S7: CKD & glomerulonephritis

Question 1

What is CKD?

Answer 1

Can result in progressive loss of renal function over months to years
Usually irreversible because the renal tissue has been replaced by extracellular matrix (scar tissue) in response to damage

Question 2

Describe the staging of CKD

Answer 2

1 – eGFR>90
2 – eGFR 60-89
3a – eGFR 45-59
3b – eGFR 30-44 
4 – eGFR 15-29
5 – eGFR<15 
A1 – urine ACR < 30mg/g 
A2 – urine ACR 30-290mg/g 
A3 – urine ACR > 300mg/g

Question 3

List risk factors for developing CKD

Answer 3

Diabetes
Hypertension
CVD
Family history of stage 5 CKD

Question 4

Describe prevention of CKD

Answer 4

Modifiable risk factors – lifestyle, smoking, obesity & lack of exercise
Uncontrolled diabetes, hypertension, proteinuria (ace-inhibitors/angiotensin receptor blockers) & lipids

Question 5

Describe handling of water in CKD

Answer 5

Reduced GFR – lose ability to maximally dilute and concentrate urine
Small glomerular filtrate but same solute load causes osmotic diuresis = nocturia (response to ADH is reduced)
Low volume of filtrate reduces maximum ability to excrete urine therefore maximum urine volume much smaller

Question 6

Describe hyperkalaemia in CKD

Answer 6

Can occur once eGFR < 20mls/min (less likely when good urine output maintained)
May require:
1) Stopping ACEi/angiotensin receptor blocker
2) Avoidance of other drugs that can increase K+
3) Altering diet to avoid foods with high potassium

Question 7

How do you treat anaemia in CKD?

Answer 7

Check iron stores first – if iron low, replace iron first

When iron is ok, check Hb, if still low -> start erythropoietin stimulating agent

Question 8

Describe management of bone mineral disease in CKD

Answer 8

Reduce phosphate intake
Phosphate binders – many contain calcium
1-alpha-calcidol
(vitamin D)

Question 9

What is established end-stage renal failure?

Answer 9

When death is likely without renal replacement therapy
eGFR<15mls/min
Symptoms: overwhelming tiredness, difficulty sleeping, difficulty concentrating, symptoms & signs of volume overload

Question 10

Describe renal replacement therapy

Answer 10

Required when native renal function declines to a level no longer adequate to support health
Usually when eGFR 8-10
3 types: haemodialysis, peritoneal dialysis & renal transplant

Question 11

Describe advantages and disadvantages of haemodialysis

Answer 11

Advantages = less responsibility, days off & proven effective long-term 
Disadvantages = time consuming, tied to dialysis times, access/line problems & fluid/food restricted

Question 12

Describe advantages and disadvantages of peritoneal dialysis

Answer 12

Advantages = continuously at home (independent), less fluid/food restrictions, easy to travel & renal function may be better preserved initially 
Disadvantages = frequent daily exchanges/overnight, responsibility, peritonitis & less long-term survival data

Question 13

Describe advantages and disadvantages of renal transplant

Answer 13

Advantages = reduced mortality & morbidity compared to dialysis, better quality of life 
Disadvantages = peri-operative risk, malignancy risk, infection risk & risk of diabetes, hypertension from meds

Question 14

What is glomerulonephritis?

Answer 14

Inflammation of the glomeruli 
4 structures in glomerulus that can be damaged:
1) Capillary endothelium 
2) Glomerular basement membrane 
3) Mesangial cells 
4) Podocytes 
Often involves the immune system

Question 15

What is the difference between nephritic and nephrotic syndrome?

Answer 15

Nephritic – inflammation disrupting the glomerular basement membrane, haematuria (‘cola’ coloured urine)
Nephrotic – podocyte damage (effacement of foot processes) leading to glomerular charge-barrier disruption, massive proteinuria (oedema)

Question 16

Describe nephrotic syndrome

Answer 16

Triad: proteinuria > 350mg/mmol, hypoalbuminaemia & oedema
Usually accompanied by high cholesterol
Other features: BP often normal, creatinine may be normal

Question 17

List causes of nephrotic syndrome

Answer 17

Primary renal disease – minimal change disease, membranous glomerulonephritis & focal segmental glomerulosclerosis
Secondary renal disease – diabetes

Question 18

Describe diabetic nephropathy

Answer 18

Leading cause of end stage renal disease
Excess glucose in blood binds to proteins
Hyaline atherosclerosis – obstructs blood flow, initially increased GFR
Over time, mesangial cells secrete more structural matrix – thickens basement membrane – decreases GFR
Treatment: hypertension, good glycaemic control, ACEi & angiotensin receptor blockers

Question 19

Describe minimal change disease

Answer 19

Most common cause of nephrotic syndrome in children under 6
Glomerular capillary fuses with foot processes
Prognosis good in children, variable with adults

Question 20

Describe membranous glomerulonephritis

Answer 20

Subepithelial deposition of immune complexes -> thickening of basement membrane
40% adult nephrotic syndrome
Treatment: immunosuppressants & treatment of underlying cause

Question 21

Describe focal segmental glomerulosclerosis

Answer 21

Primary: idiopathic
Secondary: sickle cell disease, HIV, heroin abuse & kidney hyperperfusion
Podocytes are damaged
Proteins build up in glomerulus – hyalinosis (glassy) -> leading to sclerosis
Treatment: steroids (NB: inconsistent results can lead to chronic renal failure)

Question 22

Describe management of nephrotic syndrome

Answer 22

1) Oedema – diuretics, salt & fluid restriction
2) ACEi – anti-proteinuric
3) Hypercholesterolaemia – atherogenic if long-term nephrotic
4) Treat underlying condition

Question 23

Describe nephritic syndrome

Answer 23

Triad: haematuria, reduction in GFR & hypertension
Often some proteinuria but less than nephrotic syndrome
Onset may be acute or rapidly progressive

Question 24

List common causes of nephritic syndrome

Answer 24

IgA nephropathy (Berger’s disease)
Rapidly progressive GN
Goodpasture’s
Post-streptococcal GN

Question 25

Describe IgA nephropathy

Answer 25

Most common primary glomerular disease worldwide, causing recurrent haematuria
Hypertension and IgA levels raised -> deposited in mesangium -> sclerosis of damaged segment
Treatment: control BP, antihypertensives & steroids (20% will develop advanced CKD)

Question 26

Describe rapidly progressive glomerulonephritis

Answer 26

Severe glomerular injury – leakage of fibrin; macrophages & epithelial cells proliferate
Crescent shape masses form -> reduces glomerular supply
Loss of renal function within days to weeks
Treatment: high dose steroids, immunosuppressants & plasma exchange

Question 27

Describe Goodpasture’s syndrome

Answer 27

Antibodies to type IV collagen in glomerular BM develop -> inflammation
Results in rapidly progressive glomerular nephritis, acute renal failure & lung haemorrhage
Treatment: plasma exchange, corticosteroids
Prognosis poor without treatment

Question 28

Describe post-streptococcal glomerulonephritis

Answer 28

Presents 1-3 weeks following group A B-haemolytic streptococcal infection of tonsils, pharynx or skin
Treatment: abx to treat remaining infection
Prognosis excellent in children
Around 60% adults recover completely, the rest develop hypertension or renal impairment

Question 29

Describe the management of nephritic syndrome

Answer 29

1) Blood pressure control/reduction of proteinuria – ACEi, salt restrict
2) Treatment of oedema
3) Disease specific treatment
4) CVS risk management
5) Dialysis

Question 30

What investigations do you do for a patient with suspected CKD?

Answer 30

Measure BP
Urine dipstick - look for protein
General - LFTs, U&Es
Ultrasound scan - look at kidney size

Question 31

How do you treat acidosis in CKD?

Answer 31

Give oral NaHCO3 (sodium bicarbonate) tablets

Question 32

Describe how CKD leads to bone mineral disease

Answer 32

Impaired renal function
Less activation of vitamin D:
1) Less calcium absorption, decreased plasma calcium levels & stimulation of parathyroid glands to produce more PTH
2) Impaired mineralisation of bone
Increased levels of PTH leads to more bone resorption
Increased levels of plasma phosphate due to impaired excretion by kidney (leads to further activation of parathyroid glands -> hyperplasia)

Question 33

List symptoms of having accumulated waste products in CKD

Answer 33

Uraemic symptoms
Nausea and vomiting
Reduced appetite
Pruritus - constant itch