CHEMPATH: Acute kidney injury and chronic kidney disease Flashcards Preview

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Flashcards in CHEMPATH: Acute kidney injury and chronic kidney disease Deck (47)
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1
Q

Compare and contrast AKI vs CKD.

A

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
2
Q

What are the functions of the kidney?

A
  1. Excretion of water-soluble waste
  2. Water balance
  3. Electrolyte balance
  4. Acid-base homeostasis
  5. Endocrine functions - EPO, RAS, Vit D
3
Q

What are the different stages of AKI according to KIDGO?

A

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
4
Q

Define AKI.

A

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
5
Q

What are the three categories of AKI causes?

A
  1. pre-renal
  2. intrinsic renal
  3. post-renal
6
Q

What is the aetiology of pre-renal AKI?

A

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

7
Q

Summarise RAS response to reduced circulating volume.

A
  1. Activation of central baroreceptors
  2. Activation of RAS
  3. Release of vasopressin
  4. Activation of sympathetic system
  5. Vasoconstriction, increased cardiac output, renal sodium retention
8
Q

What are the clinical causes of pre-renal AKI?

A
  • 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
9
Q

What does this show?

A

Renal artery stenosis to the left kidney

10
Q

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
A

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
11
Q

Is AKI the same as ATN?

A

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.

12
Q

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
A

D.Benign prostatic hypertrophy

13
Q

What are the post-renal causes of AKI?

A
  • (Intra-renal obstruction)
  • Ureteric obstruction (bilateral)
  • Prostatic / Urethral obstruction
  • Blocked urinary catheter
14
Q

What is the pathophysiology of post-renal AKI?

A
  • Obstruction results in increased tubular pressure
  • Immediate decline in GFR
  • GFR is normally dependent on hydraulic pressure gradient
15
Q

What are the renal complications of prolonged obstructive uropathy?

A
  • Glomerular ischaemia
  • Tubular damage
  • Long term interstitial scarring
16
Q

What are the renal causes of AKI?

A

Abnormality in any part of the nephron:

  1. Vascular Disease e.g. vasculitis
  2. Glomerular Disease e.g. glomerulonephritis
  3. Tubular Disease e.g. ATN
  4. Interstitial Disease e.g. analgesic nephropathy
17
Q

What are 5 causes of direct tubular injury causing renal AKI?

A

Ischaemia (most common)

Endogenous toxins

  • Myoglobin
  • Immunoglobulins e.g. Myeloma

Exogenous toxins - contrast, drugs

  • Aminoglycosides
  • Amphotericin
  • Acyclovir
18
Q
A

Rhabdomyolysis

19
Q

A 40 year old female presents with a rash and AKI is diagnosed. What is the most likely cause of her renal failure from the following list?

  • A.NSAIDs
  • B.Systemic vasculitis
  • C.Amyloidosis
  • D.Tumour lysis syndrome following chemotherapy for lymphoma
  • E.Myeloma
A

Systemic vasculitis

20
Q
A
21
Q

Give 2 examples of how immune dysfunction can cause renal AKI.

A
  • Glomerulonephritis
  • Vasculitis
22
Q

Give 2 examples of how infiltration/abnormal protein deposition can cause renal AKI.

A
  • Amyloidosis
  • Lymphoma
  • Myeloma-related renal disease
23
Q

What are the top 5 causes of in-hospital AKI?

A
  1. Decreased renal perfusion
  2. Medications
  3. Radiographic contrast media
  4. Postoperative
  5. Sepsis

Source: In-hospital AKI. Nash 2002

24
Q

What is the prognosis with AKI?

A

Only ~39% have a complete recovery and 19% die

25
Q

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

A

Serum creatinine

Urine output (or eGFR)

26
Q

What are the 4 phases of healing in AKI?

A
  1. Haemostasis
  2. Inflammation
  3. Proliferation
  4. Remodeling

When there is an imbalance between scarring and remodelling, scar tissue will cause chronic disease.

27
Q

What are the stages of CKD? What factors are considered?

A

GFR is measured

28
Q

Other than GFR, what can be used to predict prognosis in CKD?

A

ACR (albumin:Cr ratio)

29
Q

What are the most common causes of CKD?

A
  1. Diabetes
  2. Atherosclerotic renal disease
  3. Hypertension
  4. Chronic Glomerulonephritis
  5. Infective or obstructive uropathy
  6. Polycystic kidney disease
30
Q

What are the 4 main complications of CKD?

A

Progressive failure of homeostatic function i.e. acidosis + hyperkalaemia

Progressive failure of hormonal function i.e. anaemia + renal bone disease

Cardiovascular disease i.e. vascular calcification + uraemic cardiomyopathy

Uraemia and Death

31
Q

Why does renal acidosis occur in CKD? What are the consequences of this? How is this treated?

A

There is failure of renal excretion of protons.

Consequences:

  • Muscle and protein degradation
  • Osteopenia due to mobilization of bone calcium
  • Cardiac dysfunction

Tx: oral sodium bicarbonate

32
Q

Regarding hyperkalaemia, which of the following is true?

  • A.It can lead to ECG changes such as peaked p waves and flattened t waves.
  • B.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.
  • C.NSAIDs can lower potassium levels
  • D.Hyperaldosteronism is a common cause
  • E.All of the above
A

B..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.

NB:

  • ECG – flattened p waves and peaked T waves should be seen
  • NSAIDs – can increase K
  • Hyperaldosteronism (Conn’s) - lowers K
33
Q

List 3 medications which can cause hyperkalaemia.

A
  • ACEi
  • Spironolactone
  • ’Potassium-sparing’ diuretics
34
Q

What abnormality is shown?

A

Hyperkalaemia

35
Q

Why does anaemia occur in CKD?

A

Progressive decline in EPO producing cells with loss of renal parenchyma (usually when GFR<30mL/min) –> normochromic, normocytic anaemia

Important to exclude other common causes:

  • Iron deficiency
  • B12 and/or folate deficiency
36
Q

What medications can be used to manage anaemia in CKD?

A

Erythropoiesis-stimulating agents (ESAs):

  • Erythropoietin alfa (Eprex)
  • Erythropoietin beta (NeoRecormon)
  • Darbopoietin (Aranesp)
37
Q

Your patient with CKD has been started on an ESA but does not respond. What could be the cause?

  • A.Iron deficiency
  • B.TB
  • C.Malignancy
  • D.B12 and folate deficiency
  • E.Hyper-parathyroidism
  • F.Any of the above
A

F.Any of the above

38
Q

List 4 types of renal bone disease.

A
  1. Osteitis fibrosa
  2. Osteomalacia
  3. Adynamic bone disease
  4. Mixed osteodystrophy

May occur together

39
Q

What is the aetiology of hyperparathyroidism in CKD?

A
  • Phosphate retention
  • Low Vit D levels due to lack of 1-α-hydroxylase
40
Q

What is osteitis fibrosa?

A

Osteoclastic resorption of calcified bone and replacement by fibrous tissue due to hyperparathyroidism

41
Q

What is osteomalacia?

A

Insufficient mineralization of bone osteoid due to lack of vitamin D (due to lack of 1-alpha-hydroxylation in kidney)

42
Q

What is the cause of adynamic bone disease?

A

Excessive iatrogenic suppression of PTH in CKD –> low bone turnover and reduced osteoid

43
Q

What are the three main treatments for renal bone disease?

A
  1. Phosphate control - dietary reduction + phosphate binders
  2. Vit D receptor activators – give 1-alpha calcidol + paricalcitol (vit D analogue)
  3. Direct PTH suppression - Cinacalcet
44
Q

What is cardiovascular disease characterised by in CKD?

A

Renal vascular lesions are frequently characterised by heavily calcified plaques, rather than traditional lipid-rich atheroma

45
Q

What are the three phases of uraemic cardiomyopathy?

A
  1. Left ventricle (LV) hypertrophy
  2. LV dilatation
  3. LV dysfunction
46
Q

The following are contraindications to transplantation: true or false?

  1. HIV positive –
  2. Any malignant disease –
  3. BMI >30 –
  4. Active Sepsis –
  5. Aged above 65 years -
A
  1. HIV positive – FALSE
  2. Any malignant disease – FALSE
  3. BMI >30 – FALSE
  4. Active Sepsis – TRUE
  5. Aged above 65 years - FALSE
47
Q

What are the two types of dialysis?

A

Haemodialysis

Peritoneal dialysis

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