CHEMPATH: Acute kidney injury and chronic kidney disease Flashcards
Compare and contrast AKI vs CKD.
AKI:
- Abrupt decline in GFR
- Potentially reversible
- Treatment targeted to precise diagnosis and reversal of disease
CKD:
- Longstanding decline in GFR
- Irreversible
- Treatment targeted to prevention of complications of CKD and limitation of progression
What are the functions of the kidney?
- Excretion of water-soluble waste
- Water balance
- Electrolyte balance
- Acid-base homeostasis
- Endocrine functions - EPO, RAS, Vit D
What are the different stages of AKI according to KIDGO?
AKI Stage 1:
- sCr : x1.5- 1.9 the reference OR rise of ≥26 µmol/L
- UO: <0.5ml/kg/hr for 6-12 hrs
AKI Stage 2:
- sCr : x2.0-2.9 the reference
- UO: <0.5ml/kg/hr for _>_12hrs
AKI Stage 3:
- sCr : x≥3 the reference OR or rise of ≥354 µmol/L
- UO: <0.3ml/kg/hr for _>_24hrs OR anuria for _>_12 hours
Define AKI.
A rapid reduction in kidney function, leading to an inability to maintain electrolyte, acid-base and fluid homeostasis, defined as any of the following:
- sCR increase of _>_26.5umol/L within 2 days
- sCr _>_x1.5 the baseline, known to have occurred in the last 2 weeks
- urine volume <0.5ml/kg/hr
What are the three categories of AKI causes?
- pre-renal
- intrinsic renal
- post-renal
What is the aetiology of pre-renal AKI?
Reduced renal perfusion –>
- generalised reduction in tissue perfusion
- OR selective renal ischaemia
Pre-renal AKI occurs when normal adaptive mechanisms (RAS) fail to maintain renal perfusion
Summarise RAS response to reduced circulating volume.
- Activation of central baroreceptors
- Activation of RAS
- Release of vasopressin
- Activation of sympathetic system
- Vasoconstriction, increased cardiac output, renal sodium retention
What are the clinical causes of pre-renal AKI?
- True volume depletion
- Hypotension
- Oedematous states – fluids not in the right compartment because fluid is mostly in the interstitium
- Selective renal ischaemia
- Drugs affecting glomerular blood flow
What does this show?
![](https://s3.amazonaws.com/brainscape-prod/system/cm/385/829/353/q_image_thumb.jpg?1651673146)
Renal artery stenosis to the left kidney
Which class of drugs may predispose patients to developing pre-renal AKI? Explain each.
- A.NSAIDs
- B.Calcineurin inhibitors
- C.ACEi or ARBs
- D.Diuretics
- E.All of the above
All of the above
- NSAIDs - decrease afferent arteriolar dilatation
- Calcineurin inhibitors - decrease afferent arteriolar dilatation
- ACEi or ARBs - decrease efferent arteriolar constriction
- Diuretics – affect tubular function, decrease preload
Is AKI the same as ATN?
No, ATN occurs when prolonged insult leads to ischaemic injury i.e. prolonged AKI –> ATN
Pre-Renal AKI is not associated with structural renal damage and responds immediately to restoration of circulating volume whereas ATN does not respond.
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A 68 year old man with previously normal renal function is found to have a creatinine of 624μmol/l. Renal ultrasound shows the following appearance in both kidneys. What is the likely cause of his AKI?
- A.Right-sided kidney stone
- B.Left ureteric transitional cell carcinoma
- C.Membranous glomerulonephropathy
- D.Benign prostatic hypertrophy
- E.Amyloid
![](https://s3.amazonaws.com/brainscape-prod/system/cm/385/829/358/q_image_thumb.jpg?1651673336)
D.Benign prostatic hypertrophy
What are the post-renal causes of AKI?
- (Intra-renal obstruction)
- Ureteric obstruction (bilateral)
- Prostatic / Urethral obstruction
- Blocked urinary catheter
What is the pathophysiology of post-renal AKI?
- Obstruction results in increased tubular pressure
- Immediate decline in GFR
- GFR is normally dependent on hydraulic pressure gradient
What are the renal complications of prolonged obstructive uropathy?
- Glomerular ischaemia
- Tubular damage
- Long term interstitial scarring
What are the renal causes of AKI?
Abnormality in any part of the nephron:
- Vascular Disease e.g. vasculitis
- Glomerular Disease e.g. glomerulonephritis
- Tubular Disease e.g. ATN
- Interstitial Disease e.g. analgesic nephropathy
What are 5 causes of direct tubular injury causing renal AKI?
Ischaemia (most common)
Endogenous toxins
- Myoglobin
- Immunoglobulins e.g. Myeloma
Exogenous toxins - contrast, drugs
- Aminoglycosides
- Amphotericin
- Acyclovir
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Rhabdomyolysis