S7: CKD & glomerulonephritis Flashcards
What is CKD?
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Usually irreversible because the renal tissue has been replaced by extracellular matrix (scar tissue) in response to damage
Describe the staging of CKD
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
List risk factors for developing CKD
Diabetes
Hypertension
CVD
Family history of stage 5 CKD
Describe prevention of CKD
Modifiable risk factors – lifestyle, smoking, obesity & lack of exercise
Uncontrolled diabetes, hypertension, proteinuria (ace-inhibitors/angiotensin receptor blockers) & lipids
Describe handling of water in CKD
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
Describe hyperkalaemia in CKD
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
How do you treat anaemia in CKD?
Check iron stores first – if iron low, replace iron first
When iron is ok, check Hb, if still low -> start erythropoietin stimulating agent
Describe management of bone mineral disease in CKD
Reduce phosphate intake
Phosphate binders – many contain calcium
1-alpha-calcidol
(vitamin D)
What is established end-stage renal failure?
When death is likely without renal replacement therapy
eGFR<15mls/min
Symptoms: overwhelming tiredness, difficulty sleeping, difficulty concentrating, symptoms & signs of volume overload
Describe renal replacement therapy
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
Describe advantages and disadvantages of haemodialysis
Advantages = less responsibility, days off & proven effective long-term Disadvantages = time consuming, tied to dialysis times, access/line problems & fluid/food restricted
Describe advantages and disadvantages of peritoneal dialysis
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
Describe advantages and disadvantages of renal transplant
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
What is glomerulonephritis?
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
What is the difference between nephritic and nephrotic syndrome?
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)
Describe nephrotic syndrome
Triad: proteinuria > 350mg/mmol, hypoalbuminaemia & oedema
Usually accompanied by high cholesterol
Other features: BP often normal, creatinine may be normal
List causes of nephrotic syndrome
Primary renal disease – minimal change disease, membranous glomerulonephritis & focal segmental glomerulosclerosis
Secondary renal disease – diabetes
Describe diabetic nephropathy
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
Describe minimal change disease
Most common cause of nephrotic syndrome in children under 6
Glomerular capillary fuses with foot processes
Prognosis good in children, variable with adults
Describe membranous glomerulonephritis
Subepithelial deposition of immune complexes -> thickening of basement membrane
40% adult nephrotic syndrome
Treatment: immunosuppressants & treatment of underlying cause
Describe focal segmental glomerulosclerosis
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)
Describe management of nephrotic syndrome
1) Oedema – diuretics, salt & fluid restriction
2) ACEi – anti-proteinuric
3) Hypercholesterolaemia – atherogenic if long-term nephrotic
4) Treat underlying condition
Describe nephritic syndrome
Triad: haematuria, reduction in GFR & hypertension
Often some proteinuria but less than nephrotic syndrome
Onset may be acute or rapidly progressive
List common causes of nephritic syndrome
IgA nephropathy (Berger’s disease)
Rapidly progressive GN
Goodpasture’s
Post-streptococcal GN
Describe IgA nephropathy
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)
Describe rapidly progressive glomerulonephritis
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
Describe Goodpasture’s syndrome
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
Describe post-streptococcal glomerulonephritis
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
Describe the management of nephritic syndrome
1) Blood pressure control/reduction of proteinuria – ACEi, salt restrict
2) Treatment of oedema
3) Disease specific treatment
4) CVS risk management
5) Dialysis
What investigations do you do for a patient with suspected CKD?
Measure BP
Urine dipstick - look for protein
General - LFTs, U&Es
Ultrasound scan - look at kidney size
How do you treat acidosis in CKD?
Give oral NaHCO3 (sodium bicarbonate) tablets
Describe how CKD leads to bone mineral disease
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)
List symptoms of having accumulated waste products in CKD
Uraemic symptoms
Nausea and vomiting
Reduced appetite
Pruritus - constant itch
