Wednesday 10 November 2010

MRCP revision battle 45.1: Dialysis and complications

Back to my old nemesis renal medicine for another 7 battles...

MRCP revision battle 45.1: Dialysis and complications
MRCP revision battle 45.2: Anaemia in chronic renal failure
MRCP revision battle 45.3: Diuretics
MRCP revision battle 45.4: Proteinuria
MRCP revision battle 45.5: Renal osteodystrophy
MRCP revision battle 45.6: Radio-contrast nephropathy
MRCP revision battle 45.7: Minimal change disease

MRCP revision battle 45.1: Dialysis and complications

Lets start with a very matter-of-fact battle on dialysis and its complications

Brief overview of types of renal replacement therapy
  1. Haemodialysis
    • semi-permeable membrane
    • solute transfer by diffusion
    • excess fluid removed by creating a negative transmembrane pressure = ultrafiltration
  2. Haemofiltration
    • highly permeable membrane
    • solute transfer by convection
    • ultrafiltrate replaced by an equal volume of substitute fluid
    • takes longer and is more expensive than haemodialysis but less haemodynamic instability so used for critically ill patients
  3. Peritoneal dialysis
    • dialysis fluid put into abdominal cavity via tenchkoff catheter
    • solutes diffuse across peritoneal membrane
    • ultrafiltration achieved by adding glucose to the dialysis fluid

Complications of dialysis
  • Disequilibration syndrome
    • occurs on initial dialysis
    • manifests as nausea, vomiting, headache and altered consciousness
    • caused by rapid changes in plasma osmolality
  • Vascular disease
  • Heart valve calcification - especially aortic valve
  • Beta-2 microglobulin amyloidosis
  • Arthritis
  • Infections

Now to consider anaemia in renal failure...

MRCP revision battle 45.2: Anaemia in chronic renal failure

Anaemia is common in chronic renal failure and is usually due to:
  • decreased production of erythropoetin
  • iron deficiency

Treatment should be considered when Hb <11
The target for treatment should be Hb between 10.5 and 12.5

Correct any iron deficiency first; note that oral iron is often not enough and IV iron therapy may be needed.

If there is still anaemia the likely eryropoetin deficiency must be addressed.  Options are:
  • Eryropoetin replacement with either epoetin (=recombinant human erythropoetin) or 
  • darbepoetin (=hyperglycosylated derivative of epoetin with a longer half life)

Side effects of epoetin include:
  • hypertension (25%)
  • bone aches
  • 'flu'
  • rashes, urticaria
  • pure red cell aplasia 
    • low reticulocyte count
    • anaemia
    • antibodies
  • increased risk of DVT as increased PCV

If no response to epoetin consider if the patient has an infection, inflammatory condition or aluminium toxicity, all of which can impair epoetin's effectiveness.

Note that blood transfusions are generally avoided in renal patients as they would make matching for transplants more difficult

Cross your legs as we move on to a battle of diuretics...

MRCP revision battle 45.3: Diuretics

Before I started my revision I thought I was very au-fait with diuretics - after all, I prescribe them daily.  However, a quick bond with the British National Formulary revealed some interesting gems.  So here's a quick recap of diuretics with a sprinkling of hopefully new information.

1. Loop diuretics
  • work on the Na-K-2Cl transporter in the ascending loop of Henle
  • examples include furosemide and bumetanide
  • bumetanide is 40x more potent than furosemide for the same dose
  • both work within 30 mins (if given IV) or 1 hr (if given orally) and their action is completed within 6 hours
  • possible side effects include:
    • hypokalaemia/natraemia
    • retention if enlarged prostate
    • tinnitus 
    • pancreatitis

2. Thiazide diuretics
  • work on the Na-Cl co-transporter in the DCT
  • examples include bendroflumethiazide, indapamide and metolazone
  • they work within 1 to 2 hours and have a duration of action of 12 to 24 hours
  • possible side effects include:
    • hypokalaemia/naturaemia
    • hyperglycaemia
    • pancreatitis

3. Aldosterone antagonists
  • work by antagonising aldosterone 
  • examples include spironolactone and eplerenone 
  • possible side effects include:
    • hyperkalaemia
    • impotenence
    • gynaecomastia

Now for the differentials of proteinuria...

MRCP revision battle 45.4: Proteinuria

Normal protein excretion in urine is <150mg/day

Causes of proteinura include:
  • Renal causes
    • UTI
    • glomerulonephritis
    • myeloma
    • diabetes
    • hypertension
    • amyloid
  • Extra-renal causes
    • fever
    • exercise
    • psoriasis
    • pregnancy

Orthostatic proteinuria is proteinuria which disappears when recumbant.   The cause of this is unknown but it is felt to be benign.

On to renal osteodystrophy...

MRCP revision battle 45.5: Renal osteodystrophy

Renal osteodystrophy refers to the bone pathology which results from the endocrine and electrolyte imbalances caused by chronic renal failure.

Derangements include:
  • raised phosphate
  • low calcium
  • secondary hyperparathyroidism
  • low vitamin D
  • acidosis

The result on bones include:
  • osteomalacia
  • osteitis fibrosa cystica = hyperparathyroid bone disease
  • osteoporosis
  • osteosclerosis 'rugger jersey' spine

Management is:
  • calcichew - to bind phosphate in the gut
  • vit D analogues - eg adcal D3/calceos/calcichew = colecalciferol

On to the slightly more stimulating contrast nephropathy...

MRCP revision battle 45.6: Radio-contrast nephropathy

Radiocontrast nephropathy complicates up to 10% of procedures involving contrast.

Contrast nephropathy presents as non-oliguric acute renal failure 1 to 5 days post procedure.

Risk of contrast nephropathy can be reduced by:
  • good hydration/normal saline
  • oral n.acetyl cysteine

Risk of contrast nephropathy is increased by:
  • increased amount of contrast
  • hypovolaemia
  • myeloma
  • increasing age
  • diabetes
  • raised calcium
  • chronic renal failure

Remember that metformin must be withheld before and for 48 hrs post IV contrast due to risk of lactic acidosis. 

Now to end on a high with a battle with minimal change disease...

MRCP revision battle 45.7: Minimal change glomerulonephritis

Minimal change glomerulonephritis almost always presents as nephrotic syndrome

It is responsible for 80% of cases of nephrotic syndrome in children and around a quarter of cases in adults.

Its name 'minimal change' comes from the fact that under a light microscope the kidney looks normal; if an electron microscope is used you can see podocyte fusion.

Minimal change glomerulonephritis causes a highly selective proteinuria with only smaller proteins leaked.

Most causes are idiopathic but 10-20% are associated with:
  • NSAIDs/gold/rifampacin
  • hodgkins, thyroma
  • mononucleosis

It is believed to be T-lymphocyte mediated.

Treatment is with corticosteroids - 80% of cases respond
Cyclophosphamide can be used in non-responders.

The prognosis for minimal change glomerulonephritis is (fairly) good:
  • 1/3 recover completely
  • 1/3 suffer infrequent relapses
  • 1/3 suffer frequent relapses
  • BUT - <1% proceed to end-stage renal failure

Tomorrow's battles will be a completely random bag, then a final renal push (the end of the hattrick) will occur the day after.