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AT CHEMPATH > ChemPath: Assessment of Renal Function 2 > Flashcards

ChemPath: Assessment of Renal Function 2 Flashcards

1
Q

Define AKI.

A

Rapid reduction in kidney function, leading to inability to maintain electrolyte, acid-base and fluid homeostasis.

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2
Q

What are the three stages of AKI and what is the name of the classification used?

A

KDIGO classification

Stage 1: increase in serum creatinine by 1.5-1.9 times baseline
or UO <0.5ml/kg/hr for 6-12h

Stage 2: increase in serum creatinine by 2-2.9 times baseline
or UO <0.5ml/kg/hr for >12h

Stage 3: increase in serum creatinine by >3 times baseline
or UO <0.3ml/kg/hr for >24h

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3
Q

What is pre-renal AKI?

A

AKI caused by reduced renal perfusion

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4
Q

Describe the normal response to reduced circulating volume.

A
  • Activation of central baroreceptors and renin-angiotensin system
  • Release of vasopressin
  • Activation of sympathetic system
  • Results in vasoconstriction, increased cardiac output and renal sodium retention
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5
Q

Name and describe the two mechanisms that maintain renal blood flow despite changes in systemic blood pressure.

A
  • Myogenic stretch - if the afferent arteriole gets stretched due to high pressure, it will constrict to reduce the transmission of that pressure to the glomerulus
  • Tubuloglomerular Feedback - high chloride concentration in the early distal tubule (suggestive of high GFR) stimulates constriction of the afferent arteriole which lowers GFR and, hence, chloride concentration
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6
Q

List some causes of pre-renal AKI.

A
  • True volume depletion
  • Hypotension
  • Oedematous state
  • Selective renal ischaemia (e.g. renal artery stenosis)
  • Drugs
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7
Q

List some drugs that cause AKI and briefly state how they affect renal blood flow

A
  • ACE inhibitors - preferential dilation of efferent arteriole
  • NSAIDs - increased afferent constriction
  • Calcineurin inhibitors - same as above
  • Diuretics - affect tubular function and decrease preload
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8
Q

What is a consequence of prolonged pre-renal AKI?

A

Acute tubular necrosis (ATN)

This does NOT respond to fluid restoration (compared to pre-renal AKI which does respond)

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9
Q

What might be seen on urine microscopy in a patient with ATN?

A

Epithelial cell casts

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10
Q

What causes post-renal AKI?

A

Physical obstruction of urine flow

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11
Q

List some sites of urine obstruction.

A
  • Intra-renal
  • Ureteric
  • Prostatic/urethral
  • Blocked urinary catheter
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12
Q

Outline the pathophysiology of post-renal AKI.

A
  • GFR is dependent on a hydraulic pressure gradient
  • Obstruction results in increased tubular pressure
  • This results in an immediated decline in GFR
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13
Q

What are some consequences of prolonged renal obstruction?

A
  • Glomerular ischaemia
  • Tubular damage
  • Long-term interstitial scarring
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14
Q

List the possible sites of disease in intrinsic AKI.

A
  • Vascular (e.g. vasculitis)
  • Glomerular (e.g. glomerulonephritis)
  • Tubular (e.g. ATN)
  • Interstitial (e.g. AIN)
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15
Q

Causes of intrinsic renal AKI:
1. Direct tubular injury - what can cause this?

A
  • Ischaemia (MOST COMMON)
  • Endoengous toxins (e.g. myoglobin from rhabdo, immunoglobulin)
  • Exogenous toxins (e.g. aminoglycosides, amphotericin, aciclovir)
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16
Q

Causes of intrinsic renal AKI:
2. Immune dysfunction - what can cause this?

A

Immune dysfunction -> renal inflammation

  • Glomerulonephritis
  • Vasculitis
    (40yo presenting with systemic purpura + AKI)
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17
Q

Causes of intrinsic renal AKI:
3. Infiltration/abnormal protein deposition - what can cause this?

A
  • Amyloidosis (associated with nephrotic syndrome)
  • Lymphoma
  • Myeloma
18
Q

List the possible outcomes of AKI.

A
  • Partial recovery of renal function
  • Discharged with increased serum creatinine
  • Discharged requiring chronic dialysis
  • Death
19
Q

What are the biochemical definitions of AKI?

A
  • Increase in serum creatinine > 26.5µmol/L within 48 hours
  • Increase in serum creatinine > 1.5 times baseline within the previous 7 days
  • Urine volume < 0.5 ml/kg/hr for 6 hours
20
Q

What are the four processes of acute wound healing?

A
  • Haemostasis
  • Inflammation
  • Proliferation
  • Remodelling
21
Q

What are the stages of CKD?

A
  • Stage 1: >90
  • Stage 2: 60-89
  • Stage 3: 30-59
  • Stage 4: 15-29
  • Stage 5 (end stage): <15
22
Q

List some causes of CKD.

A
  • **Diabetes mellitus ** *
  • ** Hypertension** *
  • Chronic glomerulnephritis
  • Atherosclerotic renal disease
  • Infective or obstructive uropathy
  • Polycystic kidney disease
23
Q

What are the normal roles of the kidney?

A
  • Excretion of water-soluble waste
  • Water balance
  • Electrolyte balance
  • Acid-base homeostasis
  • Endocrine (EPO, RAS, vitamin D)
24
Q

Outline the consequences of CKD.

A
  • Progressive failure of homeostatic function (acidosis, hyperkalaemia)
  • Progressive failure of hormonal function (anaemia, renal bone disease)
  • Cardiovascular disease (vascular calcifiction, uraemic cardiomyopathy)
  • Uraemia and death
25
Q

What are the consequences of renal acidosis?

A
  • Muscle and protein degradation
  • Osteopaenia (bone buffering aka release of calcium/bicarb from bone to neutralise acid)
  • Cardiac dysfunction
26
Q

How is renal acidosis treated?

A

Oral sodium bicarbonate

27
Q

What are the consequences of hyperkalaemia?

A
  • Cardiac dysfunction (arrhythmia)
  • Muscle dysfunction

NOTE: hyperkalaemia causes membrane depolarisation

28
Q

Which medications can cause hyperkalaemia?

A
  • ACE inhibitors
  • Spironolactone (Potassium-sparing diuretics)
29
Q

What type of anaemia does chronic renal disease cause?

A

Normochromic, normocytic anaemia

30
Q

How is anaemia of chronic renal disease treated?

A

Using erythropoietin stimulating agents
* Erythropoietin alfa (Eprex)
* Erythropoietin beta (NeoRecormon)
* Darbopoietin (Aranesp)

NOTE: if CKD is not responding to erythropoiesis stimulating agents, consider iron deficiency, malignancy, B12 deficiency etc.

31
Q

List some types of renal bone disease.

A
  • Osteititis fibrosa cystica
  • Osteomalacia
  • Adynamic bone disease
  • Mixed osteodystrophy
32
Q

Outline the pathophysiology of renal bone disease.

A

CKD leads to

  1. Reduced activation of Vitamin D -> hypocalcaemia -> 2nd HPT -> PTH stimulates bone (osteoclast) to release calcium -> inc burn turnover and release of bone mineral content
  2. Can’t excrete phosphate -> phosphate retention -> phosphate-calcium crystals form and deposit -> soft tissue calcification (renal osteodystrophy) + even further reduced availability of calcium
    *FGF23 produced to help pee out phosphate
33
Q

What is osteitis fibrosa cystica?

A

Caused by osteoclastic resoprtion of calcified bone and replacement by fibrous tissue (feature of hyperparathyroidism)

34
Q

What is adynamic bone disease?

A

Overtreatment leading to excessive suppression of PTH results -> decrease osteoblast/clast activity -> low bone turnover and reduced osteoid

35
Q

Outline the treatment of renal bone disease.

A
  • Phosphate control - dietary, phosphate binders
  • Vitamin D activators - 1-alpha calcidol, paricalcitol
  • Direct PTH suppression - cinacalcet (works by increasing the sensitivity of the calcium sensing receptor)
36
Q

What is the most important consequence of CKD?

A

Cardiovascular disease - this is most likely to kill them

37
Q

What are the three phases of uraemic cardiomyopathy?

A
  • LV hypertrophy
  • LV dilatation
  • LV dysfunction
38
Q

What are the treatment options for patients with severe CKD?

A
  • Transplantation
  • Haemodialysis
  • Peritoneal dialysis
39
Q

What rises the most in acute renal failure, where the cause is dehydration?

A

Urea

(Sodium and potassium only rise a little)

40
Q

In rhabdomyolysis: what is seen on urine dip and urine microscopy?

A

Urine dip: blood +ve
Urine microscopy: RBCs absent, myoglobin casts

*Diagnostic blood test: creatine kinase

AT CHEMPATH (24 decks)

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