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MRCP Renal > MRCP2 > Flashcards

MRCP2 Flashcards

1
Q

Drugs causes of acute interstitial nephritis?

A

penicillin
rifampicin
NSAIDs
allopurinol
furosemide

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2
Q

Connective tissue causes of acute interstitial nephritis?

A

SLE
sarcoidosis
Sjögren’s syndrome

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3
Q

Infective causes of acute interstitial nephritis?

A

Hanta virus
staphylococcus

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4
Q

Pathophysiology of acute interstitial nephritis?

A

marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules

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5
Q

Presentation of acute interstitial nephritis?

A

fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension

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6
Q

Investigation findings of acute interstitial nephritis ?

A

sterile pyuria
white cell casts

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7
Q

Differentiate between pre-renal and acute tubulonephritis?

A

Pre-renal AKI - kidneys hold on to sodium to preserve volume

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8
Q

Diagnostic criteria of AKI?

A

Rise in creatinine of 26µmol/L or more in 48 hours

or

> = 50% rise in creatinine over 7 days

or
Fall in urine output to < 0.5ml/kg/hour for more than 6 hours in adults (8 hours in children)

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9
Q

What is stage 1 AKI?

A

Increase in creatinine to 1.5-1.9 times baseline,

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10
Q

What is stage 2 AKI?

A

Increase in creatinine to 2.0 to 2.9 times baseline,

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11
Q

What is stage 3 AKI?

A

Increase in creatinine to ≥ 3.0 times baseline

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12
Q

Chromosome mutation in ADPKD type 1?

A

Chromosome 16

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13
Q

Chromosome mutation in ADPKD type 2?

A

Chromosome 4

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14
Q

Ultrasound diagnostic criteria (in patients with positive family history) for ADPKD?

A

two cysts, unilateral or bilateral, if aged < 30 years
two cysts in both kidneys if aged 30-59 years
four cysts in both kidneys if aged > 60 years

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15
Q

Management of ADPKD

A

tolvaptan (vasopressin receptor 2 antagonist)

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16
Q

Criteria for ADPKD tolvaptan?

A

chronic kidney disease stage 2 or 3 at the start of treatment

rapidly progressing disease

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17
Q

Features of ADPKD?

A

hypertension
recurrent UTIs
flank pain
haematuria
palpable kidneys
renal impairment
renal stones

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18
Q

Extra renal manifestations of ADPKD?

A

liver cysts
berry aneurysms

cardiovascular system:
- mitral valve prolapse
- mitral/tricuspid incompetence
- aortic root dilation
- aortic dissection

cysts in other organs: pancreas, spleen; very rarely: thyroid, oesophagus, ovary

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19
Q

Inheritance of alports syndrome?

A

X linked dominant

type IV collagen resulting in an abnormal glomerular-basement membrane (GBM).

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20
Q

Alports + lung involvement?

A

Anti-GBM antibodies
Leads to a goodpasteurs type syndrome

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21
Q

Features of alport syndrome?

A

microscopic haematuria
progressive renal failure
bilateral sensorineural deafness
lenticonus: protrusion of the lens surface into the anterior chamber
retinitis pigmentosa
renal biopsy: splitting of lamina densa seen on electron microscopy

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22
Q

Renal biopsy: splitting of lamina densa seen on electron microscopy

A

Alport syndrome

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23
Q

Characteristic electronic microscopic of alport syndrome ?

A

characteristic finding is of the longitudinal splitting of the lamina densa of the glomerular basement membrane, resulting in a ‘basket-weave’ appearance

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24
Q

Types of amyloid?

A

AL in myeloma - A for Amyloid, L for immunoglobulin Light chain fragments

AA amyloid - serum amyloid A protein, an acute phase reactant

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25
Q

Diagnosis of amyloid?

A

biopsy of skin
rectal mucosa
abdominal fat

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26
Q

Causes of AL amyloid?

A

most common form of amyloidosis
L for immunoglobulin Light chain fragment

  • Myeloma
  • Waldenstroms
  • MGUS
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27
Q

Causes of AA amyloid?

A
  • TB
  • bronchiectasis
  • rheumatoid arthritis
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28
Q

Presentation of AL amyloid?

A

nephrotic syndrome
cardiac and neurological involvement
macroglossia
periorbital eccymoses

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29
Q

Presentation of AA amyloid?

A

renal involvement most common feature

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30
Q

What is normal anion gap?

A

8-14

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31
Q

Causes of normal anion gap + hyperchloraemic metabolic acidosis

A

gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison’s disease

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32
Q

Causes of raised anion gap + metabolic acidosis?

A

lactate: shock, hypoxia
ketones: diabetic ketoacidosis, alcohol
urate: renal failure
acid poisoning: salicylates, methanol
5-oxoproline: chronic paracetamol use#

Methanol
Uraemia (renal failure)
Diabetic ketoacidosis
Paracetamol use (chronic)
Isoniazid
Lactate
Ethanol or propylene glycol
Salicylates

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33
Q

How to calculate anion gap?

A

(sodium + potassium) - (bicarbonate + chloride)

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34
Q

Features of goodpasteurs disease?

A

pulmonary haemorrhage
rapidly progressive glomerulonephritis
this typically results in a rapid onset acute kidney injury
nephritis → proteinuria + haematuria

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35
Q

Renal biopsy in goodpasteurs disease ?

A

renal biopsy: linear IgG deposits along the basement membrane
raised transfer factor secondary to pulmonary haemorrhages

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36
Q

Management of goodpasteur disease?

A

plasma exchange (plasmapheresis)
steroids
cyclophosphamide

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37
Q

Defect in autosomal recessive ARPKD?

A

Chromosome 6 - fibrocystin

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38
Q

Renal biopsy: Multiple cylindrical lesions at right angles to the cortical surface?

A

ARPKD

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39
Q

When does ARPKD present ?

A

In utero - in babies or in early infancy with abdominal masses

Typically has liver involvement, for example portal and interlobular fibrosis.

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40
Q

Complications of arteriovenous fistulas?

A

infection
thrombosis
may be detected by the absence of a bruit
stenosis
may present with acute limb pain
steal syndrome

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41
Q

Ateriovenous fistula + absence of bruit ?

A

fistula thrombosis

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42
Q

How does calciphylaxis occur?

A

hypercalcaemia, hyperphophataemia and hyperparathyroidism

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43
Q

what can provoke or exacerbate calciphylaxis?

A

Warfarin

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44
Q

How should calciphylaxis be managed ?

A

focuses on reducing calcium and phosphate levels, controlling hyperparathyroidism and avoiding contributing drugs such as warfarin and calcium containing compounds.

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45
Q

Causes for anaemia in renal failure?

A

reduced erythropoiesis due to toxic effects of uraemia on bone marrow
reduced absorption of iron
anorexia/nausea due to uraemia
reduced red cell survival (especially in haemodialysis)
blood loss due to capillary fragility and poor platelet function
stress ulceration leading to chronic blood loss

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46
Q

What is the target haemoglobin in renal failure ?

A

10-12

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47
Q

Problems with CKD electrolytes?

A

low vitamin D (1-alpha hydroxylation normally occurs in the kidneys)
high phosphate
low calcium: due to lack of vitamin D, high phosphate
secondary hyperparathyroidism: due to low calcium, high phosphate and low vitamin D

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48
Q

CDK stage 1?

A

Greater than 90 ml/min, with some sign of kidney damage on other tests

I.e. No proteinaemia or U&E(if all the kidney tests* are normal, there is no CKD)

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49
Q

CDK stage 2?

A

60-90 ml/min with some sign of kidney damage

However if kidney tests* are normal, there is no CKD

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50
Q

CDK stage 3a?

A

45-59 ml/min, a moderate reduction in kidney function

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51
Q

CKD stage 3b?

A

30-44 ml/min, a moderate reduction in kidney function

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52
Q

CKD stage 4 ?

A

15-29 ml/min, a severe reduction in kidney function

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53
Q

CKD stage 5 ?

A

Less than 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed

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54
Q

Management of chronic prostatitis?

A

A prolonged course of a quinolone

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55
Q

What is cysinuria?

A

formation of recurrent renal stones. It is due to a defect in the membrane transport of cystine, ornithine, lysine, arginine (mnemonic = COLA)

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56
Q

What is the genetics in cystinuria?

A

chromosome 2: SLC3A1 gene
chromosome 19: SLC7A9

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57
Q

Diagnostic test for cystinuria?

A

cyanide-nitroprusside test

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58
Q

Management of cystinura?

A

hydration
D-penicillamine
urinary alkalinization

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59
Q

Causes of cranial diabetes insidious ?

A

Idiopathic
post head injury
pituitary surgery
craniopharyngiomas
infiltrative
histiocytosis X
sarcoidosis
DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)
haemochromatosis

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60
Q

Causes of nephrogenic DI?

A

genetic:
more common form affects the vasopression (ADH) receptor
less common form results from a mutation in the gene that encodes the aquaporin 2 channel

electrolytes
hypercalcaemia
hypokalaemia
lithium
lithium desensitizes the kidney’s ability to respond to ADH in the collecting ducts

demeclocycline

tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis

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61
Q

Investigation findings for diabetic insidious?

A

high plasma osmolality, low urine osmolality

a urine osmolality of >700 mOsm/kg excludes diabetes insipidus

water deprivation test

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62
Q

management of diabetic insipidous?

A

nephrogenic diabetes insipidus
- thiazides

central diabetes insipidus can be treated with desmopressin

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63
Q

How to assess diabetic nephropathy?

A

ACR > 2.5 = microalbuminuria

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64
Q

Management of diabetic nephropathy?

A

BP control: aim for < 130/80 mmHg
ACE inhibitor or angiotensin-II receptor antagonist

control dyslipidaemia e.g. Statins

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65
Q

What type of renal tubule acidosis is Fanconi

A

Type 2 renal tubule acidosis

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66
Q

Features of Fanconi syndrome?

A

type 2 (proximal) renal tubular acidosis
polyuria
aminoaciduria
glycosuria
phosphaturia
osteomalacia

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67
Q

Causes of cystinosis?

A

cystinosis (most common cause in children)
Sjogren’s syndrome
multiple myeloma
nephrotic syndrome
Wilson’s disease

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68
Q

Causes of focal segmental glomerulosclerosis?

A

idiopathic
secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy
HIV
heroin
Alport’s syndrome
sickle-cell

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69
Q

Renal biopsy of FSGS?

A

Light microscopy: focal and segmental sclerosis and hyalinosis

Electron microscope: effacement of foot processes

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70
Q

Treatment of FSGS?

A

steroids +/- immunosuppressants

untreated FSGS has a < 10% chance of spontaneous remission

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71
Q

Glomeulonephritis that presents with nephritis?

A

Rapidly progressive glomerulonephritis - aka crescentic glomerulonephritis

IgA nephropathy - aka Berger’s disease (mesangioproliferative GN)

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72
Q

Causes of rapid glomerulonephritis?

A

Goodpasture’s
ANCA positive vasculitis

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73
Q

Presentation of IgA nephropathy or mesangioproliferative GN?

A

typically young adult with haematuria following an URTI

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74
Q

Glomeulonephritis that presents as a nephritis and nephrotic syndrome?

A

Diffuse proliferative glomerulonephritis

Membranoproliferative glomerulonephritis (mesangiocapillary)

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75
Q

What type of glomerulonephritis occurs in post strep glomerulonephritis?

A

Diffuse proliferative glomerulonephritis

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76
Q

Presentation of Diffuse proliferative glomerulonephritis?

A

classical post-streptococcal glomerulonephritis in child
presents as nephritic syndrome / acute kidney injury
most common form of renal disease in SLE

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77
Q

Causes of membranoproliferazive glomerulonephritis?

A

type 1: cryoglobulinaemia, hepatitis C
type 2: partial lipodystrophy

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78
Q

Glomerulonephritis that presents as nephrotic syndrome?

A

Minimal change disease

Membranous glomerulonephritis

Focal segmental glomerulosclerosis

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79
Q

Presentation of minimal change disease?

A

typically a child with nephrotic syndrome (accounts for 80%)
causes: Hodgkin’s, NSAIDs
good response to steroids

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80
Q

What is the treatment of minimal change disease?

A

Steroids

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81
Q

Causes of membraneous glomerulonephritis?

A

presentation: proteinuria / nephrotic syndrome / chronic kidney disease
cause: infections, rheumatoid drugs, malignancy

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82
Q

Management of membraneous glomerulonephritis?

A

1/3 resolve, 1/3 respond to cytotoxics, 1/3 develop chronic kidney disease

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83
Q

Causes of FSGS?

A

may be idiopathic or secondary to HIV, heroin

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84
Q

Frank haematuria and > 45 - how should they be referred?

A

Aged >= 45 years AND:
unexplained visible haematuria without urinary tract infection, or
visible haematuria that persists or recurs after successful treatment of urinary tract infection

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85
Q

Frank haematuria and > 60 - how should they be referred?

A

Aged >= 60 years AND have unexplained nonvisible haematuria and either dysuria or a raised white cell count on a blood test

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86
Q

What is triad of haemolytic uraemia syndrome?

A

acute kidney injury
microangiopathic haemolytic anaemia
thrombocytopenia

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87
Q

In HUS, there is no role for what?

A

No role for antibiotics?

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88
Q

Management of HUS?

A
  1. Plasma exchange

eculizumab (a C5 inhibitor monoclonal antibody) has evidence of greater efficiency than plasma exchange alone in the treatment of adult atypical HUS

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89
Q

Investigations in HUS

A

Blood film - fragments
Stool culture - PCR for toxin

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90
Q

What is HSP?

A

Small vessel IgA vasculitis

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91
Q

Features of HSP?

A

palpable purpuric rash (with localized oedema) over buttocks and extensor surfaces of arms and legs
abdominal pain
polyarthritis
features of IgA nephropathy may occur e.g. haematuria, renal failur

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92
Q

Management of HSP?

A

Purely supportive

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93
Q

Kidney disease in HIV?

A
  1. HIV virus itself
  2. indinavir can precipitate intratubular crystal obstruction.
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94
Q

Features of HIV associated nephropathy?

A

massive proteinuria resulting in nephrotic syndrome
normal or large kidneys
focal segmental glomerulosclerosis with focal or global capillary collapse on renal biopsy
elevated urea and creatinine
normotension

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95
Q

Causes of unilateral hydronephrosis ?

A

Pelvic-ureteric obstruction (congenital or acquired)
Aberrant renal vessels
Calculi
Tumours of renal pelvis

PACT

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96
Q

Causes of bilateral hydronephrosis?

A

Stenosis of the urethra
Urethral valve
Prostatic enlargement
Extensive bladder tumour
Retro-peritoneal fibrosis

SUPER

97
Q

Management of hyperkalaemia?

A
  1. Stabilise with calcium gluconate
  2. combined insulin/dextrose infusion +nebulised salbutamol
  3. Calcium resonium / Loop diuretic / dialysis
98
Q

ECG features of hypokalaemia?

A

ECG features

U waves
small or absent T waves
prolonged PR interval
ST depression

99
Q

What is the presentation of IgA nephropathy?

A

young male, recurrent episodes of macroscopic haematuria
typically associated with a recent respiratory tract infection
nephrotic range proteinuria is rare
renal failure is unusual and seen in a minority of patients

100
Q

Associated conditions of IgA nephropathy?

A

alcoholic cirrhosis
coeliac disease/dermatitis herpetiformis
Henoch-Schonlein purpura

101
Q

What is the pathophysiology of IgA nephropathy?

A

mesangial deposition of IgA immune complexes
there is considerable pathological overlap with Henoch-Schonlein purpura (HSP)
histology: mesangial hypercellularity, positive immunofluorescence for IgA & C3

102
Q

How to differentiate between Post strep and IgA nephropathy?

A

Low complement –> post strep
proteinurea –> post strep
Interval between infection –> Post strep
No interval –> IgA

103
Q

Markers of good prognosis in IgA?

A

Frank haematuria

104
Q

Poor prognosis IgA?

A

Male gender
proteinurea >2g
hypertension, smoking, hyperlipidaemia, ACE genotype DD

105
Q

What is the effect of constriction of the afferent arteriol?

A

Decrease in glomerular filtration rate
Decreases renal plasma flow

106
Q

What is the affect of vasodilation of afferent arteriol?

A

Increases glomerular filtration rate
Increases renal plasma flow

107
Q

What causes vasodilation of the afferent arteriole?

A

Prostaglandin

108
Q

What is the affect of constriction of the efferent arteriol?

A

Increases glomerular filtration rate
Reduces renal plasma rate

109
Q

What is the affect of vasodilation of the efferent arteriol?

A

Decreases glomerular filtration
Increase renal plasma fow

110
Q

What causes constrriction of afferent arteriol?

A

sympathetic nerve stimulation, NSAIDs

111
Q

What causes constriction of the efferent arteriol?

A

angiotensin II

112
Q

What causes dilation of the efferent arteriol?

A

ACE Inhibitor

113
Q

What is membranoproliferative glomerulonephritis also known as?

A

mesangiocapillary glomerulonephritis

114
Q

Causes of type 1 membraneoproflierative glomerulonephritis?

A

Cryglobulinaemia
Hepatitis C

115
Q

What is the electron microscope finding for type 1 membranoproliferative glomerulonephritis/

A

electron microscopy: subendothelial and mesangium immune deposits of electron-dense material resulting in a ‘tram-track’ appearance

116
Q

Causes of type 2 membranoproliferative glomerulonephritis?

A

partial lipodystrophy (patients classically have a loss of subcutaneous tissue from their face)

factor H deficiency

117
Q

What is the electron microscope finding for type 2 membranoproliferative glomerulonephritis/

A

electron microscopy: intramembranous immune complex deposits with ‘dense deposits’

118
Q

Causes of type 3 membranoproliferative glomerulonephritis ?

A

Hepatitis B
Hepatitis C

119
Q

How to differentiate between type 1 and type 2 membranoproliferative glomerulonephritis?

A

Type 2: –> alternative pathway complement activation
Type 2 –> low circulating levels of C3

120
Q

Management of membranoproliferative glomerulonephritis?

A

Steroids

121
Q

Difference between membranoproliferative and membraneous glomerulonephritis?

A

Membraneous: Nephrotic
Membranoproliferative: Nephrotic / Nephritic

122
Q

Renal biopsy of membranous glomerulonephritis?

A

basement membrane is thickened with subepithelial electron dense deposits. This creates a ‘spike and dome’ appearance

123
Q

Causes of membranous glomerulonephritis?

A

infections: hepatitis B, malaria, syphilis
malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia
drugs: gold, penicillamine, NSAIDs
autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid

124
Q

Management of membranous glomerulonephritis?

A
  1. ACEi
  2. Immunosuppression
  3. Anticoagulation
125
Q

Causes of normal anion gap metabolic acidosis?

A

gastrointestinal bicarbonate loss:
prolonged diarrhoea: may also result in hypokalaemia
ureterosigmoidostomy
fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison’s disease

126
Q

Causes of raise anion gap metabolic acidosis?

A

lactate:
shock
sepsis
hypoxia
ketones:
diabetic ketoacidosis
alcohol
urate: renal failure
acid poisoning: salicylates, methanol

127
Q

Difference between type A and type B metabolic acidosis?

A

lactic acidosis type A: sepsis, shock, hypoxia, burns
lactic acidosis type B: metformin

128
Q

Presentation of minimal change disease?

A

Nephrotic syndrome

129
Q

Causes of minimal change disease?

A

drugs: NSAIDs, rifampicin
Hodgkin’s lymphoma, thymoma
infectious mononucleosis

130
Q

Features of minimal change disease?

A

nephrotic syndrome
normotension - hypertension is rare
highly selective proteinuria
only intermediate-sized proteins such as albumin and transferrin leak through the glomerulus

renal biopsy
normal glomeruli on light microscopy
electron microscopy shows fusion of podocytes and effacement of foot processes

131
Q

fusion of podocytes and effacement of foot processes

A

Minimal change disease

132
Q

Treatment of minimal change disease?

A

oral corticosteroids: majority of cases (80%) are steroid-responsive
cyclophosphamide is the next step for steroid-resistant cases

133
Q

Complications of nephrotic syndrome?

A

increased risk of thromboembolism
- renal vein thrombosis, resulting in a sudden deterioration in renal function
hyperlipidaemia
chronic kidney disease
immunoglobulin loss
hypocalcaemia (vitamin D and binding protein lost in urine)

134
Q

When is the onset of contrast induced nephropathy?

A

2-5 days post

135
Q

Definitation of contast induced nephropathy?

A

ephrotoxicity may be defined as a 25% increase in creatinine occurring within 3 days of the intravascular administration of contrast medi

136
Q

Preventation of contrast induced nephropathy?

A

intravenous 0.9% sodium chloride at a rate of 1 mL/kg/hour for 12 hours pre- and post- procedure

137
Q

Causes of papillary necrosis?

A

chronic analgesia use
sickle cell disease
TB
acute pyelonephritis
diabetes mellitus

138
Q

Features of papillary necrosis?

A

fever, loin pain, haematuria

139
Q

Complications of peritoneal dialysis?

A

Peritonitis
Sclerosing peritonitis

140
Q

Most common cause of infection from peritoneal dialysis?

A

Coagulase negative staph
- staph epidermis

141
Q

Management of peritoneal dialysis?

A

vancomycin (or teicoplanin) + ceftazidime added to dialysis fluid

142
Q

Indications for plasma exchange?

A

Guillain-Barre syndrome
myasthenia gravis
Goodpasture’s syndrome
ANCA positive vasculitis if rapidly progressive renal failure or pulmonary haemorrhage
TTP/HUS
cryoglobulinaemia
hyperviscosity syndrome e.g. secondary to myeloma

143
Q

Complications for plasma exchnage?

A

Hypocalcaemia
metabolic alkalosis
removal of systemic medications
coagulation factor depletion
immunoglobulin depletion

144
Q

What is the onset of post streptococcal glomerulonephritis?

A

6-14 days

145
Q

Mechanism of post streptococcal glomerulonephritis?

A

Immune complex deposition
IgG, IgM and C3

146
Q

Investiations for poster streptococcal glomerulonephritis?

A

raised anti-streptolysin O titre are used to confirm the diagnosis of a recent streptococcal infection
low C3

147
Q

Renal biopsy findings for post streptoccal glomerulonephritis?

A

electron microscopy: subepithelial ‘humps’ caused by lumpy immune complex deposits
immunofluorescence: granular or ‘starry sky’ appearance

148
Q

Causes of rapidly progressive glomerulonephritis ? And its presentation?

A

Goodpasture’s syndrome
Wegener’s granulomatosis
others: SLE, microscopic polyarteritis

149
Q

Presentation of renal cellcarcinoma?

A

haematuria
loin pain
abdominal mass
varicocele
majority are left-sided
caused by the tumour compressing veins

150
Q

Paraneoplasic effect of renal cell carcinoma?

A

may secrete erythropoietin (polycythaemia)
parathyroid hormone-related protein (hypercalcaemia), renin
ACTH

151
Q

T1 Renal cell carcinoma?

A

Tumour ≤ 7 cm and confined to the kidney

152
Q

T2 Renal cell carcinoma?

A

Tumour > 7 cm and confined to the kidney

153
Q

T3 Renal cell carcinoma?

A

Tumour extends into major veins or perinephric tissues, but not into the ipsilateral adrenal gland and not beyond Gerota’s fascia

154
Q

T4 Renal cell carcinoma?

A

Tumor invades beyond Gerota’s fascia (including contiguous extension into the ipsilateral adrenal gland)

155
Q

Most common to least renal stones?

A

Calcium oxolate ( most common)
Cystine
Uric acid
calcuim phosphate
Struvite

156
Q

Radiodense stone + contains sulphur?

A

cystine

157
Q

Radio-opaque stone ?

A

Clacium oxalte
calcium phosphate

158
Q

Radiolucent stone + in born error of metabolism?

A

Uric acid stone

159
Q

Normal / alkaline urine + radio opaque?

A

calcium phosphate

160
Q

Radio-lucent stone + Acidic urine

A

Urate stones

161
Q

radio-opaque + alkaline ?

A

struvite

162
Q

Investigations for renal stones?

A

urine dipstick and culture
serum creatinine and electrolytes: check renal function
FBC / CRP: look for associated infection
calcium/urate: look for underlying causes
also: clotting if percutaneous intervention planned and blood cultures if pyrexial or other signs of sepsis

163
Q

Size of stone to pass spontaneously?

A

< 5mm

164
Q

Management of complex calculi?

A

Percutaneous nephrolithotomy

165
Q

Stone burden of less than 2cm in pregnant females

A

Ureteroscopy

166
Q

Stone burden of less than 2cm in aggregate

A

Lithotripsy

167
Q

What are class 1 antigens of HLA?

A

class 1 antigens include A, B and C.

168
Q

What are class 2 antigens of HLA?

A

Class 2 antigens include DP,DQ and DR

169
Q

Mechanism of hyperacute rejection?

A

OCCURS IN MINUTES
due to pre-existing antibodies against ABO or HLA antigens
an example of a type II hypersensitivity reaction
leads to widespread thrombosis of graft vessels → ischaemia and necrosis of the transplanted organ
no treatment is possible and the graft must be removed

170
Q

Mechanism of acute graft failure?

A

< 6 months
usually due to mismatched HLA. Cell-mediated (cytotoxic T cells)
usually asymptomatic and is picked up by a rising creatinine, pyuria and proteinuria
other causes include cytomegalovirus infection
may be reversible with steroids and immunosuppressants

171
Q

Mechanism of chronic graft failure?

A

both antibody and cell-mediated mechanisms cause fibrosis to the transplanted kidney (chronic allograft nephropathy)
recurrence of original renal disease (MCGN > IgA > FSGS)

172
Q

Investigation of choice for renal-vascular disease?

A

MR angiography is now the investigation of choice
CT angiography
conventional renal angiography is less commonly performed used nowadays, but may still have a role when planning surgery

173
Q

Associations of retroperitoneal fibrosis?

A

Riedel’s thyroiditis
previous radiotherapy
sarcoidosis
inflammatory abdominal aortic aneurysm
drugs: methysergide

174
Q

Indications for starting renal replacement therapy?

A

Indicated by the impact of symptoms of uraemia on daily living
biochemical measures
uncontrollable fluid overload
estimated glomerular filtration rate (eGFR) of around 5 to 7 ml/min/1.73 m2 if there are no symptoms’

175
Q

What ferritin is required to start EPO?

A

100

176
Q

What must be done before starting EPO?

A

Complete iron studies

177
Q

pH > 7.2 - renal stone?

A

Struvite

178
Q

Back pain and crap renal function?

A

Think amylidosis

If previous condition: AA

If new AL

179
Q

Gold standard management:
Poorly controlled T1DM + Renal failure ?

A

Combined pancreas + kidney transplant

180
Q

Scan for prostate cancer?

A

Tecnitium - 99

181
Q

Clubbed calyxes and ring signs?

A

Analgesia nephropathy

182
Q

When should diabetic patients get ACEi?

A

ACR > 3

183
Q

Initial management of CKD-mineral bone disease:

A

Correct hyperphosphataemia first; start with dietary changes before starting a phosphate binder

184
Q

Tumour markers in trsticular cancer?

A

germ cell tumours
seminomas: seminomas: hCG may be elevated in around 20%
non-seminomas: AFP and/or beta-hCG are elevated in 80-85%
LDH is elevated in around 40% of germ cell tumours

185
Q

CMV in transplant patients?

A

here is often a leukopaenia, atypical lymphocytosis with a mild rise in transaminases and graft dysfunction. Specific organ involvement can lead to hepatitis, pancreatitis, gastrointestinal ulceration and bleeding, pneumonitis, colitis and meningoencephalitis. The diagnosis is confirmed with CMV polymerase chain reaction (PCR). Treatment for patients with invasive disease is initially IV ganciclovir.

186
Q

What can increase risk of post biopsy bleed?

A

Plasma exchange
Remove clotting factors

187
Q

Chronic prostatits treatment?

A

4 weeks of ciprofloxacin

188
Q

What type of glomerulonephritis is post strep?

A

Diffuse proliferative glomerulonephritis

189
Q

Atypical HUS vs HUS?

A

Atypical HUS caused by genetic component
Mimics TTP

However no diarrhoeal illness, and has normal ADAMST13

190
Q

Tubulointerstitial nephritis with uveitis (TINU) ?

A

Symptoms include fever, weight loss and painful, red eyes. Urinalysis is positive for leukocytes and protein.

191
Q

What is eculizumab and what is it used for?

A

Eculizumab (a C5 inhibitor monoclonal antibody) has evidence of greater efficiency than plasma exchange alone in the treatment of adult atypical HUS

192
Q

Iron replacement in CKD?

A

Give oral iron before IV

193
Q

Treating hypertension in CKD?

A

If eGFR <30 do not use hypertension algorithm

Use loop diruetic

194
Q

Indications for ACNA positive vasculitis dialysis?

A

Severe active renal disease (serum creatinine above 354 micromol/L or who require dialysis),
Pulmonary haemorrhage,
Concurrent anti-GBM autoantibody disease.

195
Q

What is dialysis disequalibrium syndrome?

A

cerebral oedema which can present as focal neurological deficits, papilloedema and a decreased level of consciousness. It can be treated with mannitol or hypertonic saline

196
Q

How do you treat dialysis disequalibrium syndrome?

A

mannitol or hypertonic saline

197
Q

Cancer + nephrotic syndrome?

A

Membranous glomerulonephritis

198
Q

Hepatitis B + Nephrotic syndrome?

A

Membranous glomerulonephritis

199
Q

Antibody implicated in idiopathy membranous glomerulonephritis?

A

anti-phospholipase A2 antibodies

200
Q

Lupus nephritis, choice of immunosuppresion?

A

Mycophenolate

201
Q

At extremes of body mass, what should be done to give a more accurate picture of renal function?

A

Cystatin C measurement

202
Q

Amyloidosis: Nephrotic or nephritic?

A

Nephrotic

203
Q

High plasma osmolality + Low urine osmolalty?

A

diabetes insipidus

204
Q

Initial test for testicular ultrasound?

A

Ultrasound
Not tumour markers

205
Q

Transplanted alports patient: Decline renal function?

A

New anti GBM anitbodies

206
Q

WHat should be done before kidney biospy?

A

Ultrasound renal tract

207
Q

Mutation in alports?

A

COL4A5 gene

208
Q

What type of antibody is ant-GBM?

A

IgG

209
Q

What type of antibody is ANCA

A

IgG

210
Q

WHat kidney issue is associated with neurofibromatosis?

A

Renal artery stenosis

211
Q

Fistula thrombosis is a complication is a contraindication to RRT

A

Fistula thrombosis is a complication is a contraindication to RRT

212
Q

Elevated PSA, testosterone?

A

Testosterone is contraindicated in elevated PSA

213
Q

HAART renal complications? :

A

Indinavir can cause renal stones

214
Q

High renin + High aldosterone

A

Renal artery stenosis

215
Q

Whait is chlorthalidone?

A

Thiazide like diuretic

216
Q

Treatment of peritoneal sepsis from peritoneal dialysis?

A

Peritoneal dialysis peritonitis: treat with intraperitoneal vancomycin + ceftazidime

217
Q

When do you supplement clacium and vitmain D in secondary hyperparathyroidism?

A

When PTH twice normal

218
Q

String bead appearance?

A

Fibromuscular dystrophy

a non-atherosclerotic, non-inflammatory condition producing segmental stenoses in all vascular beds.

FMD patients have carotid artery involvement1, hence the frequent presentation of cerebral ischaemia such as transient ischaemic attacks, strokes, headache and tinnitus2.

219
Q

ADPKD management of blood pressure?

A

blood pressure target of < 110 / 75 mmHg

220
Q

Is FSGS as diagnosis?

A

No

221
Q

Clarithromycin + Statin

A

Rhabdomyolysis

222
Q

What CK reading is supportive of rhabdomyolysis?

A

the CK is significantly elevated, at least 5 times the upper limit of normal

223
Q

Granular casts + high urine osmolality?

A

Acute tubular necrosis

224
Q

Spironolactone gynaecomastia management?

A

Eplerenone can be used in patients with troublesome gynaecomastia on spironolactone

225
Q

Features of post transplant lymphoproliferative disorder?

A

weight loss
anaemia
lymphadenopathy

226
Q

Mechanism of post transplant lymphoproliferative disorder?

A

EBV

227
Q

Management of berger’s disease?

A

IgA nephropathy management
no proteinuria, normal GFR: observe
proteinuria: ACE inhibitor
signifcant fall in GFR/not responding to ACE inhibitor: corticosteroid

228
Q

What condition causes brown lesions?

A

Secondary hyperparathyroidism

229
Q

Indication for dialysis in urea?

A

Complications of it
e.g. seizure

230
Q

What is the most common damaghe done by SLE to kidney?

A

Class IV (diffuse proliferative glomerulonephritis)

231
Q

Management of SLE nephritis?

A
  1. Treat hypertension
  2. initial therapy for focal (class III) or diffuse (class IV) lupus nephritis
    glucocorticoids with either mycophenolate or cyclophosphamide
  3. subsequent: mycophenolate
232
Q

Is plasma exchange used in HUS?

A

Rarely - only severe cases

233
Q

Management of membrane glomerulonephritis?

A

ACE inhibitors and immunosuppression with either cyclophosphamide, chlorambucil, ciclosporin or mycophenolate mofetil along with prednisolone. Rituximab has also been shown to have a benefit in the short term.

234
Q

Sickle cell disease can cause what?

A

Membranous glomerulonephritis

235
Q

US kidney: rings seen in medulla?

A

Papillary necrosis

236
Q

spikes’ on the surface of the capillary loops.

A

Membranous glomerulonephritis

237
Q

In HUS how do you confirm Ecoli?

A

Stool culture looking for Shiga toxin-producing Escherichia coli should be sent in patients with suspected haemolytic uraemic syndrome

238
Q

Apparently cycling > 3 hours per day can cause rile dysfunction

A

who knew

MRCP Renal (2 decks)

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