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MRCP Combined > Renal > Flashcards

Renal Flashcards

1
Q

What is the pathogenesis of diabetic nephropathy?

A

Increased glomerular capillary pressure

Non-enzymatic glycosylation of the BM

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2
Q

What is seen on histology of diabetic nephropathy

A

BM thickening
Kimmelstiel-Wilson nodules (nodular glomerulosclerosis)
Hyaline arteriosclerosis

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3
Q

What genetic predisposition may lead to diabetic nephropathy?

A

ACE gene polymorphisms

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4
Q

What are the stages of diabetic nephropathy?

A
  1. Hyperfiltration
  2. Silent (GFR remains elevated)
  3. Microalbuminaemia 30-300mg/day, dipstick -ve
  4. Overt nephropathy: albumin>300mg/d, dipstick +ve, HTN usually present
  5. ESRF
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5
Q

What type of renal stone does proteus mirabilis predispose to?

A

Struvite

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6
Q

Why is there a small rise in creatinine following ACEI introduction?

A

Reduced filtration pressure

Greater rise - underlying renovascular disease

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7
Q

What has the best sensitivity for detecting proteinuria in CKD?

A

Albumin:creatinine ratio

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8
Q

How is proteinuria diagnosed in CKD?

A

First pass morning ACR sample

3-70mg/mmol - repeat
>70 - confirmed

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9
Q

What are the indications to refer to nephrologist in CKD?

A

Urinary ACR>70 unless known to be caused by diabetes
Urinary ACR >30 + haematuria
Urinary ACR 3-29, persistent haematuria, declining eGFR

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10
Q

What causes bone disease in CKD?

A

Low vitamin D
As hydroxylation normally occurs in the kidneys
High phosphate due to decreased excretion

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11
Q

What are the clinical manifestations of renal bone disease?

A

Osteitis fibrosa cystica
Osteomalacia
Osteoporosis

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12
Q

What is the most common histological pattern of lupus nephritis?

A

Diffuse proliferative glomerulonephritis (also the most severe pain)

Other - rapidly progressive GN

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13
Q

What are the histological features of lupus nephritis?

A

Wire loop appearance (endothelial and mesangial proliferation)
Thickened capillary wall secondary to immune complex deposits

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14
Q

What is Henoch-Schonlein purpura?

A

IA mediated small vessel vasculitis

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15
Q

What are the symptoms of HSP?

A

Palpable purpuric rash with localised oedema over buttocks and extensor surfaces of arms and legs
Abdominal pain
Polyarthritis
Features of IgA nephropathy - haematuria and renal failure

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16
Q

What percentage of HSP patients relapse?

A

1/3

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17
Q

What is the triad of haemolytic uraemic syndrome?

A

AKI
Microangiopathic anaemia
Thrombocytopenia

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18
Q

What are the causes of HUS?

A

Verotoxigenic/enterohaemorrhagic e.coli
Also shigella
Primary - atypical (not related to diarrhoea) = complement dysregulation

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19
Q

What is the treatment of HUS?

A 
Supportive
Fluids
Dialysis
Blood transfusion
Atypical - plasma exchange
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20
Q

What is Goodpasture’s disease?

A

Small vessel vasculitis associated with pulmonary haemorrhage and rapidly progressive glomerulonephritis

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21
Q

What is the cause of Goodpasture’s syndrome?

A

Anti-GBM antibodies against type 4 collagen

Associated with HLA DR2

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22
Q

How is Goodpasture’s syndrome diagnosed?

A

Linear IgG deposits on GBM on renal biopsy

Increased TLCO

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23
Q

What is the management of Goodpasture’s syndrome and a common complication

A

Plasmaphresis
Complication - hypocalcaemia

Also steroids, CYC

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24
Q

What are 8 indications for plasma exchange?

A 
GBS
Myasthenia gravis
Goodpasture's syndrome
TTP
HUS
Cryoglobulinaemia
ANCA +ve vasculitis if severe
Hyperviscosity syndrome
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25
Q

What are 4 complications of plasmaphresis?

A

Hypocalcaemia (due to presence of citrate used as anticoagulant for extra-corporeal system which binds to calcium)
Metabolic alkalosis
Remove of systemic medications
Coag factor/Ig depletion

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26
Q

What is the inheritance of PKD?

A

Autosomal dominant

T1 - 85% = chromosome 16 which encodes for polycystin 1

T2 - 15% = chromosome 4

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27
Q

How is PKD screened for?

A

Abdominal ultrasound - good pickup rate of type 1

However if wanting to donate a kidney therefore screening for type 2 needed as well - genetic screening

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28
Q

What is the management of PKD?

A

Manage HTN

Tolvaptan

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29
Q

How does tolvaptan work in PKD?

A

Vasopressin receptor 2 antagonist - binds to V2 receptors in collecting ducts to reduced cell proliferation, cyst formation, fluid excretion

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30
Q

What are the extra-renal manifestations of PKD?

A

Liver cysts
Berry aneurysms
MV prolapse
Aortic root dilation and aortic dissection

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31
Q

What is fibromuscular dysplasia?

A

Non-atherosclerotic non-inflammatory disease of blood vessels that causes abnormal growth in the wall of an artery

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32
Q

What are the features of fibromuscular dysplasia?

A

Hypertension
CKD/AKI secondary to ACEI initiation
Flash pulm oedema secondary to fluid retention and diastolic ventricular dysfunction

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33
Q

What percentage of renal artery stenosis is caused by fibromuscular dysplasia?

A

10%

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34
Q

How is fibromuscular dysplasia diagnosed?

A

USS - asymmetric kidneys
Duplex USS
Contrast catheter angiography of the renal artery

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35
Q

What hormones do testicular teratomas secrete?

A

hCH and AFP

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36
Q

What scan is used to diagnose reflux nephropathy?

A

Micturating cystography

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37
Q

What scan is used to diagnose renal scarring?

A

DMSA scan

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38
Q

What is the mechanism of action of ciclosporin?

A

Inhibits calcineurin which is a phosphatase involved in T cell activation

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39
Q

What are the side effects of tacrolimus?

A

Impaired glucose tolerance

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40
Q

What is the mechanism of action of MMF?

A

Blocks purine synthesis by inhibition of IMPDH, therefore inhibits proliferation of B and T cells

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41
Q

When does CMV syndrome occur post renal transplant?

A

Between 1st and 6th month

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42
Q

What is the diagnosis and treatment of CMV syndrome?

A

PCR

Ganaciclovir

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43
Q

What is the pathophysiology of hyperacute organ rejection?

A

Pre-formed antibody such as ABO incompatibility or HLA mismatch

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44
Q

What are the features of hyperacute organ rejection?

A

Kidney becomes mottled, dusky, vessels thrombose following completion of vascular anastamosis.
If left in - abscess formation

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45
Q

What are the characteristics of acute organ rejection?

A

Occurs during first 6 months
T cell mediated
Medical management

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46
Q

What are the features of renal artery thrombosis, a complication of renal transplant?

A

Sudden complete loss of urine output

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47
Q

What would suggest a urine leak post renal transplant?

A 
Diminished urine output
Rising creatinine
Fever
Abdo pain
USS --> perigraft collection, necrosis of ureter tip
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48
Q

What are the complications of peritoneal dialysis?

A

Coagulase -ve staph peritonitis (epidermis)

Sclerosing peritonitis

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49
Q

What is the diagnosis of renal vascular disaese?

A

MR angiography

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50
Q

What are the biochemical features of renal artery stenosis?

A

High aldosterone
High renin
Low K

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51
Q

Why is renin low in primary hypoaldsteronism?

A

Resulting hypertension causes excessive renal perfusion, which results in decreased renin production

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52
Q

What are 4 risk factors for Wilm’s tumour?

A

Beckith-Wiedemann syndrome
WAGR syndrome
Hemihypertrophy
Mutation in WT1 gene on chromosome 11

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53
Q

What cell does renal cell cancer arise from?

A

Proximal tubule epithelium

54
Q

What is the most common histological subtype of renal cancer?

A

Clear cell

55
Q

What are 3 risk factors for renal cell carcinoma?

A

Smoking
VHL
Tuberous sclerosis

56
Q

What are the endocrine effects of renal cell carcinoma?

A

Secretes EPO, PTH, renin, ACTH

57
Q

What is Stauffer syndrome?

A

Paraneoplastic hepatic dysfunction syndrome seen in renal cell carcinoma

Presents as cholestasis/hepatosplenomegaly

58
Q

What is the cause of Stauffer syndrome?

A

Increased IL-6

59
Q

What is the treatment of renal cell carcinoma?

A

Partial/total nephrectomy
Alpha-IFN and IL-2
Receptor tyrosine kinase inhibitors e.g. sorafenib

60
Q

What are 5 causes of retroperitoneal fibrosis?

A 
Riedel's thyroiditis
Prev radiotherapy
Sarcoid
Inflammatory AAA
Methysergide
61
Q

What are the features of retroperitoneal fibrosis?

A

Lower back/flank pain
Fever
Lower limb oedema

62
Q

What are the biochemical features of rhabdomyolysis?

A

High CK, K, phosphate (release from myocytes)
Low Ca (myoglobin binds calcium)
Myoglobinuria
Metabolic acidosis

63
Q

What are 5 causes of rhabdomyolysis?

A 
Seizure
Collapse
Ecstasy
McArdle's syndrome
Statins
64
Q

On which chromosome is MHC coded for?

65
Q

Where does spironalactone act?

A

Cortical collecting duct

66
Q

What are 5 indications for spironalactone?

A 
Ascites
Hypertension
Heart failure
Nephrotic syndrome
Conn's syndrome
67
Q

What are 2 side effects of spironalactone?

A

Hyperkalaemia

Gynaecomastia

68
Q

What are 5 causes of metabolic acidosis with normal anion gap?

A 
GI bicarb loss
Renal tubular acidosis
Acetazolamide
Ammonium chloride injection
Addison's
69
Q

What are 5 causes of metabolic acidosis with raised anion gap?

A

Lactic acidosis (e.g shock, burns, metformin)
Ketones (DKA, alcohol)
Urate (renal failure)
Acid poisoning (salicylates, methanol)

70
Q

How is diabetes insipidus diagnosed?

A

Water deprivation test

High plasma osmo, low urine osmo

71
Q

Name 5 causes of cranial DI

A 
Pituitary surgery
Haemochromatosis
Head injury
Idiopathic
DIDMOAD (Wolfram's syndrome)
72
Q

What is the cause of nephrogenic DI?

A

Mutation in AVPR2 receptor

Less common - aquaporin 2 channel mutation

Other: High Ca, low K, lithium, democlocycline

73
Q

What is the treatment of diabetes insipidus?

A

Cranial - desmopressin

Nephro - thiazides

74
Q

What is the cause of congenital nephrogenic DI?

75
Q

What are the biochemical features of alcoholic ketoacidosis?

A

Metabolic acidosis
High anion gap
Elevated ketones
Normal/low glucose

76
Q

What is the treatment of alcoholic ketoacidosis?

A

Infusion of saline and thiamine

77
Q

What is the mechanism of action of beta lactams?

A

Inhibit cell wall formation

78
Q

Which antibiotics inhibit protein synthesis?

A

Aminoglycosides
Chloramphenicol
Macrolides
Tetracyclines

79
Q

Which antibiotics inhibit DNA synthesis?

A

Quinolones
Metronidazole
Sulphonamides
Trimethoprim

80
Q

What is the mechanism of action of rifampicin?

A

Inhibits RNA synthesis

81
Q

What are 3 causes of rapidly progressive glomerulonephritis?

A

SLE
GPA
Goodpasture’s

82
Q

What are 3 causes of nephritic syndrome?

A

Rapidly progressive glomerulonephritis
IgA nephropathy
Alport syndrome

83
Q

What is seen on histology in Rapidly progressive GN

A

Crescents

Goodpasture’s - linear IgG deposits

84
Q

What is the treatment of IgA nephropathy?

A

Monitoring
Steroids if persistent proteinuria
Steroids 3rd line or falling eGFR

85
Q

How is IgA nephropathy dianosed?

A

Mesangial hypercellularity

Positive immunofluorescence for IgA and C3

86
Q

How many days/weeks post URTI does IgA nephropathy occur?

87
Q

What are the features of Alport syndrome

A

BL SN deafness
Lenticonus
Retinitis pigmentosa
Nephritic syndrome –> ESRF

88
Q

What is seen on electron microscopy in Alport syndrome?

A

Splitting of lamina densa - basket weave appearance

89
Q

Which conditions can present as both nephritic and nephrotic syndrome?

A

Diffuse proliferative GN

Membranoproliferative GN

90
Q

What are the causes of diffuse proliferative GN?

A

SLE

1-2 weeks post strep (B haemolytic strep usually pyogenes)

91
Q

What is seen on histology in diffuse proliferative GN?

A

Wire looping of capillaries
Subepithelial humps
Starry sky

92
Q

What are the causes of membranoproliferative GN?

A
  1. Cryoglobulinaemia, hep C

2. Partial lipdodystrophy, factor H deficiency

93
Q

What factor is seen in lipodystrophy?

A

C3b nephritic factor

94
Q

What is seen on electron microscopy in membranoproliferative GN?

A
  1. Tram track

2. Dense deposits

95
Q

What are 5 causes of minimal change disease?

A

Idiopathic
NSAIDs
Rifampicin
EBV

96
Q

What is the pathophysiology of minimal change disease?

A

T cell and cytokine mediated damage to GBM –> polyanion loss and increased glomerular permeability to serum albumin

97
Q

How is minimal change disease diagnosed?

A

Light microscopy is normal

Electron microscopy - fusion of podocytes, effacement of foot processes

98
Q

What percentage of minimal change patients are responsive to steroids?

99
Q

What is 2nd line treatment of minimal change disease if resistant to steroids?

A

Cyclophosphamide

100
Q

What are 5 complications of nephrotic syndrome?

A 
Arterial and venous thromboses (loss of antithrombin)
Hyperlipidaemia
Increased infection (loss of Ig)
Low calcium (Loss of vit D)
CKD
101
Q

What are the most common causes of nephrotic syndrome in adults?

A

Membranous GN - 1/3

Focal segmental glomerulosclerosis - 1/3

102
Q

What are the causes of secondary membranous GN?

A 
Hep B
Malaria
Syphilis
Malignancy
Gold
Penicillamine
NSAIDs
SLE
RA
103
Q

Which antibodies are seen in primary membranous GN?

A

Anti-phospholipase A2

104
Q

What is seen on histology on membranous GN?

A

Spike and dome appearance of basement membrane

105
Q

What is the treatment of membranous GN?

A

ACEI/ARB to reduce proteinuria
Watch and wait
Steroids

106
Q

What are the causes of focal segmental glomerulosclerosis?

A 
Idiopathic
IgA nephropathy/reflux
Heroin
Alport's syndromee
Sickle cell
107
Q

What is seen on histology of focal segmental glomerulosclerosis?

A

Focal and segmental glomerulosclerosis
Light microscopy - hyalinosis
Electron microscopy - effacement of foot processes

108
Q

What is a risk factor for amyloidosis?

A

Multiple myeloma

Chronic inflammation

109
Q

What is seen on histology for nephrotic syndrome caused by amyloidosis?

A

Positive stain for Congo-Red, which when combined with polarised light appears apple-green

110
Q

What are 2 causes of intrinsic AKI?

A

Acute tubular necrosis

Acute interstitial nephritis

111
Q

What is the pathophysiology of acute tubular necrosis?

A

Hypovolaemia or prolonged renal ischaemia/direct toxicity from nephrotoxins

Causes reduced glomerular perfusion and filtration –> renal cell hypoxia –> necrosis of renal tubular epithelium

112
Q

What is seen on urinalysis in acute tubular necrosis?

A

Granular, muddy brown urinary casts

No white cells

113
Q

Name some toxins that can cause acute tubular necrosis.

A

Aminoglycosides
Myoglobin
Radiocontrast
Lead

114
Q

What are the causes of acute interstitial nephritis?

A 
NSAIDs
Penicillins
PPIs
Ciprofloxacin
Allopurinol
25% other - SLE, sarcoid, Sjogrens
115
Q

What is the triad of acute interstitial nephritis?

A

Rash
Fever
Eosinophilia

Also - arthralgia and hypertension

116
Q

What is seen on urinalysis in acute interstitial nephritis?

A

White cell and/or red cell casts

117
Q

What are the 4 types of renal tubular acidosis?

A

1: distal
2: proximal
3: mixed
4: hyperK

118
Q

What are 4 causes of type 1 renal tubular acidosis?

A

RA
SLE
Sjogrens
Amphotericin B toxicity

119
Q

Deficiency of carbonic anhydrase leads to which type of renal tubular acidosis?

A

Type 3 (mixed)

120
Q

Fanconi syndrome is a cause of which type of renal tubular acidosis?

A

Type 2 (proximal)

121
Q

Name 3 other causes of type 2 RTA.

A

Idiopathic
Wilson’s disease
Acetazolamide

122
Q

What is the pathophysiology of type 1 and type 2 RTA?

A

Type 1: inability to secrete H+ in DVT

Type 2: decreased HCO3 reabsorption in PCT

123
Q

What are the cases of type 4 RTA?

A

Hypoaldosteronism eg. Addisons, diabetes, SLE, ACEIs, BB, amyloid

124
Q

What is the pathophysiology of type 4 RTA?

A

Reducing in aldosterone –> reduction in PCT ammoniuim excretion

125
Q

What blood gas abnormality is seen on types 1, 2, and 3 RTA?

A

Low K

Hyperchloraemic metabolic acidosis (normal anion gap)

126
Q

What blood gas abnormality is seen on type 4 RTA?

A

High K

Hyperchloraemic metabolic acidosis

127
Q

What is the treatment of type 1 and 2 RTA?

A

Type 1: correct low K before acidosis. Chronic - PO bicarb prevents urinary K loss

Type 2: bicarb. 2nd line hydrochlorthiazide and K

128
Q

Fludrocortisone is the treatment of which type of RTA?

129
Q

What are the complications of type 1 and 2 RTA?

A

Renal stones
Growth restriction
Renal failure

130
Q

Osteopetrosis, cerebral calcification, XS bone growth are complications of which type of RTA?

MRCP Combined (58 decks)

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