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SPM- Renal > Chronic Kidney Disease > Flashcards

Chronic Kidney Disease Flashcards

1
Q

Why is eGFR a better measure of renal function?

A

Large reductions in eGFR can occur with little increases in serum creatinine

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2
Q

What is a normal eGFR?

A

Above 90

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3
Q

How does eGFR change with age?

A

The number of functional nephrons an individual has reduces with age and so eGFR naturally declines with age

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4
Q

What might cause someone to have an abnormally raised creatinine but with normal renal function?

A

Creatinine is produced by muscle so body builders with a raised muscle mass will have higher serum creatinine levels

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5
Q

How can you investigate for proteinuria?

A

Urine dip

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6
Q

What test is very valuable in patients with CKD and is associated with a poor prognosis?

A

A:CR- Albumin to creatinine level

Albumin in the urine is a marker of declining renal function

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7
Q

What is the most common cause of CKD in the UK?

A

Diabetic nephropathy

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8
Q

How is CKD defined?

A

The presence of abnormal kidney structure or function for at least 3 months.

Note- eGFR naturally declines with age so there should be structural/functional changes (causing symptoms)

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9
Q

What two criteria are involved in the staging for CKD?

A

eGFR- Gives the G stage

A:CR- Gives the A stage

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10
Q

What are the eGFR values for G1?

What does this mean in real terms?

A

Greater than or equal to 90

This is normal or high eGFR

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11
Q

What are the eGFR values for G2?

What does this mean in real terms?

A

60-89

Mildly decreased eGFR

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12
Q

What are the eGFR values for G3a?

What does this mean in real terms?

A

45-59

Mildly to moderately decreased eGFR

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13
Q

What are the eGFR values for G3b?

What does this mean in real terms?

A

30-44

Moderately to severely decreased eGFR

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14
Q

What are the eGFR values for G4?

What does this mean in real terms?

A

15-29

Severely decreased eGFR

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15
Q

What are the eGFR values for G5?

What does this mean in real terms?

A

<15- This is end stage renal disease

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16
Q

What is the A:CR for A1?

A

0-3

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17
Q

What is the A:CR for A2?

A

3-30 (Microalbuminuria)

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18
Q

What is the A:CR for A3?

A

> 30 (Macroalbuminuria)

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19
Q

What measurement is associated with the greatest increased risk of CVD and so death?

A

Increasing A:CR

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20
Q

What are some causes of CKD?

A

Renal Artery stenosis (prolonged hypo-perfusion)
Diabetic nephropathy
IgA Nephropathy
Polycystic Kidney Disease
Vasculitic kidney disease
Prolonged exposure to nephrotoxic medications
Prolonged outflow obstruction- BPH, Tumour, Strictures, Fibrosis, Compression, Stones

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21
Q

Describe the pathological process involved in diabetic retinopathy?

A

Hyperglycaemia leads to glycosylation of the basement membrane proteins. This leads to mesangial expansion /thickening of the basement membrane (forms Kimmelsteil- Wilson Nodules). Mesangial expansion causes the slits between podocyte to widen and there is dysfunction at the glomerulus allowing proteins and other molecules to freely filter at the glomerulus

There is also hyaline arteriosclerosis which causes glomerular sclerosis, and when it occurs at the efferent arteriole causes the initial hyper-filtration stage

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22
Q

Summarise the changes that occur in diabetic retinopathy?

A

Hyperglycaemia leads to glycosylation of basement membrane proteins
Mesangial expansion (form Kimmelsteil- Wilson Nodules)
Filtration slits between podocytes widen causing dysfunction
Hyaline arteriosclerosis- leading to glomerular sclerosis

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23
Q

What screening test should be done at every diabetic check to investigate for diabetic nephropathy?

A

Urine dip for protein/albumin

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24
Q

Not every single case of proteinuria in diabetics will be due to diabetic nephropathy, what else might indicate it is likely to be due to diabetes?

A

No haematuria- if haematuria is present think nephritic
Presence of other microvascular complications (Retinopathy, neuropathy)
Long history of diabetes (>10 years)
Gradual deterioration over time
No obstructive symptoms
-Ve immunology work up (ANCA, ANA)

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25
Q

Are type 1 or type 2 diabetics more at risk for diabetic nephropathy?

A

Type 1- Longer exposure to hyperglycaemia

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26
Q

What histological features may be seen with diabetic nephropathy?

A

Kimmelsteil-Wilson Nodules- due to mesangial expansion
Abnormal glomerulus- glomerular sclerosis
Loss of open capillary loops

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27
Q

What type of nephropathy is seen within a couple of days of a mucosal infection in certain patients?

A

IgA nephropathy

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28
Q

Why might some patients develop proteinuria 1-2 days after the onset of a URTI or GI infection?

A

They have IgA nephropathy, with abnormal IgA
When is infection of the mucosal surfaces and so IgA levels are increased. IgG binds to this IgA to form circulating immune complexes which deposit in the kidneys causing damange leading to proteinuria

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29
Q

What type of hypersensitivity reaction is IgA nephropathy?

A

Type III- abnormal IgA that is bound by IgG as the body does not recognise them as self

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30
Q

What is the treatment for diabetic nephropathy?

A

Improved glycaemic control
Manage other risk factors- HTN (Target 130/90), Smoking
ACEi or ARB for HTN
Statins to reduce CVD risk

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31
Q

What features will be seen on a urine dip for IgA nephropathy?

A

Haematuria and proteinuria

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32
Q

What must be done for diagnosis of IgA nephropathy?

A

Renal biopsy under USS guidance

Looks for IgA deposits in the mesangium

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33
Q

Where does IgA deposition occur in IgA nephropathy?

A

In the mesangium- tissue that provides structural support to the capillaries of the glomerulus

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34
Q

What would you suspect if someone has a rash on their legs or buttocks and they have a renal biopsy suggestive of IgA nephropathy?

A

HSP- Henoch-Schonlein Purpura (HSP)

Also due to abnormal IgA that is not recognised as self and IgA binds to it to form circulating immune complexes. Causes systemic vasculitis due to wide spread deposition.

Both the renal and skin biopsy will show IgA deposition

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35
Q

What are some of the symptoms of HSP?

A

Purpuric rash typically affecting the shins and buttocks
Abdo pain
Nausea and vomiting
Arthritis (this is none erosive so not permanent)

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36
Q

What is the treatment for IgA nephropathy?

A

Immunosuppression- e.g. Steroids
Reduce other risk factors- ACEi/ARBs for HTN, Statins
Treat mucosal infection if required

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37
Q

If suspecting IgA nephropathy what investigations should be done?

A

Urine dip- Proteins/Albumin, Haematuria
Urine ACR
Renal biopsy
(And standard things, monitor renal function as large declines mean dialysis may be needed)

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38
Q

What kidney condition can cause CKD and has a very strong genetic component?

A

Polycystic kidney disease

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39
Q

What is the inheritance pattern of polycystic kidney disease?

A

Autosomal dominant- PKD1 gene

There is also a recessive type that is associated with later onset and less severe kidney disease

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40
Q

Why does polycystic kidney disease cause CKD?

A

Large cysts develop in the kidneys that disrupt the function of the nephron. There is compression of blood vessels which causes the kidneys to think they are in a low fluid state- this can drive HTN that is not responsive to normal therapy

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41
Q

Why might polycystic kidney disease cause hypertension?

A

Large cysts form which can compress blood vessels leading the kidneys to think they are in a low fluid state. Resulting RAAS activation increase sodium reabsorption and increases potassium excretion- driving fluid retention

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42
Q

What is the triad of HSP?

A

Purpuric rash
Abdo pain
Arthritis

43
Q

How might someone with polycystic kidneys disease present?

A

Loin pain- (Could be kidney stones so do a urine dip)
Haematuria
Hypertension
Signs of fluid retention (raised JVP, peripheral oedema)

44
Q

Why might someone with polycystic kidney disease be prone to developing kidney stones?

A

Cysts compress collecting ducts leading to urinary stasis

Stasis of urine increases the risk of developing kidney stones

45
Q

What gene is responsible for autosomal dominant PKD?

A

PKD1

46
Q

What investigations should be done for someone presenting with features of PKD (loin pain, fluid overload, hypertension)?

A

If suspecting any urinary stones the gold standard investigation is a CT KUB.

Renal USS
Bloods- U&Es, FBC, Creatinine, eGFR
Urine dip- May show haematuria and proteins
If suspecting fluid overload- ECG, ECHO, BNP

47
Q

What is a dangerous pathology associated with PKD?

A

Aneurysms- these patients are at risk of developing arterial aneurysms. These should be investigated with angiograms- e.g. MRAngiogrgam for intra-cerebral aneurysms

48
Q

What is the treatment for PKD?

A

Reduce other risk factors
Manage HTN with ACEi or ARBs (not calcium channel blockers as this can lead to increased cyst formation)
Fluid retention
Decompression of problematic cysts
Tolvaptans- ADH Antagonists are under trial

49
Q

If someone has a family history of PKD what should be done?

A

Regular renal ultra sound for screening- should begin from early 20s

50
Q

What vascular conditions can cause CKD?

A

Renal artery stenosis/ fibro-muscular dysplasia

Causes prolonged hypo-perfusion

Note a vascular occlusion is also a pre-renal cause of AKI

51
Q

How might a patient with renal artery stenosis present?

A

Uncontrolled HTN, as lowering of blood pressure with medical therapy causes further reduction in renal perfusion resulting in RAAS activation
Fluid overload- heart murmurs, S3, pulmonary oedema, raised JVP

52
Q

What is the main cause of renal artery stenosis?

A

Atherosclerotic disease

53
Q

How might renal fibro-muscular dysplasia present differently to renal artery stenosis?

A

Presents in younger women whereas renal artery stenosis is associated with risk factors for atherosclerotic disease (increasing age, HTN, smoking, high lipids)

CT/MRAngiogram would show strictures and narrowing rather than a stenosed vessel

54
Q

Why might patients with renal artery stenosis have a history of AKI after starting anti-hypertensives?

A

Anti-hypertensives reduce the blood pressures and result in further renal hypo-perfusion

55
Q

What investigations should be done for a patient with suspected renal artery stenosis?

A

Examine for signs of fluid overload
Bloods- BNP, Renin and Aldosterone (likely to be high), Urea and electrolytes, Lipids and cholesterol (CV risk factors)
Imaging- CT/MRI Angiogram

56
Q

What is the treatment for renal artery stenosis?

A

Widen the vessel- angioplasty, stenting, grafts

If CV risk factors due to atherosclerotic disease treat these too- Statins, smoking cessation

57
Q

Why is an MRI angiogram preferred for renal artery stenosis over a CT angiogram?

A

CT contrast can be nephrotoxic

Gadolinium used for MRAngiography is not

58
Q

How can HIV cause renal disease?

A

HAART agents are nephrotoxic

HIV virus itself can cause HIV associated glomerulonephritis- Causes Focal Segmental Glomerulonephritis most commonly

59
Q

What is rapidly progressive glomerulonephritis?

A

Type of nephritic syndrome- inflammation of the glomeruli which causes cell proliferation of cells (in a crescent shape) that leads to renal failure

60
Q

What are some causes of rapidly progressive glomerulonephritis?

A

Type I- Anti-GM Antibodies e.g. Good Pastures Syndrome
Type 2- Immune Complexes- Post Strep Glomerulonephritis, IgA Nephropathy, HSP
Type 3- Neither Anti- GBM or Immune Complexes- Often a caused by ANCA vasculitis

Can cause Intrinsic AKI.

61
Q

How might you investigate the cause of rapidly progressive AKI?

A

Renal Biopsy and immunofluorescence

And the clinical Hx

62
Q

What anti-body body causes good pastures syndrome?

A

Anti-GBM

63
Q

Where does Good Pasture cause issues?

A

Kidneys- cause of nephritic syndrome (can be an intrinsic cause of AKI)
Lungs- Haemoptysis

64
Q

What is Post-Streptococcal Glomerulonephritis?

A

Starts with a strep infection (Group A beta haemolytic) which causes antibody generation. Antibodies produced which leads to circulating immune complexes which deposit in the glomerulus. Leads to inflammation of the glomerulus. Produces a nephritic syndrome (includes haematuria)

65
Q

Who is normally affected by post-streptococcal glomerulonephritis?

A

Children
6 weeks after impetigo
1-2 weeks after pharyngitis

66
Q

For any suspicion of intrinsic causes of renal damage what investigation should be done?

A

Renal USS- except in children. Give steroids first as most likely to be minimal change disease so see if there is a response to this.

67
Q

Who should be screened for the development of CKD?

A

(Screen people with conditions that put them at risk of AKI)

Pre- Renal:
CV Disease (IHD, CCF, PVD…)
Hypertension

Renal Disease Risks-
Diabetes
Post AKI- Monitor for 2-3 years
Multi-system disease that could have renal involvement e.g. SLE
Family history of ESRD or hereditary kidney disease (e.g. Polycystic kidney disease)

Post Renal Risks
Recurrent renal stones
Structural renal tract disease (e.g. BPH)
Outflow obstructions

68
Q

If patients are taking known nephrotoxic drugs how often should they have their renal function checked? How is this done? Give some examples of such medications?

A

Patients taking nephrotoxic drugs should have their renal function tested at least once per year. This should include an ACR and eGFR. Lithium, ACEi ARBs, Calcineurin inhibitors (e.g Tacrolimus/Ciclosporin)

69
Q

What should be done if an abnormal eGFR is found?

A 
History and examination
Blood pressure
Fluid status
Urinalysis
A:CR Ratio
Repeat the eGFR- after two weeks to exclude AKI and 3 times over 90 days to observe for progression
70
Q

How often should someone with ESRD (eGFR<15) have their eGFR/ACR checked?

A

At least 4 times a year according to NICE guidelines

NICE have provided guidance on how often patients with CKD should be monitored. However, this doesn’t take into account co-morbidities (increased rate or progression), treatment changes or fluctuations in CKD

71
Q

When should a renal USS be considered for patients with CKD?

A

If there is accelerated progression
Persistent visible or invisible haematuria
Symptoms of outflow obstruction
Family history of polycystic kidney disease
eGFR<30
If a renal biopsy is indicated (i.e. suspecting intrinsic disease)- this should always be done under USS guidance

72
Q

What factors would indicate referral to a nephrologist?

A

GFR< 30
ACR> 70 (unless known to be due to diabetes and already treated appropriately)
ACR >30 with haematuria
Sustained decrease in GFR in 12 months (> 25% reduction+change in eGFR category or 15 or more drop in eGFR)
Poorly controlled hypertension requiring at least 4 therapeutic doses (could be RA stenosis)
Suspected renal artery stenosis
Rare or genetic cause expected

73
Q

What are some risk factors for CKD progression?

A

Diabetes- esp. if poorly controlled
HTN
Smoking
Multi-system diseases such as SLE, HIV, HSP
Chronic outflow obstruction- BPH, Strictures, Tumour
Long term use of nephrotoxics- ACEi/ARBs, Lithium, Calcineurin inhibitors (e.g. Tacrolimus)

74
Q

What should be done to treat the risk factors for CKD progression?

A 
Proteinuria- ACEi/ARBs
HTN- Treat according to NICE guidelines
Smoking cessation
Reduce chronic NSAID use
Urology if outflow obstruction- e.g. BPH
Manage diabetes and SLE properly
75
Q

What are some of the complications of renal failure?

A

Reduced elimination of waste products- uraemia
Electrolyte imbalance
Fluid retention + HTN
Acid/Base imbalance
Reduced vitamin D activation
Reduced EPO production
Reduced excretion of renally excreted drugs- e.g. Lithium

76
Q

Which kidney functions can dialysis take over for RRT? Which does it not replace?

A

Electrolyte imbalance
Fluid overload
Acid base imbalance

It cannot take over:
EPO production
Vitamin D activation

77
Q

What are the signs of fluid overload in renal failure?

A 
Pitting oedema
Pulmonary oedema
Raised JVP
Hepatomegaly
Third heart sound
Development of CCF due to overload
Hypertension
78
Q

What is the management for fluid overload in diabetic patients?

A

Diuretics- Loop diuretics such as furosemide are more potent, spironolactone is potassium sparing
Salt restriction
Fluid restriction

79
Q

What electrolyte imbalance may cause confusion, fits or coma?

A

Sodium

80
Q

What electrolyte imbalance is associated with the development of cardiac arrhythmias? Describe the changes seen on and ECG?

A

Hyperkalaemia

Tall Tented T waves, Widened QRS complex, Prolonger PR interval, Cardiac arrest

81
Q

What is the acute management of hyperkalaemia?

A

Calcium gluconate to stabilise the cardiac membranes
Insulin and dextrose/glucose (e.g. 6-10 units of actrapid in 50mls 50% glucose) - drives potassium into cells
Salbutamol
Ion exchange resins- Calcium Resonium
Loop Diuretics- such as furosemide which decreases potassium

82
Q

What is the long term management for hyperkalaemia?

A

Reduced potassium intake- refer to a dietician
Review medications
Drugs that cause RAAS blockage can cause increased potassium
Furosemide reduces serum potassium

83
Q

What type of acid base imbalance is seen in CKD?

A

Kidneys are capable of producing bicarbonate ions as the hydrogen ion can be excreted in the filtrate. Failure of this results in a failure to buffer H+ in the serum and so leads to a metabolic acidosis

84
Q

What compensatory mechanisms are seen in metabolic acidosis?

A

Increased ventilation to reduced PCO2 which forms carbonic acid in solution. Resp compensation therefore increases PO2 and decreases PCO2. Patients may therefore feel breathless

85
Q

What is the management for metabolic acidosis due to CKD? Why is it not great and must be done by a specialist?

A

Sodium bicarbonate can be given

But this also increases the sodium load which can cause fluid retention and HTN. So it needs to be given by a specialist

86
Q

What symptom might a patient with metabolic acidosis describe?

A

Dyspnoea, due to their respiratory compensation increasing ventilatory rate

87
Q

What endocrine disturbance is seen in patients with CKD? Why?

A

Secondary hyperparathyroidism- this is due to reduced activation of vitamin D

88
Q

What is the stimulus for PTH release?

A

Low serum calcium

89
Q

What are the effects of PTH?

A

Increase extracellular calcium through four mechanisms:

1) Increase bone resorption- stimulate osteoclasts (releases calcium and phosphate)
2) Increased activation of vitamin D at the kidney
3) Increase phosphate excretion- this is because phosphate binds to serum calcium (making this physiologically unavailable) therefore acts at the PCT to increase phosphate excretion in the urine (high phosphate also stimulates PTH release)
4) Increases re-absorption of calcium from the filtrate in the DCT

90
Q

What effect does PTH have on phosphate

A

PTH increases bone resorption by stimulating osteoclasts- so it causes phosphate release from the bone
Also increases excretion of phosphate in the urine by reducing re-absorption

Overall decreases phosphate

91
Q

Where is vitamin D synthesised?

A

By keratinocytes in the epidermal layer of the skin when exposed to sunlight

Also comes from some foods

92
Q

Describe the activations stages of vitamin D? Which stage is stimulated by PTH?

A

First hydroxylation is done at the liver to 25 OH Vit D

Second hydroxylation is done by the tubular cells at the kidney to form the active form 1,25 Dihydroxy Vit D

93
Q

What does activated, 1,25 dihydroxy vitamin D do?

A

Increases calcium absorption in the GI tract

94
Q

Why does CKD cause secondary hyper-parathyroidism?

A

Reduced Vitamin D activation which causes a low serum calcium (as active Vit D increases absorption of calcium in the GI tract). Low calcium is a stimulus for PTH release

95
Q

What stimulates PTH release?

A

Low calcium

High phosphate

96
Q

What bone changes might be seen on an X-Ray?

A

Brown tumours

Rugger Jersey Spine (Vertebral bodies look like black and white rugby jersey)

97
Q

What is the management for secondary hyperparathyroidism in CKD?

A

Give activated vitamin D- cacitriol
Phosphate binders
Phosphate restriction
Parathyroidectomy

98
Q

What blood pressure changes might be seen for a patient with CKD? What is the treatment?

A

Fluid retention causes HTN

Treat according to guidelines- not that calcium channel blockers should never be used for PKD

99
Q

Why might anaemia be seen in patients with CKD?

A

EPO is produced by the kidneys
This is reduced with CKD

Check Hb regularly

100
Q

What is the treatment for anaemia in CKD? What should be done before this though?

A

EPO injections may be required

Investigate for other causes of anaemia too before starting on EPO: Iron Studies, B12 and Folate

101
Q

When might a renal biopsy be required?

A

If glomerulonephritis or intrinsic renal disease is suspected. Immunofluorescence could then be done

102
Q

What should be checked when checking fluid status?

A 
BP 
Mucous membranes
Eyes- sunken eyes are a marker of dehydration, conjunctival pallor
Ascites
Skin turgor
JVP
Blood pressure
Heart Rate
Extra heart sounds
Auscultate for pulmonary oedema
Capillary refill time
Peripheral oedema- ankle or sacral

Check weight measurements, fluid chart, observations

103
Q

If suspecting myeloma what tests should be done?

A

Urine checked for bence jones proteins
Serum electrophoresis
Serum or urinary light chains

104
Q

What does active vitamin D do?

A

Increases calcium absorption in the GI tract

Increased calcium re-absorption at the filtrate

SPM- Renal (9 decks)

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