MRCP revision battle 5.1: Nephrotic Syndrome

After yesterdays big push today's revision was less epic, mainly because I started reading "The Lovely Bones" by Alice Sebold and I just got too involved.  My motivation to revise also wasn't helped by the first onexamination question I did being 'renal based', with renal medicine being my personal black hole of knowledge... it doesn't matter how many facts I try to throw into it, it still remains just as black.

So, today's battles are:
5.1 nephrotic syndrome
5.2 renal vein thrombosis
5.3 IgA glomerulonephritis
5.4 acute epiglottis



Battle 5.1: Nephrotic syndrome


Nephrotic syndrome is a classic triad of:

• >3g proteinuria
• hypoalbuminaemia <25 and
• oedema

It is also strongly associated with hypercholesterolaemia


80% of the time it is associated with glomerulonephritis, a fiendishly complex set of conditions.


The rest of the time its possible causes are many and varied:

• diabetes mellitus
• leprosy/malaria/HBV
• myeloma/lymphoma
• amyloidosis
• SLE
• gold/penicillamine/NSAIDS/captopril/interferon alpha/heroin
• pre-eclampsia
• accelerated hypertension
• sickle cell disease
• Alports
• rarely visico-ureteric reflux

I'm afraid I don't have a clever way/inclination to remember that list, I just hope that by reading it a few times in the exam a faint light of recognition may go on at the appropriate time.


Happily I do have a way of remembering the potential complications of nephrotic syndrome, which is good since sneaky MRCP examiners may be trying to get you to guess nephrotic syndrome from a description of the complications alongside part of the classic triad.

My mnemoric is BOB, I HIT HIM:

• B12 deficiency
• Osteomalacia
• Budd-Chiari
• Infections
• Hyperlipidaemia
• Immunosupression
• Thrombosis (including renal vein thrombosis)
• Hyponatraemia
• Iron deficiency
• Malnutrition

Treatment for nephrotic syndrome is to restrict salt, treat the cause, prophylactic heparin, treat any hypertension and potentially give furosemide or ACE-i.


On to 5.2... renal vein thrombosis

MRCP revision battle 5.2: Renal vein thrombosis

Renal vein thrombosis can occur due to:

• nephrotic syndrome inducing a hypercoagulable state
• invasion of the renal vein by renal cell carcinoma
• thombophillia

It is often asymptomatic, but equally may present with haematuria, loin pain, palpable mass or a sudden worsening of renal function.


Treatment is with warfarin, anticoagulated to INR 2-3 for 3-6 months.

 Follow me to battle 5.3....

MRCP revision battle 5.3: IgA Glomerulonephritis

As if the glomerulonephropathies aren't tricky enough (hence why series 5 of the battles only discusses one of them) they can also have a series of pseudonyms/ 'nicknames.'  For example, IgA nephropathy also goes by the labels 'Bergers disease' and 'mesangioproliferative glomerulonephritis'.  For simplicity, I'll just refer to it as IgA nephropathy.


IgA nephropathy is the commonest GN in adults, and it classically affects young males after an URTI.  So, in the exam look out for the 25 yr old man who has haematuria following a sore throat.

Symptoms may just be micro/macro haematuria, or match the nephrotic syndrome triad.

Incidence is increased in those from the far east, and those with HLA DQw7 or HLA B35.

Associations include cirrhosis, dermatitis herpetiformis, ank spon, Wiskott-Aldrich syndrome and chronic liver or lung disease.


IgA is positive in 50% of cases and C3 tends to be raised.


25% of cases progress to end stage renal disease.

Frank haematuria is associated with a good prognosis.
Being male, having proteinuria, hypertension, smoking or high lipids are all associated with a poor prognosis.


Phew, thats one of the GN covered... a few more to face at a later date... now lets diversify for the last battle of the day to acute epiglottis.

MRCP revision battle 5.4: Acute Epiglottitis

Since the introduction of the Hib vaccine the potentially life-threatening condition of acute epiglottitis has happily become rare.  Except, of course, in the MRCP exam.

The commonest cause of acute epiglottis was always h.influenzae, but many other pathogens can also cause it.

Presentation tends to be a 'toxic' looking patient with fever and stridor, often with a preceding sore throat.


Treatment is with a 3rd generation cephalosporin.



That's it for today, but if you fancy testing yourself on yesterday's battles click here to go to war 4...

MRCP questions: War 4

As with previous 'wars' after 'battles' these are just a few quick questions to see if your brain cells have retained the information provided in battles 4.1 to 4.5.

Jot down your answers on a piece of paper then compare them to my answers here


Question 1: 
What pattern would COPD produce on spirometry?

Question 2:
With what condition is thermoactinomyces vulgaris associated?

Question 3:
In which zone of the lungs would fibrosis secondary to EAA classically occur?


Question 4:
Can you name 11 causes of lung fibrosis?

Question 5:
Can you name at least 10 causes of clubbing?


answers here