AKI/CKD Flashcards
Compare AKI vs CKD
Definition of an AKI
rapid reduction in kidney function
-> inability to maintain electrolyte, acid-base and fluid homeostasis
medical emergency - need nephrologist
Chemical markers definition of AKI
AKI Stage 1: Increase in sCr by ≥26 µmol/L, or by 1.5 to 1.9x the reference sCr
AKI Stage 2: Increase in sCr by 2.0 to 2.9x the reference sCr
AKI Stage 3: Increase in sCr by ≥3x the reference sCr, or increase by ≥354 µmol/L
Summarise pre-renal AKI
reduced renal perfusion - either because of generalised reduction in tissue perfusion, or selective renal ischemia (renal artery stensosis)
No structural abnormality
Pre-renal AKI occurs when normal adaptive mechanisms fail to maintain renal perfusion
Physiological response to reduced circulating volume
activates central baroreceptors -> activation RAS -> vasopression, activation SNS -> vasoconstriction, increased CO, increased Na retention
Myogenic response -> afferent arteriole constricts with increased systemic pressure, and dilates with reduced pressure
tubuloglomerular feedback mechanism: increase in GFR -> increase in chloride ions in the early distal tubule -> afferent arteriole constriction -> decrease in GFR -> reduced chloride ions in distal tubule
Causes of pre-renal AKI
True volume depletion
* Lady in nursing home – v dehydrated
* Diabetes insipidus
Hypotension
Oedematous states
* Renal failure
* Heart/liver failure – ascites/peripheral oedema
Selective renal ischaemia
* Atherosclerotic disease
Drugs affecting glomerular blood flow
What is this
L renal artery stensosis
Kidney not being perfused as it should
Which class of drugs may predispose patients to developing pre-renal AKI?
NSAIDs
Calcineurin inhibitors
ACEi or ARBs
Diuretics
All of the above
All:
NSAIDs - decrease afferent arteriolar dilatation
Calcineurin inhibitors - decrease afferent arteriolar dilatation
ACEi or ARBs - decrease efferent arteriolar constriction
Diuretics – affect tubular function, decrease preload
What is acute tubular necrosis
When AKI becomes very established
If AKI goes on it -> ischemia of kidney -> ATN – harder to reverse
(doesnt respond to restoration of circulating volume)
Examples of causes of intrinsic AKI
May represent abnormality of any part of nephron
- Vascular Disease e.g. vasculitis
- Glomerular Disease e.g. glomerulonephritis
- Tubular Disease e.g. ATN
- Interstitial Disease e.g. analgesic nephropathy eg because of NSAIDs
Direct tubular injury as a mechanism of renal injury
Most commonly ischaemic (Pre renal -> ATN)
Endogenous toxins
* Myoglobin – muscle break down = myoglobin = blocks tubules
* Immunoglobulins
Exogenous toxins - contrast, drugs
* Aminoglycosides
* Amphotericin
* Acyclovir
Cola coloured urine and big bruise
Rhabdomyolysis
Cola urine is due to myoglobin
Systemic vasculitis
Non blanching rash
Young
AKI when so young – got to think about intrinsic renal cause
Examples of immune dysfunction -> renal inflammation
Glomerulonephritis
vasculitis
Examples of infiltration/abnormal protein deposition -> renal injury
Amyloidosis
lymphoma
myeloma-related renal disease
BPH
Really dilated calaceas - both are like this so the obstruction must be distal to the kidneys
This is hydronephrosis
Summarise post-renal AKI
Hallmark is physical obstruction to urine flow
(Intra-renal obstruction)
Ureteric obstruction (bilateral)
Prostatic / Urethral obstruction
Blocked urinary catheter
Pathophysiology of obstructive uropathy
GFR is dependent on hydraulic pressure gradient
Obstruction results in increased tubular pressure
Immediate decline in GFR
Huge increase in creatinine - more tahn in intrinsic AKI
Why do some AKIs resolve and others don’t
Acute wounds heal via four phases:
* Haemostasis
* Inflammation
* Proliferation
* Remodeling
Pathological responses to renal injury are characterized by imbalance between scarring and remodeling
Replacement of renal tissue by scar tissue results in chronic disease
Sequence of CKD
Stages of CKD
What do you use to risk stratify a patient with CKD
GFR and albumin creatinine ratio (ACR)
predicts risk of event and mortality in future
Regarding hyperkalaemia, which of the following is true
- It can lead to ECG changes such as peaked p waves and flattened t waves.
- In those with CKD, dietary intake is a major cause and high potassium levels are found in foods such as milk, chocolate, dried fruits and tomatoes.
- NSAIDs can lower potassium levels
- Hyperaldosteronism is a common cause
- All of the above
In those with CKD, dietary intake is a major cause and high potassium levels are found in foods such as milk, chocolate, dried fruits and tomatoes.
Renal dietitian will see them regularly
Would be flattened P waves and tall tented T -> VT -> VF
NSAIDs increase K
High aldosterone lower K
Any of above
Cant just assume epo is going to improve Hb – need to look for the other causes if they don’t respond
Summarise the development of hyperparathyroidism in CKD
Not excreting phos -> increase FGF23 = pee out phos = lower level 1aOH vit D = secondary hyperPTH
More PTH = more reistant bone is to PTH = viscious cycle
Summarise osteitis fibrosa
Osteoclastic resorption of calcified bone and replacement by fibrous tissue
due to secondary hyperparathyroidism
can get brown’s tumour
Summarise osteomalacia
Insufficient mineralisation of bone osteoid
due to reduced levels of active Vit D
Summarise adynamic bone disease
Excessive suppression of PTH results in low turnover and reduced osteoid
Very little osteoblast activity
CVD as a consequence of CKD
-Vascular calcification - lesions are heavy calcified plaques rather than lipid rich atheroma
-Uraemic cardiomyopathy
Uraemia -> cardiac muscle dysfunction -> cardiomyopathy
Most important consequence of CKD
Risk of cardiac event directly predicted by GFR
