AKI/CKD Flashcards by Emily Southall

Compare AKI vs CKD

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Definition of an AKI

rapid reduction in kidney function
-> inability to maintain electrolyte, acid-base and fluid homeostasis

medical emergency - need nephrologist

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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

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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

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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

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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

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What is this

L renal artery stensosis
Kidney not being perfused as it should

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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

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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)

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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

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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

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Cola coloured urine and big bruise

Rhabdomyolysis
Cola urine is due to myoglobin

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Systemic vasculitis

Non blanching rash
Young
AKI when so young – got to think about intrinsic renal cause

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Examples of immune dysfunction -> renal inflammation

Glomerulonephritis
vasculitis

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Examples of infiltration/abnormal protein deposition -> renal injury

Amyloidosis
lymphoma
myeloma-related renal disease

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BPH
Really dilated calaceas - both are like this so the obstruction must be distal to the kidneys

This is hydronephrosis

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Summarise post-renal AKI

Hallmark is physical obstruction to urine flow

(Intra-renal obstruction)
Ureteric obstruction (bilateral)
Prostatic / Urethral obstruction
Blocked urinary catheter

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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

Recovery from obstructive uropathy

immediate relief of obstruction resture GFR fully

Prolonged obstruction -> glomerular ischemia, tubular damage, long term interstitial scarring

What two measures do we use to define severity of acute kidney injury?

Creatinine
UO

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

commonest causes of CKD

**Diabetes and obesity** Atherosclerotic renal disease Hypertension Chronic Glomerulonephritis Infective or obstructive uropathy Polycystic kidney disease

functions of the kidney

Excretion of water-soluble waste Water balance Electrolyte balance Acid-base homeostasis Endocrine functions: EPO, RAS, Vit D

Consequences of CKD

1]Progressive **failure of homeostatic function** -Acidosis -Hyperkalaemia 2]Progressive **failure of hormonal function** -Anaemia -Renal Bone Disease 3]**Cardiovascular disease **– ultimately the thing that kills the patients -Vascular calcification -Uraemic cardiomyopathy **4]Uraemia and Death**

Summarise renal acidosis

Metabolic acidosis Failure of renal excretion of protons -> low bicarb acidic env results in: * Muscle and protein degradation * Osteopenia due to mobilization of bone calcium * Cardiac dysfunction Treated with oral sodium bicarbonate (when pts' bicarb gets to 20mmol/L) – not fixing problem – just making the environment more healthy

**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

Consequences of high K

Potassium is the major intracellular cation Hyperkalaemia causes membrane depolarization * Cardiac function * Muscle function

Causes of high K

Common sequelae of CKD Especially among diabetics Medications * ACEi – can increase K * Spironolactone * ’Potassium-sparing’ diuretics

Anaemia of chronic renal disease

decline in eruthropoietin-producing cells, loss of renal parenchyma noted when GFR <30 Normochromic, normocytic anaemia vs IDA (microcytic) or B12/folate (macrocytic)

Mx of anaemia of chronic renal disease

erythropoiesis-stimulating agenst (ESAs) * Erythropoietic alfa (Eprex) * Erythropoietin beta (NeoRecormon) * Darbopoietin (aranesp) - longer acting Monitor BP because it can cause a rise

**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 renal bone disease

Complex entity resulting in reduced bone density, bone pain and fractures: -Osteitis fibrosa -Osteomalacia -Adynamic bone disease -Mixed osteodystrophy – combination of above

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

Treatment of renal bone disease

Phosphate control * Dietary * Phosphate binders Vit D receptor activators * 1-alpha calcidol - *Usually give 25OH vit d – but in these need to give active form – so 1 a calcidol* * Paricalcitol Direct PTH suppression * Cinacalcet

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

Three phases of uraemic cardiomyopathy

L ventricle hypertrophy LV dilatation LV dysfunction

True false - these are CI to transplant 1. HIV 2. BMI 3. Active sepsis 4. >65yrs 5. Any malignant disease

1. F 2. F 3. T 4. F 5. F

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AKI/CKD Flashcards

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