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Year 2 - BRS > 9.6 - Chronic kidney disease and renal failure > Flashcards

9.6 - Chronic kidney disease and renal failure Flashcards

1
Q

What are the homeostatic functions of the kidneys? (3)

A
  • electrolyte balance
  • acid-base balance
  • volume homeostasis
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2
Q

What happens to the homeostatic functions of the kidneys in kidney disease? (5)

A
  • increased potassium
  • decreased bicarbonate
  • decreased pH
  • increased phosphate
  • salt and water imbalance
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3
Q

What are the excretory functions of the kidneys? (5)

A
  • nitrogenous waste
  • hormones
  • peptides
  • ‘middle sized molecules’ (molecular weight 2-5000Da)
  • salt and water
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4
Q

What happens to the excretory functions of the kidneys in kidney disease? (3)

A
  • increased urea
  • increased creatinine
  • decreased insulin requirement (low insulin clearance so more stays in system)
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5
Q

What are the endocrine functions of the kidneys? (2)

A
  • erythropoietin
  • 1-alpha hydroxylase (for vitamin D)
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6
Q

What happens to the endocrine functions of the kidneys in kidney disease? (3)

A
  • anaemia
  • decreased calcium
  • increased parathyroid hormone
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7
Q

What are the glucose metabolism functions of the kidneys? (2)

A
  • gluconeogenesis
  • insulin clearance
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8
Q

In kidney disease what is there an overall increased risk of?

A

Cardiovascular risk increased

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9
Q

What does clinical presentation of kidney failure depend on? (2)

A
  • rate of deterioration
  • cause of kidney failure
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10
Q

How does rate of deterioration affect clinical presentation of kidney disease?

A
  • slow rate of deterioration = body good at adapting e.g. some patients present with urea 50 (very low) but their body is used to it since it has developed over years so they do not feel unwell
  • acute renal failure presents quicker as body has not adapted
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11
Q

How does cause of kidney failure affect clinical presentation of kidney disease - 2 examples?

A
  • Goodpasture’s disease (antibodies against glomerular basement membrane) - may present with haemoptysis (lung involvement due to antibodies against lung too) –> blood test to find renal failure
  • skin rash (purpura) –> blood test to find renal failure
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12
Q

What is the most important equation with regard to acidosis/alkalosis?

A

CO2 + H2O <–> H2CO3 <–> H+ + HCO3-

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13
Q

What do small shrunken kidneys on ultrasound indicate?

A

Chronic kidney disease

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14
Q

What is the first thing to determine about a patient that presents with kidney disease?

A

What is their fluid status? Hyper/hypo/normovolaemic (look at blood pressure and skin turgor to determine)

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15
Q

How does kidney failure affect salt and water balance (1), and what does this lead to (3)?

A

Kidney failure tends to REDUCE secretion of salt and water (increased amounts retained) leading to:

  • hypertension
  • oedema
  • pulmonary oedema
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16
Q

In what kind of circumstances can salt and water loss be seen in? (3)

(Kidney failure tends to increase salt and water retention)

A
  • tubulointerstitial disorders - damage to concentrating mechanism
  • right after kidney transplant - damage to tubules and increased urine excretion
  • kidney obstruction relief - kidney cannot concentrate urine and you get kidney failure
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17
Q

What can be a cause of acute kidney injury (AKI)?

A

Hypovolaemia

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18
Q

What does hyponatraemia mean (and what does it not mean)?

A
  • hyponatraemia does NOT mean reduced total body sodium
  • hypervolaemia - it has got to do with how much free water you have (more in hyponatraemia)
  • to treat this, you may not want to give them salt but instead remove the excess free water
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19
Q

Describe how metabolic acidosis happens in renal failure.

A
  • reduced secretion (and therefore excretion) of H+ ions which means you become acidotic
  • cells take up this H+
  • (the cells taking up the H+ also forces K+ out of the cells, leading to hyperkalaemia)
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20
Q

What does metabolic acidosis in renal failure do to K+?

A

The cells taking up the H+ also forces K+ out of the cells, leading to hyperkalaemia

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21
Q

What are the two causes of hyperkalaemia (in renal failure)?

A
  • reduced distal tubule potassium secretion
  • acidosis
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22
Q

What are the symptoms of hyperkalaemia (dependent on chronicity - more chronic, fewer symptoms)? (3)

A
  • cardiac arrhythmias
  • neural and muscular activity
  • vomiting
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23
Q

What ECG changes are seen in hyperkalaemia? (6)

A
  • peaked T waves
  • P waves broaden, have reduced amplitude and disappear (severe)
  • QRS widening
  • heart block
  • asystole
  • VT/VF (ventricular tachycardia/ventricular fibrillation)
24
Q

In kidney failure, what does reduced EPO cause?

A

Anaemia

25
Q

In kidney failure, what does reduced 1,25-Vit D levels cause? (3)

A
  • reduced intestinal calcium absorption
  • hypocalcaemia
  • hyperparathyroidism
26
Q

How does chronic renal failure cause hyperparathyroidism?

A
  • phosphate retention (usually excreted by kidneys)
  • this contributes to low levels of 1,25-Vit D (along with reduced 1-alpha hydroxylase)
  • this leads to hypocalcaemia –> hyperparathyroidism
27
Q

What does reduced EPO and 1,25-Vit D (–> hyperparathyroidism) in kidney failure cause overall?

A

Increased cardiovascular risk

28
Q

What is the major predictor of end stage renal failure?

A

CKD (chronic kidney disease)

29
Q

What is the major outcome for a patient with CKD?

A

Cardiovascular disease - i.e. a patient with CKD is more likely to die from CV disease than end stage renal failure (despite CKD being major predictor of end stage renal failure)

30
Q

What standard cardiovascular risk (3) and additional risks (3) are there for kidney failure patients?

A

Standard cardiovascular risk:

  • hypertension
  • diabetes
  • lipid abnormalities

Additional risks:

  • inflammation
  • oxidative stress
  • mineral/bone metabolism disorder
31
Q

What are the two main things we want to treat during initial management of kidney failure?

A
  • fluid balance
  • hyperkalaemia
32
Q

Initial management of kidney failure - how do we manage fluid balance?

A
  • hypovolaemic - give fluids
  • hypervolaemic - trial of diuretics/dialysis
33
Q

Initial management of kidney failure - how do we manage hyperkalaemia? (3)

A
  • drive K+ into cells - sodium bicarbonate, insulin dextrose (caution)
  • drive K+ out of body - diuretics/dialysis
  • gut absorption - potassium binders
34
Q

How does sodium bicarbonate work to drive K+ into cells?

A
  • binds to H+ to push equation to the right
  • H+ come out of cell into blood to equalise this, and K+ goes back into cell
35
Q

Why do we need to be careful with insulin dextrose to treat hyperkalaemia?

A
  • associated with hypoglycaemia
  • only used when potassium > 6.5 or there are ECG changes (follow trust guidelines)
36
Q

What are the two types of dialysis?

A
  • haemodialysis
  • peritoneal dialysis
37
Q

What do we use to determine long term management of kidney failure?

A

End stage renal failure risk assessment

38
Q

What are the different types of long term management options for kidney failure? (4)

A
  • conservative treatment
  • home therapy
  • in centre therapy
  • transplantation
39
Q

What are some conservative long term treatment options for kidney failure? (5)

A
  • erythropoietin injections to correct anaemia
  • diuretics to correct salt-water overload
  • phosphate binders
  • 1,25-Vit D supplements
  • symptom management
40
Q

What are the home therapy long term treatment options for kidney failure? (2)

A
  • haemodialysis
  • peritoneal dialysis/assisted programmes
41
Q

What does centre therapy for long term treatment of kidney failure include?

A

Haemodialysis - 4h, 3x a week

42
Q

What is the kidney failure risk equation (KFRE)?

A
  • validated risk prediction tool for kidney replacement therapy in the next two to five years for adults with STABLE CKD stages 3A to 5
  • NOT to be used in patients with rapidly changing eGFR
43
Q

What is the kidney failure risk equation calculated from? (4)

A
  • age in years
  • sex
  • CKD-EPI eGFR
  • urine albumin creatinine ratio (ACR)
44
Q

What are the uses of the kidney failure risk equation? (2 + 3)

A
  • patient understanding of their CKD diagnosis especially in the context of multi-morbidity
  • identification of high risk CKD patients:
    • targeted patient engagement/education
    • aggressive risk factor management
    • referral to secondary care
45
Q

What is important to keep in mind when taking blood from patients with kidney failure?

A

Avoid taking blood/inserting IV lines into the veins in the antecubital fossa or cephalic vein at wrist level, as we need access for haemodialysis and these can cause scaring (stenosis) - use veins at back of hand

46
Q

If a kidney failure patient is fit for transplantation, why do we avoid transfusions?

A

Transfusions sensitise patients to the antigens in the blood of the donor, and if they then get a kidney donation from someone else who shares similar antigens to the blood donor there is increased risk of transplant failure

47
Q

What different methods are there for assessing GFR/kidney function? (5)

A
  • urea
  • creatinine
  • radionuclide studies
  • creatinine clearance
  • inulin clearance
48
Q

Is urea a good indicator of GFR and why?

A
  • poor indicator
  • confounded by diet, catabolic state, GI bleeding (bacterial breakdown of blood in gut), drugs, liver function etc
49
Q

Is creatinine a good indicator of GFR?

A
  • good indicator
  • but affected by muscle mass, age, race, sex etc
  • need to look at the patient when interpreting the result (if they are small/big, M/F etc)
  • we look at the TREND of creatinine which is useful
50
Q

Are radionuclide studies good indicators of GFR?

A
  • EDTA clearance etc
  • reliable but expensive
  • used for donors
51
Q

Is creatinine clearance a good indicator of GFR and why?

A
  • difficult for elderly patients to collect an accurate 24h urine sample
  • overestimates GFR at low GFR (as a small amount of creatinine is also secreted into urine)
52
Q

Is inulin clearance a good indicator of GFR?

A

Laborious - used for research purposes only

53
Q

What is the main factor used to calculate estimated GFR (eGFR)?

A

Serum creatinine

54
Q

What kind of acid-base disturbance is a decrease in GFR associated with?

A

Metabolic acidosis - healthy kidneys responsible for removing H+ from body

55
Q

What two equations are used to calculate estimated GFR (and which is used by NICE guidance)?

A
  • Modification of Diet in Renal Disease (MDRD)
  • CKD Epidemiology Collaboration (CKD-EPI) - used in NICE guidance
56
Q

Describe the GFR and ACR categories and risk of adverse outcomes - NICE guidance classification

A

GFR in order of increasing risk:

  • > /=90 (normal and high) - G1
  • 60-89 (mild reduction related to normal range for a young adult) - G2
  • 45-59 (mild-moderate reduction) - G3a
  • 30-44 (moderate-severe reduction) - G3b
  • 15-29 (severe reduction) - G4
  • <15 (kidney failure) - G5

ACR categories in order of increasing risk:

  • <3 (normal to midly increased) - A1
  • 3-30 (moderately increased) - A2
  • > 30 (severely increased) - A3

Year 2 - BRS (84 decks)

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