay, urethral obstruction/urolithiasis
- Urinary leakage e.g. damage to ureter, bladder, proximal urethra leading to uroabdomen
Your patient has an AKI and shows jaundice. What might you be suspicious of and why is this important?
AKI + jaundice = lepto until proven otherwise
Lepto is zoonotic
*according to Tom Hackney
Can use SNAP antibody test for this or send PCR or MAT to external lab
What clinical exam findings might make you suspicious of an AKI?
- Signs associated with fluid loss - dehydration/hypovolaemia
- Signs associated with concurrent illness e.g. sepsis
- Renal pain ± palpable enlargement - renal pain is a consistent finding in kidney disease
- Uremic halitosis and oral ulceration (rare) -> urea causes mucosal damage as it is acidic
What changes might you see on biochemistry in an AKI?
- Azotaemia
- Hyperphosphataemia (relatively marked)
- Hyperkalaemia (to a possibly dangerous level); hypokalaemia is possible
- Hypocalcaemia
- (Elevated hepatic parameters in leptospirosis)
What changes might you see on urinalysis in an AKI?
- Inappropriate USG
- Proteinuria
- Glucosuria
- Get a sample for culture and sensitivity -> may see WBCs/bacteria on cytology
USG is a marker of kidney function from:
a) the last few minutes
b) the last few hours
c) the last few days
d) the last few weeks
b) the last few hours
This means that if the AKI happened within the last hour, you might not see this on USG.
Describe the changes you might see on ultrasound with an AKI
- Kidneys may appear normal or enlarged (can measure in length or in relation to aortic diameter)
- **Parenchyma **may look normal but slightly oedematous (oedematous)
- Peri-renal free fluid may be seen with lepto (dogs) or lymphoma (cats)
- May see hydronephrosis with obstruction or pyelonephritis
- Could take renal biopsy but there is a risk of bleeding
What might radiography/CT be used for with regards to an AKI?
- Identification of obstruction - can use contrast
Treatment of AKI
- Treat any concurrent/causative disease
- Fluid therapy - 8-10x maintenance for 2 weeks, then 4 weeks to get down from 6x to just maintenance
- Goal is to maintain volume status and renal perfusion.
- Closely monitor to avoid volume overload
