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Met 3b > Renal > Flashcards

Renal Flashcards

1
Q

In CKD what replaces the normal glomeruli and tubules?

A

Fibrosis

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2
Q

What is the prevalence of CKD in adults?

A

3 to 7 percent

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3
Q

Which races are prone to CKD?

A

Blacks and Asians (2-3x)

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4
Q

What is the biggest cause of CKD in the UK?

A

Diabetes

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5
Q

What is the second biggest cause of CKD in the UK?

A

Glomerular nephritis

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6
Q

What is the third biggest cause of CKD?

A

Hypertension

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7
Q

What the common causes of CKD?

A 
DM
GN
HTN
Pyelonephritis
Vascular disease
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8
Q

In which age group is CKD most common?

A

The elderly

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9
Q

Describe the natural history of CKD?

A

Hyperfiltration > microalbuminuria > macroalbuminura > nephrotic syndrome and proteinuria > CKD

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10
Q

What mode of inheritance is polycystic kidney disease?

A

Autosomal dominant

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11
Q

Explain the genetics behind polycystic kidney disease?

A

Single mutation of either one of two interacting genes

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12
Q

In polycystic kidney disease, is the patient predisposed to CKD?

A

Yes

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13
Q

What complications may arise in polycystic kidney disease?

A

Subarachnoid haemorrhage

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14
Q

Where are cysts found in polycystic kidney disease?

A

Liver
Kidneys
Ovaries

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15
Q

How is polycystic kidney disease diagnosed?

A

USS

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16
Q

How is polycystic kidney disease managed?

A

Treat hypertension
Deal with complications such as infected cysts
Tolvaptan slows progression
Transplant

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17
Q

When is a patient with polycystic kidneys likely to reach CKD stage 5?

A

Middle age

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18
Q

What other considerations, outside of treatment, must be made in CKD?

A

Screen family

Organise a pre emptive transplant

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19
Q

What is a normal GFR?

A

100ml/min

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20
Q

What can naturally influence GFR?

A

Age, sex, race and muscle mass

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21
Q

Which stages of CKD are normal and do not require treatment?

A

1 and 2

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22
Q

What is CKD stage 1?

A

eGFR

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23
Q

What is CKD stage 2?

A

eGFR 60-90 with a kidney problem

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24
Q

What is CKD stage 3?

A

eGFR 30-60

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25
Q

What is CKD stage 4?

A

eGFR 15-30

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26
Q

What is CKD stage 5?

A

eGFR less than 12

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27
Q

What is the most common reason for mortality in stages 3 and 4?

A

Another cause

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28
Q

What is the PCR?

A

The ratio of protein to creatine in the urine - divided by 100 gives the rough 24h urine protein

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29
Q

When is PCR inaccurate?

A

Extremes of muscle mass

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30
Q

Which value of PCR is significant?

A

over 100

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31
Q

What PCR will put you in the nephrotic range?

A

over 250

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32
Q

What stage of CKD needs urgent renal replacement therapy?

A

5

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33
Q

What are the primary targets in CKD treatment?

A

Reducing BP

Reducing proteinuria

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34
Q

In CKD which drugs are used to lower protein and adjust BP?

A

ACE-I e.g. ramipril

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35
Q

What factors must be considered when managing CKD?

A 
BP
Reducing proteinuria
Diabetic control
Cholesterol
Prophylactic aspirin 
Healthy living
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36
Q

Why may anaemia be present in CKD?

A

Lack of EPO production

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37
Q

Why is calcium often high with osteoporosis in CKD?

A

Kidneys cannot activate vitamin D so PTH is elevated to release calcium from bones

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38
Q

Why else might PTH be high in CKD?

A

High phosphate as not lost in urine can cause PTH to rise

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39
Q

How is metabolic acidosis treated in CKD?

A

Bicarbonate tablets

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40
Q

What is a major side effect of bicarbonate tablets?

A

Raised BP

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41
Q

What stages of CKD should be referred onto nephrology?

A

4 and 5

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42
Q

Define an AKI?

A

Acute, usually reversible decline in kidney function

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43
Q

How is AKI defined?

A

Pre renal
Intrinsic renal
Post renal

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44
Q

What may cause pre renal AKI?

A

Hypovolaemia

Renal artery stenosis

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45
Q

What is the UK prevalence of AKI?

A

38000/year

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46
Q

What is the mortality rate of those with AKI?

A

15.2 percent

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47
Q

What is a stage 1 AKI?

A

Creatinine over 250mmol or 150-200 percent from baseline

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48
Q

What is a stage 2 AKI?

A

200-300 percent rise in creatinine from baseline

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49
Q

What is a stage 3 AKI?

A

Over 300 percent rise in creatinine from baseline or creatinine over 350mmol
OR
Creatinine over 45 on RRT

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50
Q

What is a stage 3 AKI if on RRT?

A

Creatinine over 45

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51
Q

Which artery enters the kidney?

A

Afferent renal artery

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52
Q

Which artery exits the kidney?

A

Efferent renal artery

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53
Q

What is the normal glomerular filtration pressure?

A

10mmHg

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54
Q

What factors normally maintain renal perfusion?

A

RAAS

Sympathetic nervous system

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55
Q

What may cause a pre renal AKI?

A

Loss of blood
Loss of plasma
Loss of salt and water

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56
Q

Which conditions can cause reduced kidney perfusion in the absence of hypovolemia?

A

Cardiac nephrotic syndrome (nephrotic syndrome with CCF)

3rd Spacing - loss of intravascular volume to other parts of the body

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57
Q

Which type of AKI can be seen on a urine dip?

A

intrinsic

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58
Q

What are the signs of pre renal AKI?

A

Not visible JVP due to volume depletion

Orthostatic hypotension

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59
Q

When would pre renal AKI have a raised JVP?

A

Cardiac nephrotic syndrome or in co existing CCF

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60
Q

What are the first line investigation in AKI?

A

Urine dip
Urine sodium
Blood test shows raised creatinine

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61
Q

How is pre renal AKI treated?

A

Volume replacement ( or improve cardiac function in CCF)

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62
Q

What treatments are contraindicated in pre renal AKI?

A

Catheter

Diuretics

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63
Q

Does GN normally present as an AKI?

A

No, usually CKD

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64
Q

Which syndrome may cause intrinsic AKI?

A

Nephrotic syndrome

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65
Q

What musculoskeletal signs are seen in intrinsic AKI?

A

Myalgia
Bone pain
Joint pain

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66
Q

Which signs are often seen on examination with intrinsic AKI?

A

Depleted fluid status
Rash
Uveitis
Hearing loss or neurodeficit

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67
Q

What is the gold standard test for intrinsic AKI?

A

Renal biopsy

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68
Q

Which drugs are most likely to cause intrinsic AKI?

A

Antibiotics

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69
Q

Which tests should be done in intrinsic AKI?

A 
Urine culture and microscopy
GN Screen
PCR
Electrophoresis
Blood film
Creatinine
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70
Q

Which diseases affect the kidney interstitium?

A

Tubular interstitial nephritis

Acute tubular necrosis

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71
Q

Which drugs can cause tubular interstitial nephritis?

A

NSAIDs and antibiotics

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72
Q

Which white blood cells are present in acute tubular necrosis?

A

Eosinophils

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73
Q

What is seen on microscopy with acute tubular necrosis?

A

Protein casts

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74
Q

What is a complication of acute tubular necrosis due to protein casts?

A

Cast nephropathy due to obstructive casts

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75
Q

Which form of AKI can lead to acute tubular necrosis?

A

Pre renal AKI

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76
Q

Which drug can cause direct acute tubular necrosis?

A

Gentamycin

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77
Q

Which condition can cause acute tubular necrosis?

A

Rhabdomyolysis

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78
Q

How is acute tubular necrosis managed?

A

Self resolving

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79
Q

If acute tubular necrosis does not resolve, what is the complication?

A

Cortical necrosis

80
Q

How is interstitial nephritis treated?

A

Stop offending medication

Start steroids

81
Q

What SHOULD NOT be done when treating intrinsic AKI?

A

Catheter

82
Q

How is intrinsic AKI initially treated?

A

IV fluids and diuretics

83
Q

How can obstruction be classified in post renal AKI?

A

Outside
Within lumen
Within wall

84
Q

Which type of AKI presents with pain?

A

Post renal

85
Q

Which urine symptoms may be present in post renal AKI?

A

Anuria

Haematuria

86
Q

What may be present on examination with post renal AKI?

A

Palpable bladder due to retention

87
Q

Which lab investigations must be done in post renal AKI?

A

Urine and bloods

88
Q

What imaging must be done on post renal AKI?

A

USS and CT

89
Q

What signs are seen on a CT with post renal AKI?

A

Mickey Mouse sign

Grossly dilated renal pelvis

90
Q

What is the initial management of a post renal AKI?

A

Catheter

91
Q

After a catheter, what is the next step in the management of a post renal AKI?

A

anterograde or retrograde drainage

92
Q

What complication can lead to ECG in AKI?

A

Hyperkalemia

93
Q

What are the complications of AKI?

A

Hyperkalemia
Metabolic acidosis
Pulmonary oedema

94
Q

Is hyperkalemia a medical emergency?

A

Yes

95
Q

How is hyperkalemia treated?

A

IV calcium
Insulin and dextrose
IV salbutamol
Dialysis

96
Q

Why does pulmonary oedema occur in AKI?

A

Salt and water retention

97
Q

How is pulmonary oedema treated?

A

High dose IV diuretics
Dialysis
Vasodilation
Venesection (maybe)

98
Q

What is complication of AKI resolution?

A

Diuresis

99
Q

When might diuresis occur after AKI?

A

After acute tubular necrosis or obstruction

100
Q

How is diuresis monitored?

A

Blood pressure
Pulse
Assess fluid status using daily weights

101
Q

How is diuresis treated?

A

IV fluids

102
Q

What is the diagnostic criteria for nephrotic syndrome?

A

Proteinuria >3g/day

Hypoalbuminaemia

103
Q

Which medications can cause nephrotic syndrome?

A

NSAIDs

Herbal medications

104
Q

Which non specific symptoms may be seen in nephrotic syndrome?

A

Frothy urine
Low BP
Oedema

105
Q

What would show on urine dip with nephrotic syndrome?

A

Protein (+/- blood)

106
Q

When does PCR underestimate protein in the urine?

A

In muscular people

107
Q

When does PCR overestimate protein in the urine?

A

In frail people with little muscle

108
Q

What is PCR 15-30?

A

Trace

109
Q

What is PCR 30-100?

A

1+

110
Q

What is PCR 100-300?

A

2+

111
Q

What does PCR 300-1000 indicate?

A

3+

112
Q

What does PCR over 1000 indicate?

A

4+

113
Q

When might PCR results be a false positive for nephrotic syndrome?

A

When albumin is not the greatest protein component in urine e.g. in multiple myeloma

114
Q

Which fluid compartment expands with nephrotic syndrome?

A

Interstitial fluid

115
Q

What complications can arise from oedema?

A

Pleural effusion

Ascites

116
Q

Why does pulmonary oedema occur in nephrotic syndrome?

A

It leads to congestive cardiac failure

117
Q

Why does oedema occur in nephrotic syndrome?

A

Primary sodium retention (overfill hypothesis)

118
Q

Why does primary sodium retention occur in nephrotic syndrome?

A

Increase in the sodium/potassium pump activity

119
Q

What can further increase water retention in oedema?

A

ANP

120
Q

What is the underfill hypothesis?

A

Low serum albumin so low colloid oncotic pressure activates RAAS that causes salt and water retention

121
Q

In which type of nephrotic syndrome is oedema due to the undersell hypothesis?

A

Sudden onset

122
Q

What are the first line investigations in nephrotic syndrome?

A

Urine - PCR, microscopy, and dipstick
FBC, clotting, Us and Es +/- nephritic screen
USS KUB

123
Q

What is the gold standard test to confirm nephrotic syndrome?

A

Renal biopsy

124
Q

What conditions can cause nephrotic syndrome?

A

Minimal change disease
FSGS
Membranous nephropathy
Amyloidosis

125
Q

In which group of patients with nephrotic syndrome, is a biopsy not recommended?

A

Young children

126
Q

What is seen on light microscopy with minimal change disease?

A

Nothing

127
Q

What is seen on electron microscopy with minimal change disease?

A

Fusion of podocytes

128
Q

What is the main cause of minimal change disease?

A

Primary/idiopathic

129
Q

What are secondary causes of minimal change disease?

A

Drugs
Cancer
Infection
Allergy

130
Q

In which age group is minimal change disease most prevalent?

A

Children under 5

131
Q

What affect does minimal change disease have on blood pressure?

A

Normal or low

132
Q

What effect is there on renal function in minimal change disease?

A

None - unless in pre renal AKI

133
Q

Is there microscopic haematuria in minimal change disease?

A

No - but possible in adults

134
Q

What are the classifications of FSGS?

A

Primary idiopathic and secondary

135
Q

How is secondary FSGS identified?

A

Histological lesion

136
Q

In primary FSGS what symptoms are present?

A

Nephrotic syndrome
Microscopic haematuria
Hypertension
Renal impairment

137
Q

What is the most common cause of secondary FSGS?

A

Hypertension

138
Q

Is nephrotic syndrome present in secondary FSGS?

A

No

139
Q

Which underlying conditions can cause secondary FSGS?

A

Hypertension
HIV
Obesity

140
Q

Which drugs can cause secondary FSGS?

A

Heroin

Pamidronate

141
Q

Which part of the glomerulus is affected in FSGS?

A

Segmental part

142
Q

Why does sclerosis occur in FSGS?

A

Excess collagen deposition due to damage

143
Q

When is membranous nephropathy the most common cause of nephrotic syndrome?

A

In non diabetic adults

144
Q

What are the risk factors for membranous nephropathy?

A

Older
Male
White

145
Q

What is seen on histology with minimal change disease?

A

Thickened capillary loops

Sub endothelial immunoglobulin deposition

146
Q

Which medical conditions can cause secondary membranous nephropathy?

A

SLE
Malignancy
Infection
Sarcoidosis

147
Q

Which drugs can cause membranous nephropathy?

A

Penicillamine
Gold
Anti TNF

148
Q

Which infections can cause membranous nepthropathy?

A

Hepatitis B and C
HIV
Malaria
Syphillis

149
Q

When can amyloidosis cause membranous nephropathy?

A

In minimal change disease

150
Q

What is a major cause of membranous nephropathy in infants?

A

Congenital

151
Q

What is the treatment for oedema?

A

Fluid restrict to less than 1l a day

Diuretics

152
Q

What is the first line diuretic in oedema?

A

Loop diuretics e.g. furosemide

153
Q

What is the second line diuretic in oedema?

A

Aldosterone antagonists e.g. spironolactone

Thiazide like diuretic metolazone

154
Q

How does a thiazide diuretic work?

A

By inhibiting the sodium/chloride symporter

155
Q

What the complications of oedema?

A

Infection
Thromboembolism
Renal impairment
Dyslipidaemia

156
Q

Which age group is more prone to infection from oedema?

A

Children

157
Q

Why does thromboembolism occur more often in oedema?

A

Decrease ATIII

158
Q

What is the first line treatment to reduce proteinuria?

A

ACE-I

159
Q

What is the second line treatment to reduce proteinuria?

A

ARBs (e.g. losartan)

160
Q

How do ACE-I and ARBs reduce proteinuria?

A

Reduce intraglomerular pressure

161
Q

How should dyslipidaemia be managed?

A

Statins

162
Q

Which type of kidney condition takes longer to respond to steroids?

A

FSGS

163
Q

How is idiopathic membranous nephropathy treated?

A

Steroids + beta calcinin inhibitor (e.g. cyclophosphamide and nitofinab)

164
Q

What would GN show on a urine dip?

A

Blood +/- protein

165
Q

What amount of protein is seen in the urine in early GN?

A

1 to 1.5g

166
Q

What does GN show in urine microscopy?

A

Renal casts

167
Q

What symptoms are present in aggressive GN?

A

AKI
Oedema
Hypertension

168
Q

What is the first line investigation in GN?

A

Urine dip

169
Q

What is the second line investigation in GN?

A

Urine microscopy and culture

170
Q

How may rapidly processing GN appear?

A

Rapidly rising creatinine

171
Q

What symptoms characterise nephritic syndrome?

A

Blood in the urine
Hypertension
Mild oedema

172
Q

What on urine microscopy is trademark of GN?

A

Red cell casts

173
Q

What are protein casts?

A

Tamm-Horsfall protein matrix formed in the tubles

174
Q

Which conditions can cause immune mediated GN?

A 
Small vessel vasculitis
SLE
Anti GBM disease (Goodpastures)
IgA nephropathy
Cryroglobinaemia
175
Q

Which antibodies are present in small cell vasculitis?

A

ANCA

176
Q

What can cause GN post infection?

A 
Hep B
Hep C
HIV
Post - strep
Subacute bacterial endocarditis
177
Q

Which malignancies cause GN?

A

Lymphoma

Multiple myeloma

178
Q

What should be your top differential with blood on urine dip?

A

UTI (common things are common)

179
Q

Explain the pathogenesis of GN?

A

Ig mediated > deposition of antibodies (IgA, GBM antibodies, immunocomplexes) > activation of complement > chemokine release > leukocyte recruitment > glomerular inflammation and crescent formation

180
Q

Which chemotactic factor is involved in the pathogenesis of GN?

A

C5a

181
Q

How is a crescent formed in GN?

A

Glomerular necrosis and extra cells infiltrating the urinary space

182
Q

Which leukocytes are recruited in GN?

A

Neutrophils
Macrophages
Lymphocytes

183
Q

What will be seen on Us and Es with GN?

A

Raised urea and creatinine

Reduced bicarbonate

184
Q

What is the gold standard test to diagnose GN?

A

Renal biopsy

185
Q

Why is a nephritic screen not done on every patient with suspected GN?

A

High cost

186
Q

What on the nephritic screen is checked using immunofluorescence?

A

ANCA

187
Q

What is the problem with immunofluorescence of ANCA?

A

Many false positives

188
Q

What types of ANCA may be present?

A

Cytoplasmic (cANCA)

Perinuclear (pANCA)

189
Q

Which types of ANCA are used finding ELISA purified antigens?

A 
Proteinase 3 (cANCA)
Myeloperoxidase (pANCA)
190
Q

Which GN disease is linked to pANCA?

A

Microscopic polyangitis (small vessel vasculitis)

191
Q

Which GN is linked to cANCA?

A

Wegeners

192
Q

What can cause false positive ANCA results?

A

Endocarditis

193
Q

What is the first line treatment for vasculitis?

A

High dose glucorticoids (pred or hydro)
Cytotoxic agents such as cyclophosphamide (steroid sparing)
Consider plasma exchange to remove ANCA antibodies

194
Q

What is the second line treatment for vasculitis?

A

Rituximab

195
Q

How does vasculitis typical present in GN?

A

Microscopic haematuria that may progress to AKI

196
Q

Other than nephritic syndrome, how may ANCA associated vasculitis present?

A

Pulmonary renal syndrome

197
Q

What are the signs and symptoms of pulmonary renal syndrome?

A

Haemoptysis due to pulmonary haemorrhage
Pulmonary nodules
GN

Met 3b (5 decks)

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