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renal system > Chronic Kidney Disease > Flashcards

Chronic Kidney Disease Flashcards

1
Q

What is the function of the kidneys?

A
  • Body fluid homeostasis
  • Regulation of vascular tone
  • Excretory function
  • Electrolyte homeostasis
  • Acid-base balance
  • Endocrine function (erythropoietin, vitamin D)
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2
Q

What is the traditional definition of CRD?

A

Irreversible and significant loss of renal function… and thus problems kidney function

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3
Q

How do we assess for kidney disease?

A
  • Filtration (excrete out) function
  • Filtration (keep in) function
  • Anatomy
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4
Q

How do we assess kidney excretory function?

A

Use estimates of GFR (eGFR) from creatinine blood test

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5
Q

How is stage 1 kidney disease described?

A
  • Kidney Damage / Normal or high GFR

- GFR>90

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6
Q

How is stage 2 kidney disease described?

A
  • Kidney damage/mild reduction in GFR

- GFR 60-89

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7
Q

How is stage 3 kidney disease described?

A
  • Moderately impaired

- GFR 30-59

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8
Q

How is stage 4 kidney disease described?

A
  • Severely impaired

- GFR15-29

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9
Q

How is stage 5 kidney disease described?

A
  • Advanced or on dialysis

- GFR <15

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10
Q

What leads to glomerular filtration?

A

Pressure differences

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11
Q

What is the relationship between creatinine and GFR?

A

Creatinine will dramatically increase once 60% of total kidney function is loss

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12
Q

What problems are there with measuring creatinine as a measure of kidney damage?

A

Variations in muscle mass between:

  • Ages
  • Ethnicities
  • Genders
  • Weights
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13
Q

How do we assess kidney filtering function?

A

Check for presence of blood or protein un urine

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14
Q

What crosses the GBM?

A
  • Water
  • Electrolytes
  • Urea
  • Creatinine
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15
Q

What crosses the GBM but is reabsorbed in the proximal tubule?

A
  • Glucose

- Low molecular weight proteins (a2 macroglobulin)

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16
Q

What does not cross the GBM?

A
  • Cells (RBC, WBC)

- High molecular weight proteins (albumin, globulins)

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17
Q

If urine is filtering properly what should not be in the urine?

A

Blood or protein

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18
Q

How can urine be examined?

A
  • Urinalysis to check for blood or protein

- Protein quantification (PCR)

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19
Q

How is the anatomy of the kidneys assessed

A
  • Histology

- Radiology

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20
Q

What is the current definition of CKD?

A

Chronic kidney disease (CKD) is defined by either the presence of kidney damage (abnormal blood, urine or x-ray findings) or GFR<60 ml/min/1.73m^2 that is pre##sent for ≥3 months

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21
Q

What is the prevalence of CKD?

A
  • Estimates vary
  • ~8-12% UK
  • Mostly stage 3
  • Increases with age
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22
Q

What are the potential complications of CKD?

A
  • Acidosis
  • Anaemia
  • Bone disease
  • Cardiovascular
  • Death & Dialysis
  • Electrolytes
  • Fluid overload
  • Gout
  • Hypertension
  • Iatrogenic issues
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23
Q

When are complications more likely to occur in CKD?

A

With worsening GFR

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24
Q

What does risk of mortality increase with?

A

Worsening renal function

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25
Q

What is the aetiology of CKD?

A
  • Diabetes
  • Glomerulonephritis (and all the causes of that)
  • Hypertension
  • Renovascular disease
  • Polycystic kidney disease
  • CKD
  • Myeloma
  • IgA nephropathy
  • Chronic exposure to nephrotoxins
  • Reflux nephropathy and scarring
  • Chronic obstructive nephropathy
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26
Q

Give examples of renovascular disease which can lead to CKD?

A

renal artery stenosis from atherosclerosis or fibromuscular dysplasia

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27
Q

Why does renovascular disease lead to CKD?

A
  • It leads to ischaemic nephropathy

- Persistently decreased renal perfusion - ongoing heart failure or cirrhosis

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28
Q

What is the clinical approach to CKD?

A

Detection of the underlying aetiology
-Treatment for specific disease

Slowing the rate of renal decline
-Generic therapies

Assessment of complications related to reduced GFR
-Prevention and Treatment

Preparation for Renal Replacement Therapy

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29
Q

What are the signs and symptoms of CKD?

A
  • Anaemic pallor
  • Hypertension
  • SOB
  • Kidney abnormalities
  • Itch and cramps
  • Cognitive changes
  • GI symptoms
  • Change in urine output
  • Haematuria
  • Proteinuria
  • Peripheral oedema
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30
Q

What is important to explore in the history of CKD?

A
  • Previous evidence of renal disease
  • Family history
  • Systemic diseases
  • Drug exposure
  • Pre/post renal factors
  • Uraemic symptoms
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31
Q

What is important to explore on examination of CKD?

A
  • Vital signs
  • Volume status
  • Systemic illness
  • Obstruction
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32
Q

What previous evidence of renal disease may there be?

A
  • Raised urea/creatinine
  • Proteinuria/haematuria
  • Hypertension
  • Lower urinary tract symptoms
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33
Q

What may there be a family history of in CKD?

A
  • Polycystic kidney disease

- Alport syndrome

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34
Q

What history of systemic disease may there be in CKD?

A
  • Diabetes mellitus
  • Collagen vascular diseases (SLE, scleroderma, vasculitis)
  • Malignancy (Myeloma, breast, lung, lymphoma)
  • Hypertension
  • Sickle cell disease
  • Amyloidosis
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35
Q

What drug exposure may there be in CKD?

A
  • NSAIDs
  • Penicillins/aminoglycosides
  • Chemotherapeutic drugs
  • Narcotic abuse
  • ACE inhibitor / ARBs
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36
Q

What pre-post renal factors may be present in a CKD history?

A
  • Congestive cardiac failure
  • Diuretic use
  • Nausea, vomiting, diarrhoea
  • Cirrhosis
  • LUTS / pelvic disease
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37
Q

What uraemic symptoms may be present in a CKD history?

A
  • Nausea, anorexia, vomiting
  • Pruritis
  • Weight loss
  • Weakness, fatigue, drowsiness
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38
Q

What signs of obstruction may be present on examination of CKD?

A
  • Percussible bladder
  • Enlarged prostate
  • Flank masses
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39
Q

What signs of volume deplete may there be on examination of CKD?

A
  • Orthostatic BP

- Skin turgor/temperature

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40
Q

What signs of fluid overload may there be on examination of CKD?

A
  • Raised JVP
  • Crepitation’s
  • Ascites
  • Oedema
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41
Q

What signs of systemic illness in CKD may be present on examination of the skin?

A

Rash

  • Malar (lupus)
  • Purpuric (vasculitis)
  • Macular (AIN)
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42
Q

What signs of systemic illness in CKD may be present on auscultation?

A

Cardiac murmurs (endocarditis)

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43
Q

What signs of systemic illness in CKD may be present on examination of the abdomen?

A
  • Bruits

- Palpable organs

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44
Q

What signs of systemic illness in CKD may be present on examination of the skin?

A
  • Livedo reticularis (vasculitis, atheroembolism),

- Splinter haemorrhages (endocarditis)

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45
Q

What signs of systemic illness in CKD may be present on examination of the bones and joints?

A
  • Tender (malignancy)
  • Inflammed (lupus)
  • Gouty tophi
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46
Q

What signs of systemic illness in CKD may be present on examination of the pulses?

A

Absent (vascular disease)

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47
Q

What blood tests should be carried out to identify the underlying aetiology of CKD?

A
  • U+Es

- FBCs

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48
Q

What urine tests should be carried out to identify the underlying aetiology of CKD?

A
  • Urine dip
  • Urine PCR or ACR
  • 24 hour collection
49
Q

What biochemistry could be carried out to help identify the aetiology of CKD?

A
  • Urea, creatinine, electrolytes (Na, K, Cl)
  • Bicarbonate
  • Total protein, albumin
  • Calcium, phosphate
  • Liver function tests
  • Creatine kinase
  • Immunoglobulins, serum protein electrophoresis
50
Q

What haematology tests could be carried out to help identify the aetiology of CKD?

A

FBC

  • Hb
  • MCV
  • MCH
  • WBC
  • Platelets
  • % hypochromic RBCs
51
Q

What should be looked at in a coagulation screen to help identify the aetiology of CKD?

A
  • PT
  • APPT
  • +/- Fibrinogen
52
Q

What investigation should be carried out to detect haemolytic uraemic syndrome?

A

Blood count and film

53
Q

What investigation should be carried out to detect Myeloma?

A

Serum and urine electrophoresis

54
Q

What investigation should be carried out to detect intrinsic renal disease?

A

Urine protein: creatinine ratio

55
Q

What investigation should be carried out to detect rhabdomyolysis?

A

CK

56
Q

What investigation should be carried out to detect anti-GBM disease?

A

Anti-GBM

57
Q

What investigation should be carried out to detect ANCA associated vasculitides?

A
  • ANCA

- ELISA for anti MPO or PR3

58
Q

What investigation should be carried out to detect Connective tissue diseases, SLE, MCGN, Cryoglobulinaemia, Infection related glomerulonephritis?

A

C3, C4, Auto antibody screen

59
Q

How does renal disease often present?

A

Renal disease is often asymptomatic – only sign may be abnormal BP or urinalysis

60
Q

What is involved in protein quantification?

A
  • Protein creatinine ratio (PCR)
  • Albumin creatinine ratio
  • 24 hour urine collection
61
Q

What imaging techniques can be used to detect the aetiology of CKD?

A
  • Ultrasound
  • Plain radiology
  • CT
  • Nuclear medicine
  • MRI
62
Q

What are the benefits of ultrasound?

A
  • Non-invasive
  • No ionising radiation
  • May provide information about chronicity of renal disease
63
Q

What are the disadvantages of ultrasound?

A
  • No functional data

- Operator dependent

64
Q

What potential interventions are there to slow the rate of renal decline?

A
  • BP control
  • Control proteinuria
  • Reverse contributing factors
  • Allopurinol
  • Dietary protein restriction
  • Fish oils
  • Lipid lowering
  • Control acidosis
65
Q

What is high BP associated with regard to renal decline?

A

Faster decline in GFR

66
Q

Treating high BP slows progression particularly when they have…

A

Proteinuria

67
Q

How can acidosis be assessed?

A
  • Bicarbonate

- pH

68
Q

How can anaemia be assessed?

A
  • Blood count
  • Blood film
  • Haematinics
69
Q

How can bone disease be assessed?

A
  • Calcium phosphate
  • Albumin
  • Parathyroid hormone
70
Q

How can CV risk be assessed?

A
  • History of chest pain
  • BP
  • Cholesterol
71
Q

How can risk of death and dialysis be assessed?

A

Renal function including urea, creatinine and eGFR

72
Q

How can electrolyte abnormalities be assessed?

A

Electrolytes in serum including potassium

73
Q

How can fluid overload be assessed?

A

Examination including

  • BP
  • Oedema
  • JVP
  • CXR
74
Q

How can gout be assessed?

A

History and examination

75
Q

How can hypertension be assessed?

A

BP +/- 24 hour tape

76
Q

How can iatrogenic issues be assessed?

A

Ask about medication

77
Q

When is metabolic acidosis usually seen in CKD?.

A

GFR <20mls/min

78
Q

When is metabolic acidosis most marked?

A

In tubular interstitial disease

79
Q

What can metabolic acidosis make worse?

A
  • Hyperkalaemia

- Renal bone disease

80
Q

How is metabolic acidosis treated?

A
  • Oral Na

- Bicarbonate

81
Q

When is anaemia usually seen in CKD?

A

GFR <20mils/min

82
Q

Why does anaemia occur in CKD?

A
  • Normochronic, normocytic
  • Reduced erythropoietin production
  • Reduced red cell survival
  • Increased blood loss
83
Q

When is anaemia usually treated in CKD

A

Usually treat if < 10g/dl or symptomatic

84
Q

What is the treatment for anaemia in CKD?

A
  • Iron replacement

- ESA therapy

85
Q

What leads to hyperphosphataemia?

A

Reduced GFR

86
Q

What does loss of renal tissue lead to lack of?

A

Activated Vitamin D which leads to an indirect reduction in calcium absorption

87
Q

What are the clinical features of renal bond disease?

A
  • Low calcium
  • High phosphate
  • Secondary hyperparathyroidism (elevated PTH)
  • May progress to tertiary hyperparathyroidism
88
Q

What does vitamin D derived from sunlight or diet require to become active?

A

Hydroxylation by 1a hydroxylase in the kidney

89
Q

Why is there lack of activation of vitamin D in renal disease?

A

There is low 1s hydroxylase so low activation of vitamin D

90
Q

Why does low vitamin D lead to low calcium?

A
  • Reduced intestinal absorption

- Reduced tubular reabsorption

91
Q

Why is secondary hyperparathyroidism associated with renal bone disease?

A

There is resulting stimulation of PTH secretion in order to try to correct everything through increased action on the bone, gut and kidneys

92
Q

Why can secondary hyperparathyroidism sometime progress to tertiary?

A

Prolonged hypersecretion can become uncontrolled

93
Q

What is high phosphate associated with?

A

Vascular and cardiac calcification

94
Q

How does increased PTH increased bone turnover?

A

Increases the number and activity of osteoclasts and osteoblasts

95
Q

How is renal bone disease managed?

A

Control of phosphate

  • Diet
  • Phosphate binders (CaCO3 Ca acetate, sevelamer, lanthanum)

Normalise calcium and PTH

  • Active vitamin D analogues (calcitriol)
  • Tertiary disease: parathyroidectomy and calcimetics
96
Q

Why does hyperkalaemia occur in renal disease?

A
  • Normally excreted by exchange with Na + in distal tubule

- Reduced delivery of Na+ to distal tubule as GFR falls

97
Q

Give examples of foods to avoid if you have high serum potassium.

A
  • Orange
  • Banana
  • Potato based foods
  • Tomato
  • Chocolate
98
Q

When may hyperkalaemia become fatal?

A

K > 7mmol/l (NR 3.5-4.5) may induce a fatal cardiac arrhythmia

99
Q

What is the treatment for acute hyperkalaemia?

A

Stabilise
-Calcium gluconate

Shift

  • Salbutamol
  • Insulin-dextrose

Remove

  • Dialysis
  • Calcium resonium
100
Q

What is the treatment for chronic hyperkalaemia?

A
  • Diet

- Drug modifications

101
Q

When is fluid/volume overload usually problematic?

A

Usually problematic when GFR < 20mls/min

102
Q

Why does fluid/volume overload occur in renal disease?

A
  • Unable to excrete an excess Na+ load

- Na+ and Water retention

103
Q

How does fluid/volume overload present?

A
  • Oedema

- Hypertension

104
Q

What is the treatment for fluid/volume overload?

A
  • Na restriction
  • Fluid restriction
  • Loop diuretics
105
Q

What is hypertension often associated with in renal disease?

A

Volume overload

106
Q

How should hypertension in renal disease be treated?

A
  • Treatment as per slowing rate of progression
  • Most important in proteinuric renal disease
  • ACEI may offer additional advantage
  • Otherwise tailored therapy
  • Aim <125/75 in CKD with significant proteinuria, 130/80 no proteinuria
107
Q

What drugs can cause AKI on top of CKD?

A
  • Contrast agents

- Antibiotics

108
Q

What is build up of urea toxin called?

A

Uraemic pericarditis

109
Q

How should acidosis in reduced GFR be managed?

A

Bicarb

110
Q

How should anaemia in reduced GFR be managed?

A
  • EPO

- Iron

111
Q

How should bone disease CV risk in reduced GFR be managed?

A

Diet and phosphate binders

112
Q

How should in reduced GFR be managed?

A
  • BP
  • Aspirin
  • Cholesterol
  • Exercise
  • Weight
113
Q

How should death and dialysis in reduced GFR be managed?

A

Counsel and prepare

114
Q

How should electrolytes in reduced GFR be managed?

A

Diet and consider drugs

115
Q

How should fluid overload in reduced GFR be managed?

A
  • Salt and fluid restriction

- Diuretics

116
Q

How should gout in reduced GFR be managed?

A

Optimise +/- meds

117
Q

How should hypertension in reduced GFR be managed?

A
  • Weight
  • Diet
  • Fluid balance
  • Drugs
118
Q

How should iatrogenic issues in reduced GFR be managed?

A

BE AWARE

119
Q

What preparation is there for ESRD and RRT?

A
  • Education & information
  • Selection of modality
  • Planning access
  • Deciding when to start RRT
  • Multidisciplinary team

renal system (26 decks)

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