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MRCP Renal > General > Flashcards

General Flashcards

1
Q

Causes of acute interstitial nephritis?

A

drugs: the most common cause, particularly antibiotics
- penicillin
- rifampicin
- NSAIDs
- allopurinol
- furosemide
systemic disease: SLE, sarcoidosis, and Sjögren’s syndrome
infection: Hanta virus , staphylococci

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2
Q

What are the histological features of acute interstitial nephritis?

A

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

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3
Q

Features of acute interstitial nephritis?

A

fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension

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4
Q

Investigation for interstitial nephritis?

A

sterile pyuria
white cell casts

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5
Q

What is Tubulointerstital nephritis with uveitis?

A

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

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6
Q

Causes of pre-renal AKI?

A

lack of blood flow (ischaemia) to the myocardium causes a myocardial infarction

hypovolaemia secondary to diarrhoea/vomiting
renal artery stenosis

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7
Q

Causes of intrinsic AKI?

A

glomerulonephritis
acute tubular necrosis (ATN)
acute interstitial nephritis (AIN), respectively
rhabdomyolysis
tumour lysis syndrome

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8
Q

Causes of post renal AKI?

A

kidney stone in ureter or bladder
benign prostatic hyperplasia
external compression of the ureter

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9
Q

What is the definition of oliguria?

A

urine output of less than 0.5 ml/kg/hour

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10
Q

Treatment of hyperkalaemia?

A

Stabilise membrane:
1. Intravenous calcium gluconate

Short term sift into cells:
* Combined insulin/dextrose infusion
* Nebulised salbutamol

Removal from body:
* Calcium resonium (orally or enema)
* Loop diuretics
* Dialysis

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11
Q

Difference between pre-renal uraemia and acute tubular necrosis?

A

Prerenal uraemia - holds onto sodium to preserve volume

Increased sodium loss (>40) in ATN
Urine osmolality > 500 in pre-renal AKI
Poor response to fluid challenge in ATN
Pre-renal AKI: Raised urea:creatinine ratio
Brown granular casts in urine in ATN
Fractional sodium excretion <1% in AKI, > 1% in ATN

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12
Q

What is fractional sodium excrertion?

A

(urine sodium/plasma sodium) / (urine creatinine/plasma creatinine) x 100

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13
Q

What is fractional urea excretion?

A

fractional urea excretion = (urine urea /blood urea ) / (urine creatinine/plasma creatinine) x 100

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14
Q

What is the diagnostic criteria of autosomal dominant polycystic kidney disease?

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

Where is the gene mutation in autosomal dominant polcysytic kidney disease type 1?

A

Chromosome 16 - PDK1 gene

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16
Q

Where is the gene mutation in autosomal dominant polycystic kidney disease type 2?

A

Chromosome 4 - PKD2

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17
Q

Treatment for ADPKD?

A

Tolvaptan - vasopressin receptor 2 antagonist
Slows cyst development

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18
Q

Features of ADPKD?

A

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

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19
Q

Extra renal manifestation of ADPKD?

A

Liver cysts - hepatomegaly
Berry anneurysms
Mitral valve prolapse
Mitral/tricuspid incompetence
Aortic root dilation
Aortic dissection
Cyst in other organs: pancreas

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20
Q

Genetics behind Alports syndrome?

A

X-linked dominant pattern
Codes for collagen type IV at glomerular basement membrane

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21
Q

Features of Alport’s 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

What is the characteristic sign on renal biopsy found in Alport’s 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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23
Q

Components of amyloid?

A

Fibrillary component
Non-fibrillary - amyloid-P

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24
Q

What is amyloidosis

A

Extracellukar deposition of an insoluble fibrillar protein

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25
Q

How is amyloid diagnosed?

A

Biopsy: Skin, abdominal fat
Congo red staining - apple green birefringence
Serum amyloid precursor scan (SAP)

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26
Q

Types of amyloidosis?

A

AL amyloidosis
AA amyloid
Beta 2 microglobulin amylodosis

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27
Q

Most common type of amyloid? And its causes?

A

AL amyloidosis
The L stands for light chain fragment

Causes:
- myeloma
- Waldenstrom’s
- MGUS

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28
Q

What is AA amyloidosis

A

A stands for “ acute phase”

Causes:
TB
Bronchiectasis
Rheumatoid arthritis

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29
Q

What is beta 2 micro globulin amyloidosis

A

Precursor is beta 2 microglobulin - component of HLA complex

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30
Q

How is anion gap calculated?

A

(sodium + potassium) - (bicarbonate + chloride)

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31
Q

What is a normal anion gap?

A

A normal anion gap is 8-14 mmol/L

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32
Q

Causes of normal or hypercholraemic 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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33
Q

Causes of raised anion gap?

A

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

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34
Q

What is the auto antibody in Goodpasteurs?

A

Anti-GBM
Antibody against type IV collagen

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35
Q

What HLA type of goodpasteurs associated with?

A

HLA DR2

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36
Q

What are the 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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37
Q

Investigation findings in goodpasteurs?

A

Linear IgG deposits in basement membrane

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38
Q

Management of goodpasteurs disease?

A

Plasma exchange
Steroids
Cyclophosphamide

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39
Q

Alports patient + Failing renal transplant ?

A

Presence of anti-GBM antibodies
Leading to goodpasteur’s like syndrome

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40
Q

Where is the gene defect in ARPKD?

A

Chromsome 6
Fibrocystin mutation

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41
Q

How long does it take a arteriovenous fistula to form?

A

6-8 weeks

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42
Q

Complications of ateriorvenous fistula?

A

Infection
Thrombosis
Stenosis
Steal Syndrome

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43
Q

Features of benign prostatic hyperplasia?

A

Lower urinary tract features:
- Weak or intermittent flow
- Straining
-Hesitancy
- Terminal dribbling
- Incomplete emptying

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44
Q

Management of BPH?

A
  1. Alpha 1 antagonists - tamsulosin
    - introduce is score > 8
  2. 5- alpha reductase inhibitors - finasteride
  3. Combination therapy
  4. Transurethral resection of prostate
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45
Q

How to assess BPH?

A

Urinary frequency volume chart
Score with international prostate symptom score

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46
Q

Mechanism of alpha 1 antagonists in BPH?

A

Decrease smooth muscle tone of prostate and bladder

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47
Q

Mechanism of 5 alpha reductase inhibitors?

A

block the conversion of testosterone to dihydrotestosterone (DHT), which is known to induce BPH

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48
Q

Side effects of 5 alpha reductase?

A

erectile dysfunction, reduced libido, ejaculation problems, gynaecomastia

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49
Q

Bladder cancer risk factors ?

A

Transitional cell carcinoma:
- Smoking
- exposure to aniline dyes
- Rubber manufacture
- Cyclophosphamide

Squamous cell carcinoma:
- Schistosomiasis
- Smoking

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50
Q

What is calciphylaxis?

A

Severe rare complication of end stage renal failure
Painful necrotic skin tissues

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51
Q

Risk factors of developing calciphylaxis?

A

Hypercalcaemia
Hyperphophataemia
Hyperparathyroidism
Warfarin

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52
Q

Causes for anaemia in renal disease?

A

Reduced erythropoietin
Reduced erythropoiesis due to toxic effect of uraemia on bone marrow
Reduced iron absorption
Reduced renal cell survival - haemodialysis
Blood loss in capillary fragility

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53
Q

What is a brown tumour and what is it seen in?

A

Benign fibrotic erosive bony lesion
Localised rapid osteoclastic tumour
Results from hyperparathyroidism

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54
Q

CKD bone disease pathophysiology?

A

Low vitamin D - not able to be activated by kidneys
High phosphate - due to kidneys note filtering
- high pshopahte drags calcium from the bones
Low calcium
- Induces Secondary hyperparathyroidism: due to low calcium, high phosphate, low vitamin D

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55
Q

What bone disease is caused by hyperparathyroidism?

A

Osteitis fibrosa cystica

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56
Q

Causes of CKD?

A

diabetic nephropathy
chronic glomerulonephritis
chronic pyelonephritis
hypertension
adult polycystic kidney disease

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57
Q

CKD staging?

A

1 Greater than 90 ml/min, with some sign of kidney damage on other tests (if all the kidney tests* are normal, there is no CKD)
2 60-90 ml/min with some sign of kidney damage (if kidney tests* are normal, there is no CKD)
3a 45-59 ml/min, a moderate reduction in kidney function
3b 30-44 ml/min, a moderate reduction in kidney function
4 15-29 ml/min, a severe reduction in kidney function
5 Less than 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed

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58
Q

Best antihypertensive in proteinuric renal disease?

A

e.g. diabetic nephropathy
ACEi

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59
Q

What may be noted when starting an ACEI

A

Reduces filtration pressure
May note rise in creatinine
- eGFR rise of 25%
- creatinine rise of 30% acceptable

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60
Q

How can CKD bone disease be managed?

A

Reduce phosphate
Reduce PTH

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61
Q

Management of CKD?

A

Sevalamer
- non calcium base binder, binds dietary phosphate
- reduces uric acid levels

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62
Q

Best test to quantify proteinuria in CKD?

A

Albumin: Creatinine ratio

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63
Q

What is considered a significant proteinuria?

A

albumin creatinine ratio > 3mg/mmol

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64
Q

How to best measure ACR?

A

First pass morning urine

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65
Q

According to ACR who should be referred to renal?

A
  1. a urinary albumin:creatinine ratio (ACR) of 70 mg/mmol or more, unless known to be caused by diabetes and already appropriately treated
  2. a urinary ACR of 30 mg/mmol or more, together with persistent haematuria (two out of three dipstick tests show 1+ or more of blood) after exclusion of a urinary tract infection
  3. consider referral to a nephrologist for people with an ACR between 3-29 mg/mmol who have persistent haematuria and other risk factors such as a declining eGFR, or cardiovascular disease
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66
Q

When should an ACEI be introduced for proteinuria?

A
  1. ACR > 30 mg/ml + hypertension
  2. ACR > 70 mg/ml REGARDLESS OF BLOOD PRESSURE
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67
Q

Risk factors for chronic pyelonephritis ?

A

vesicoureteral reflux in children
obstruction e.g. recurrent renal stones

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68
Q

Investigation findings of chronic pyelonephritis?

A

Blunted calyx
Corticomedullary scaring with atrophy tubule
Eosinophilic casts

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69
Q

Most common complication post renal transplant?

A

Ureteric anastomotic leak

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70
Q

What are the types of organ rejection?

A
  1. Hyperacute
  2. Acute
  3. Chronic
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71
Q

Mechanism of hyper acute organ rejection?

A

Occurs Immediately.
Through presence of pre formed antibody - ABO incompatibility - IgM

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72
Q

Mechanism of acute organ rejection?

A

Occurs over 6 months
T cell mediated
Tissue infiltrates and vascular lesions - mononuclear infiltrates

Most cases can be managed medically

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73
Q

Mechanism of chronic organ rejection?

A

Occurs > 6 months
Vascular changes predominate
Myointimal proliferation

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74
Q

What is cystinuria?

A

Autosomal recessive condition
Recurrent renal stones
Membrane transporter defect: cystine, ornithine, lysine, arginine ( COLA)

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75
Q

Genetics of cystinuria?

A

Chromosome 2: SLC3A1 gene
Chromosome 19: SLC7A9

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76
Q

How is cystinuria diagnosed?

A

Cyanide - nitroprusside test on urine

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77
Q

Management of cystinuria?

A

hydration
D-penicillamine
urinary alkalinization

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78
Q

Causes of cranial diabetic insipidius?

A

idiopathic
post head injury
pituitary surgery
craniopharyngiomas
infiltrative
Haemochromatosis
DIDMOAD

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79
Q

What is DIDMOAD?

A

DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)

Also known as Wolfram syndrome

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80
Q

Causes of nephrogenic diabetes insipidus?

A

genetic: the more common form affects the vasopression (ADH) receptor, the 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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81
Q

Features of diabetes insipidus?

A

Poluria
Polydipsia

High plasma osmolality
Low urine osmolality

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82
Q

How should diabetes insipidus be tested?

A

Water deprivation test

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83
Q

Management of nephrogenic diabetes insipidus?

A

Thiazides

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84
Q

Management of cranial diabetes insipidus

A

Desmopressin

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85
Q

Phases of diabetic nephropathy?

A
  1. Hyperfiltration - increased eGFR ( reversible)
  2. Latent phase
    - most patients do not develop microalbuminuria for 10 years
  3. Proteinuria
    - microalbuminuria 30-300mg/day
  4. Overt nephropathy
    - Persistent proteinuria > 300 mg/day
    - Hypertension
    - Glomerulosclerosis + Kimmelstiel wilson nodules
  5. End stage renal failure
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86
Q

Bacteria associated with epididymo-orchitis?

A

Young / sexual:
- Chlamydia
- Neisseria

Older / low risk sex:
- ecoli

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87
Q

Features of epididymo-orchitis?

A

Unilateral testicular swelling
Discharge
MUST EXCLUDE TORSION.

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88
Q

Management of epididymo-orchitis?

A

If unknown organism,: Ceftriaxone 500 mg IM + Doxy

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89
Q

Side effect of erythropoietin?

A

accelerated hypertension potentially leading to encephalopathy and seizures (blood pressure increases in 25% of patients)
bone aches
flu-like symptoms
skin rashes, urticaria
pure red cell aplasia* (due to antibodies against erythropoietin)
raised PCV increases risk of thrombosis (e.g. Fistula)
iron deficiency 2nd to increased erythropoiesis

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90
Q

Why people fail to respond to EPO?

A

iron deficiency
inadequate dose
concurrent infection/inflammation
hyperparathyroid bone disease
aluminium toxicity

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91
Q

What is Fanconi syndrome?

A

Generalised reabsorptive disorder of renal tubule in proximal convolute tubule
Results in:
- type 2 (proximal) renal tubular acidosis
- polyuria
- aminoaciduria
- glycosuria
- phosphaturia
- osteomalacia

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92
Q

Causes of Fanconi syndrome?

A

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

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93
Q

Features of fibromuscular dysplasia?

A

Hypertension
CKD - secondary to ACEi
Flash pulmonary oedema

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94
Q

What is fibromuscualr dysplasia?

A

Renal artery stenosis accounts for 90% of renal disease
Fibromuscular dysplasia counts of remaining 10%

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95
Q

Amount of potassium required as maintenance per day?

A

1 mol/kg/ day

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96
Q

What is focal segmental glomerulosclerosis?

A

Glomerulonephritis
Cause of nephrotic syndrome
Typically presents in young adults

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97
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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98
Q

What are the findings of focal segmental glomerulosclerosis on biopsy?

A

focal and segmental sclerosis and hyalinosis on light microscopy
effacement of foot processes on electron microscopy

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99
Q

Management of FSGS?

A

Steroids +/- immunesuppression

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100
Q

Presentation of nephrotic vs nephritic syndromes ?

A
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101
Q

What glomerulonephritides general present as nephritic syndrome?

A

Rapidly progressive glomerulonephritis
IgA nephropathy

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102
Q

Causes of rapidly progressive glomerulonephritis?

A

Goodpasteurts
ANCA positive vasculitis

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103
Q

Causes of IgA nephropathy?

A

Berger’s disease
Mesangioproliferative GN
Overlap of hence schonlein purpura

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104
Q

What presents as a mixed nephritic / nephrotic syndrome?

A

Diffuse proliferative glomerulonephritis
Membranoproliferative glomerulonephritis

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105
Q

Features 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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106
Q

Features of membrane proliferative glomerulonephritis (mesangiocapillary) ?

A

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

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107
Q

Types of nephrotic syndrome?

A

Minimal change disease
Membranous glomerulonephritis
Focal segmental glomerulosclerosis

108
Q

Features of minimal change disease ?

A

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

109
Q

Features of membraneous glomerulonephritis?

A

presentation: proteinuria / nephrotic syndrome / chronic kidney disease
cause: infections, rheumatoid drugs, malignancy
1/3 resolve, 1/3 respond to cytotoxics, 1/3 develop chronic kidney disease

110
Q

Features of focal segmental glomerulosclerosis?

A

may be idiopathic or secondary to HIV, heroin
presentation: proteinuria / nephrotic syndrome / chronic kidney disease

111
Q

Disorders with glomerulonephritis and low serum complement?

A

post-streptococcal glomerulonephritis
subacute bacterial endocarditis
systemic lupus erythematosus
mesangiocapillary glomerulonephritis

112
Q

Causes of transient or spurious non-visible haematuria?

A

urinary tract infection
menstruation
vigorous exercise (this normally settles after around 3 days)
sexual intercourse

113
Q

Causes of persistent non-visible haematuria?

A

cancer (bladder, renal, prostate)
stones
benign prostatic hyperplasia
prostatitis
urethritis e.g. Chlamydia
renal causes: IgA nephropathy, thin basement membrane disease

114
Q

Drugs that give red/orange urine?

A

Rifampicin
Doxorubicin

115
Q

What is Henoch-Scholein purpura?

A

IgA mediated small vessel vasculitis
Overlap with IgA nephropathy (Berger’s disease)

116
Q

Features of hence schonlein purpura?

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 failure

117
Q

What is Berger’s disease?

A

an IgA nephropathy

118
Q

How does Berger’s disease present?

A

Macroscopic haematuria in young people
Following upper respiratory tract infection

119
Q

Associated conditions with IgA Nephropathy?

A

alcoholic cirrhosis
coeliac disease/dermatitis herpetiformis
Henoch-Schonlein purpura

120
Q

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

121
Q

Differences between IgA nephropathy and post-strep glomerulonephritis?

A
122
Q

Management of IgA nephropathy?

A

Isolated haematuria / minimal proteinuria: Nil

Persistent proteinuria (500-1000 mg/day):
1. ACEi
2. Immunosuppression or corticosteroids ( if does not respond to ACEi)

123
Q

What is the prognosis of IgA nephropathy?

A

25% get ESRF

markers of good prognosis: frank haematuria
markers of poor prognosis: male gender, proteinuria (especially > 2 g/day), hypertension, smoking, hyperlipidaemia, ACE genotype DD

124
Q

Features of HIV associated nephropathy?

A

There are five key features of HIVAN:

  1. Massive proteinuria resulting in nephrotic syndrome
  2. normal or large kidneys
  3. focal segmental glomerulosclerosis with focal or global capillary collapse on renal biopsy
  4. elevated urea and creatinine
  5. normotension
125
Q

How can nocturia be managed in lower rinary tract symptoms for men?

A

Moderating fluid intake at night
Furosemide 40mg in later afternoon
Desmopressin

126
Q

Management of overactive bladder?

A

Antimuscarinics
Oxybutynin -
Tolterodine

127
Q

Management of overactive bladder?

A

Antimuscarinics
Oxybutynin -
Tolterodine

128
Q

Features of type one membranoproliferazive glomerulonephritis?

A

cause: cryoglobulinaemia, hepatitis C
renal biopsy
electron microscopy: subendothelial and mesangium immune deposits of electron-dense material resulting in a ‘tram-track’ appearance

129
Q

Features of type 2 membranoproliferazive glomerulonephritis?

A

causes: partial lipodystrophy (patients classically have a loss of subcutaneous tissue from their face), factor H deficiency
caused by persistent activation of the alternative complement pathway
low circulating levels of C3

130
Q

Renal biopsy result for type 1 membranoproliferative glomerulonephritis?

A

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

131
Q

Renal biopsy result for Type 2 membranoproliferative glomerulonephritis?

A

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

132
Q

Renal biopsy result for Type 2 membranoproliferative glomerulonephritis?

A

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

133
Q

Causes of type 3 membranoproliferazive glomerulonephritis?

A

Hep B and Hep C

134
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

135
Q

Causes of raised anion gap metabolic acidosis?

A

Lactate:
- shock
- sepsis
- Hypoxia

Ketones:
- Diabetic Ketoacidosis
- alcohol

Urate:
- renal failure

136
Q

Causes of lactic acidosis type A?

A

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

137
Q

Causes of lactic acidosis type B?

A

Metformin

138
Q

How does minimal change disease present?

A

Nephrotic syndrome

139
Q

Causes of minimal change disease ?

A

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

140
Q

Pathophysiology of minimal change disease?

A

T cell damage to GBM –> polyanion loss
Reduction of electrostatic charge –> Increased glomeruli permeability to serum albumin

141
Q

Features of minimal change disease?

A

Nephrotic syndrome
Normotension
Highly selective proteinuria
Renal biopsy - shows normal glomeruli
– electron microscopy shows fusion of podocytes and effacement of foot processes

142
Q

Management of minimal change disease ?

A

Corticosteroids
Cyclophosphamide

143
Q

What patient group typically gets minimal change disease ?

A

Children

144
Q

What is the triad of nephrotic syndrome?

A

Proteinuria > 3g / 24 hours
Hypoalbuminaemia
Oedema

**Pro-thrombotic: Due to loss of anti-thrombin III, Proteins C and S, rise in fibrinogen levels

144
Q

What is the triad of nephrotic syndrome?

A

Proteinuria > 3g / 24 hours
Hypoalbuminaemia
Oedema

**Pro-thrombotic: Due to loss of anti-thrombin III, plasminogen, Proteins C and S, rise in fibrinogen levels

145
Q

Most common cause for nephrotic syndrome?

A

Glumerulonephritis 80%

Systemic disease
- diabetes mellitus
- systemic lupus erythematosus
- amyloidosis

Drugs
- Gold
- Penicillamine

146
Q

Complications of nephrotic syndrome?

A

VTE
- due to loss of antithrombin III and plasminogen
Hyperlipidaemia
CKD
Hypocalcaemia

147
Q

How should nephrotoxicity due to contrast media be prevented?

A

IV 0.9% at 1ml/kg/hour for 12 hours pre and post
Withold metformin

148
Q

Risk factors for nephrotoxicity from contrast?

A

known renal impairment (especially diabetic nephropathy)
age > 70 years
dehydration
cardiac failure
the use of nephrotoxic drugs such as NSAIDs

149
Q

What the papilla of the kidney?

A

Ducts leading from the pyramids into the pelvis

150
Q

What are the causes of papillary necrosis?

A

Causes
chronic analgesia use
sickle cell disease
TB
acute pyelonephritis
diabetes mellitus

151
Q

Features of papillary necrosis?

A

fever, loin pain, haematuria
IVU - papillary necrosis with renal scarring - ‘cup & spill’

152
Q

Complications of peritoneal dialysis?

A

Coagulase negative staph - staph epidermis
Staph aureus
Sclerosing peritonitis

153
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

154
Q

Complications for plasma exchange ?

A

hypocalcaemia: due to the presence of citrate used as an anticoagulant for the extracorporeal system
metabolic alkalosis
removal of systemic medications
coagulation factor depletion
immunoglobulin depletion

155
Q

Pathophysiology of post strep glomerulonephritis?

A

Onset 7-14 days post infection
Infection of group A beta haemolytic strep
Caused by immune complex IgG, IgM, C3

156
Q

What are the features of post-streptococcal glomerulonephritis?

A

Visible haematuria
Proteinuria
Hypertension
Oliguria
Low C3

157
Q

Renal biopsy features of streptococcal glomerulonephritis?

A

acute, diffuse proliferative glomerulonephritis
endothelial proliferation with neutrophils

Electron microscopy: Subepithelial “humps” - lumpy immune complex deposits

Immunoflurescnece: Starry sky appearance

157
Q

Renal biopsy features of streptococcal glomerulonephritis?

A

acute, diffuse proliferative glomerulonephritis
endothelial proliferation with neutrophils

Electron microscopy: Subepithelial “humps” - lumpy immune complex deposits

Immunoflurescnece: Starry sky appearance

158
Q

Associations of renal cell cancer?

A

more common in middle-aged men
smoking
von Hippel-Lindau syndrome
tuberous sclerosis
incidence of renal cell cancer is only slightly increased in patients with autosomal dominant polycystic kidney disease

159
Q

Features of renal cell cancer?

A

Haematuria
Loin pain
Abdominal mass

Parneoplastic hepatic dysfunction

Left sided varicocele

Ectopic hormone secretion:
- may secrete EPO
- PTH
- ACTH

Stauffer Syndrome

160
Q

What is stuffer syndrome?

A

Paraneoplastic disorder with renal cell carcinoma
Presents with cholestasis / hepatosplenomegally
Secondary to increased IL-6

161
Q

T staging for renal cell cancer?

A

T1 Tumour ≤ 7 cm and confined to the kidney
T2 Tumour > 7 cm and confined to the kidney
T3 Tumour extends into major veins or perinephric tissues, but not into the ipsilateral adrenal gland and not beyond Gerota’s fascia
T4 Tumor invades beyond Gerota’s fascia (including contiguous extension into the ipsilateral adrenal gland)

162
Q

Management of renal cell cancer?

A

< 7 cm - partial nephrectomy
Alpha interferon and interleukin-2 reduce tumour size
TKI - sorafenib, sunitinib

162
Q

Management of renal cell cancer?

A

< 7 cm - partial nephrectomy
Alpha interferon and interleukin-2 reduce tumour size
TKI - sorafenib, sunitinib

163
Q

Pain management for renal stones?

A

IM dicolenfac for severe pain
Alpha blockers no longer used

164
Q

Fever + renal colic: When should imaging be done?

A

CT KUB immediately

165
Q

Management of renal stones < 5 mm

A

Will normally pass spontaneously
Can consider lithotripsy and percutaneous nephrolithotomy

166
Q

Management: Renal stone less than 2 cm ?

A

Lithotripsy

167
Q

Management: Renal stone less than 2 cm in pregnant female?

A

Ureteroscopy

168
Q

Management: Complex renal calculi / stag horn?

A

Percuetanous nephrolithotomy

169
Q

Ureteric calculi less than 5 mm ?

A

Manage expecantlt

170
Q

How can stones be prevented?

A

Thiazide diuretics (increased distal tubule calcium resorption)

171
Q

What is the relative importance HLA antigens of renal transplant?

A

HLA matching for a renal transplant the relative importance of the HLA antigens are as follows DR > B > A

172
Q

Classes of type 1 HLA receptor?

A

A
B
C

173
Q

Classes of type 2 HLA receptor

A

DP
DQ
DR

174
Q

Hyper acute rejection of kidney, what type of hypersensitivity?

A

Type II hypersensitivity

175
Q

Acute graft failure hypersensitivity?

A

Cell mediated cytotoxic T cells

176
Q

In transplant, what is the initial immunosuppression option?

A

Ciclosporin / tacrolimus with monoclonal antibody

177
Q

Maintenance immunosuppression in renal transplant?

A

Ciclosporin . tacrolimus
With mycophenolate

178
Q

Mechanism of cyclosporin?

A

inhibits calcineurin, a phosphotase involved in T cell activation

179
Q

Tacrolimus mechanism?

A

lower incidence of acute rejection compared to ciclosporin
also less hypertension and hyperlipidaemia
however, high incidence of impaired glucose tolerance and diabetes

180
Q

Mechanism of MMF?

A

Blocks purine synthesis, inhibition of IMPDH
Inhibits B and T cells

181
Q

Side effect of MMF?

A

GI side effects
Marrow suppression

182
Q

Monoclonals used in renal transplant?

A

selective inhibitors of IL-2 receptor
daclizumab
basilximab

183
Q

Best investigation for renal vascular disease?

A

MR angiography

184
Q

Features of rhabdomyolysis?

A

acute kidney injury with disproportionately raised creatinine
elevated creatine kinase (CK)
myoglobinuria
hypocalcaemia (myoglobin binds calcium)
elevated phosphate (released from myocytes)
hyperkalaemia (may develop before renal failure)
metabolic acidosis

185
Q

Causes of rhabdomyolysis?

A

seizure
collapse/coma (e.g. elderly patients collapses at home, found 8 hours later)
ecstasy
crush injury
McArdle’s syndrome
drugs: statins (especially if co-prescribed with clarithromycin)

186
Q

Management of rhabdomyolysis?

A

IV fluids
Urinary alkalisation

187
Q

Associated conditions with scrotal pain?

A

Polycystic kidney disease
Cystic fibrosis
Von-Hippel Lindau

188
Q

Mechanism of spironolactone?

A

Aldosterone antagonist

189
Q

Indicates for spironolactone ?

A

ascites: patients with cirrhosis develop a secondary hyperaldosteronism. Relatively large doses such as 100 or 200mg are often used
hypertension
heart failure (see RALES study below)
nephrotic syndrome
Conn’s syndrome

190
Q

Adverse effects of spironolactone?

A

hyperkalaemia
gynaecomastia: less common with eplerenone

191
Q

Classification of kidney dysfunction?

A

class I: normal kidney
class II: mesangial glomerulonephritis
class III: focal (and segmental) proliferative glomerulonephritis
class IV: diffuse proliferative glomerulonephritis
class V: diffuse membranous glomerulonephritis
class VI: sclerosing glomerulonephritis

192
Q

Features of class IV diffuse proliferative glomerulonephritis? (from SLE)

A

glomeruli shows endothelial and mesangial proliferation, ‘wire-loop’ appearance

193
Q

Features of testicular cancer?

A

a painless lump is the most common presenting symptom
pain may also be present in a minority of men
hydrocele
gynaecomastia

194
Q

How does gynaecostmastia occur?

A

germ-cell tumours → hCG → Leydig cell dysfunction → increases in both oestradiol and testosterone production, but rise in oestradiol is relatively greater than testosterone
leydig cell tumours → directly secrete more oestradiol and convert additional androgen precursors to oestrogens

195
Q

Who gets what type of testicular cancer?

A

Seminoma - 35 year old
Non-seminomas - 25 year old

196
Q

Best imaging modality of testicular cancer?

A

Ultrasound

197
Q

Features of film’s tumour?

A

abdominal mass (most common presenting feature)
painless haematuria
flank pain
other features: anorexia, fever
unilateral in 95% of cases
metastases are found in 20% of patients (most commonly lung)

198
Q

Association of Wilm’s tumour?

A

Beckwith-Wiedemann syndrome
as part of WAGR syndrome with Aniridia, Genitourinary malformations, mental Retardation
hemihypertrophy
around one-third of cases are associated with a loss-of-function mutation in the WT1 gene on chromosome 11

199
Q

What is thin basemement membrane disease?

A

An inherited disorder of type IV collagen that causes thinning of the basement membrane
Multiple family members with microscopic haematuria
Diagnosis: Biopsy

200
Q

Renal stone risk factors?

A

dehydration
hypercalciuria, hyperparathyroidism, hypercalcaemia
cystinuria
high dietary oxalate
renal tubular acidosis
medullary sponge kidney, polycystic kidney disease
beryllium or cadmium exposure

201
Q

Urate stone risk factors?

A

gout
ileostomy: loss of bicarbonate and fluid results in acidic urine, causing the precipitation of uric acid

202
Q

Drugs that cause calcium stones?

A

drugs that promote calcium stones: loop diuretics, steroids, acetazolamide, theophylline

203
Q

Drugs that prevent calcium stones?

A

Thiazide

204
Q

Management of metastatic prostate cancer?

A
  1. Anti-androgen therapy - synthetic GnRH agonist or antagonists
  2. Bicalutamide
  3. Cyproterone acetate
  4. Abiraterone
  5. Bilateral orchiectomy
205
Q

Mechanism of GnRH agonists / antagonists in metastatic prostate cancer?

A

Paradoxically result in lower LH levels longer term by causing overstimulation, resulting in disruption of endogenous hormonal feedback systems. The testosterone level will therefore rise initially for around 2-3 weeks before falling to castration leves

Initially therapy is often covered with an anti-androgen to prevent a rise in testosterone - ‘tumour flare’. The resultant stimulation of prostate cancer growth may result in bone pain, bladder obstruction and other symptoms

206
Q

Mechanism of bicalutamide?

A

non-steroidal anti-androgen receptor blocker

207
Q

Mechanism of cyproterone ?

A

steroidal anti-androgen
prevents DHT binding from intracytoplasmic protein complexes
used less commonly since introduction of non-steroidal anti-androgens

208
Q

Mechanism of abiraterone?

A

androgen synthesis inhibitor
option for the treatment of hormone-relapsed metastatic prostate cancer in patients who have no or mild symptoms after androgen deprivation therapy has failed, and before chemotherapy is indicated

209
Q

What is the pathophysiology of Berger’s disease?

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

210
Q

Causes of membranous glomerulonephritis?

A

idiopathic: due to anti-phospholipase A2 antibodies
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

211
Q

What tumour marker is associated with seminoma?

A

beta HCG

212
Q

What are the features of renal cell carcinoma?

A

Classical triad:
- haematuria
- loin pain
- abdominal mass

Pyrexia of unknown origin

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

Paraneoplastic hepatic dysfunction

213
Q

Features of atypical haemolytic uraemia syndrome?

A

full blood count
anaemia: microangiopathic hemolytic anaemia characterised by a haemoglobin level less than 8 g/dL with a negative Coomb’s test
thrombocytopenia
fragmented blood film: schistocytes and helmet cells
U&E: acute kidney injury
stool culture
looking for evidence of STEC infection
PCR for Shiga toxins

214
Q

What is the mechanism of atypical haemolytic uraemia syndrome?
Mechanism of atypical haemolytic uaemic syndrome?

A

Atypical haemolytic uraemia syndrome

Complement dysfunction

215
Q

What is the most common glomerulonephritis from SLE?

A

Diffuse proliferative glomerulonephritis

216
Q

In nephrotic syndrome, loss of what makes it anticoagulable?

A

Antithrombin III

217
Q

Causes of retroperitoneal fibrosis?

A

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

218
Q

Mechanism of spironolactone?

A

Aldosterone antagonists acts on the cortical collecting ducts as a diuretic
Inhibits mineralocorticoid in cortical collecting duct

219
Q

Features of type 2 membranoproliferative glomerulonephritis?

A

causes: partial lipodystrophy (patients classically have a loss of subcutaneous tissue from their face), factor H deficiency
caused by persistent activation of the alternative complement pathway
low circulating levels of C3
C3b nephritic factor is found in 70%
an antibody to alternative-pathway C3 convertase (C3bBb)
stabilizes C3 convertase
renal biopsy
electron microscopy: intramembranous immune complex deposits with ‘dense deposits’

220
Q

When does contact nephropathy occur?

A

2-3 days after administration

221
Q

What type of antibody is involved in HSP?

A

IgA

222
Q

Side effect of tacrolimus ?

A

hypertension and hyperglycaemia.
Hyperlipidaemia
Accelerate cardiovascular disease
Tremors

223
Q

Most common cause of death from CKD?

A

Ischaemic heart disease

224
Q

Nephrotic syndrome + Acute flank pain + deteriorating renal function?

A

Renal vein thrombosis

225
Q

Management of membranous glomerulonephritis?

A
  1. ACEi
  2. Immunosuppression
  3. Anticoagulation
226
Q

Electronic microscopic findings of membraneous glomerulonephritis?

A

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

227
Q

Causes of membraneous glomerulonephritis?

A

idiopathic: due to anti-phospholipase A2 antibodies
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

228
Q

How does calcium resonium helps remove potassium?

A

Increases excretion by preventing enteral absorption

229
Q

Hypertension + High aldosterone + Low renin?

A

Primary aldosteronism

230
Q

Hypertension + High aldosterone + High renin ?

A

Bilateral renal artery stenosis

231
Q

Normotension + High aldosterone + High renin

A

Barter syndrome

232
Q

How does alcohol binge cause polyuria?

A

Alcohol bingeing can lead to ADH suppression in the posterior pituitary gland subsequently leading to polyuria. This is similar to cranial diabetes insipidus or partial cranial diabetes insipidus and typically causes hypernatremia with a raised serum osmolality and decreased urine osmolality.

233
Q

What should be co-prescribed with anti-androgens in prostate cancer?

A

GnRH and Cyproterone

risk of tumour flare.

This phenomenon is secondary to initial stimulation of luteinising hormone release by the pituitary gland resulting in increased testosterone levels.

234
Q

What type of renal stone does proteus cause?

A

Struvite stone (magnesium ammonium phosphate)

235
Q

What is a common complication of plasma exchange?

A

Hypocalxaemia

236
Q

What is bicalutamide?

A

non-steroidal, anti-androgen therapy. It works by blocking the androgen receptors and is typically used together with a gonadotropin-releasing hormone (GnRH) analogue or orchidectomy in the management of advanced prostate cancer.

237
Q

How to manage someone on Spiro, with gynaecomastia?

A

Eplerenone

238
Q

Fluids in a hypercholaemic metabolic acidosis?

A

Large volume resuscitation with normal saline leads to an overload of chloride ions into the blood. The increased chloride ions, force bicarbonate into the cells and in doing so reduce the available bicarbonate for the pH buffering system.The result is a hyperchloraemic metabolic acidosis.

239
Q

Most common inheritance of nephrogenic diabetes insidipus? Most common gene mutation?

A

X linked dominant
Vasopressin mutation: AVPR2 (arginine vasopressin receptor 2)

240
Q

How does fibromuscular dysplasia appear on ultrasound?

A

asymmetric kidneys → fibromuscular dysplasia

241
Q

Drug to prevent oxalate stones?

A

pyridoxine reduces urinary oxalate secretion

242
Q

How to prevent uric acid stones?

A

Allopurinol
Urinary alkalisation

243
Q

What virus should you be worried about in starting transplant / immunosuppression in transplants ?
How does it present?

A

CMV

sclera are jaundiced and she has widespread lymphadenopathy with hepatomegaly

244
Q

What immunosuppression can be used in pregnancy?

A

Azithromycin

245
Q

Presentation of fibromuscular dysplasia?

A

Young female
Hypertension
Asymmetric kidney

246
Q

Management of T1/T2 prostate cancer?

A

T1 = localised within prostate

conservative: active monitoring & watchful waiting
radical prostatectomy
radiotherapy: external beam and brachytherapy

247
Q

Management of T3/T4 prostate cancer?

A

T3/T4 - localised advanced prostate cancer
Hormonal therapy
radical prostatectomy: erectile dysfunction is a common complication

248
Q

What type of drugs is gosrelin and how does it work in prostate cancer?

A

GnRH AGONIST

paradoxically result in lower LH levels longer term by causing overstimulation, resulting in disruption of endogenous hormonal feedback systems. The testosterone level will therefore rise initially for around 2-3 weeks before falling to castration leves

249
Q

Best imaging for vesicoureteric reflux?

A

micturating cystourethrogram (MCUG).

250
Q

What can artificially lower PSA?

A

finasteride

251
Q

Presentation and management of CMV?

A

CMV infection is one of the most important in transplant receptors - clinically is characterized by fever, deranged transaminases, leukopenia and thrombocytopenia. Diagnosed by PCR and treated with ganciclovir

252
Q

Varicoele + malignancy

A

think RCC

253
Q

What are stag horn calculi?

A

Struvite

254
Q

Most common cause of adult nephrotic syndrome ?

A

FSGS

255
Q

What kidney stone is semi opaque on X-ray?

A

cystine stones

256
Q

What kidney stone is radio-lucent?

A

Urate
Xanthine

257
Q

What complement protein is low in partial lipodystrophy?

A

C3

258
Q

Oliguria + Haematuria + Epistaxis + Sinusitis
what autoantibody?

A

granulomatosis with polyangiitis (GPA)
cANCA

259
Q

history of asthma, and sometimes peripheral neuropathy, oliguria and haematuria?

A

eosinophilic granulomatosis with polyangiitis (EGPA, formerly Churg-Strauss syndrome),
pANCA

260
Q

Fibromusclar dysplasia appearance on MR angiogram ?

A

String bead appearance

261
Q

Gene mutation in vasopressin 2 receptor (ADH) diabetes insidious?

A

V2R gene

262
Q

What is the other name for a rapidly progressive glomerulonephropathy?

A

Crescentic

263
Q

What are variables for eGFRR

A

Creatinine
Age
Gender
Ethnicity

MRCP Renal (2 decks)

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