Chronic Kidney Disease Flashcards
(28 cards)
Define CKD?
Reduced GFR and/or evidence of kidney damage
This MUST be chronic, i.e: CKD cannot be diagnosed on the basis of 1 measurement
Methods of measuring GFR?
Can be measure in nuclear medicine (impractical, time-consuming and expensive)
Estimation by creatinine clearance
24 hour urine collection (often inaccurate)
Disadvantage of estimating GFR by creatinine clearance (most common method)?
Over-estimates GFR as creatinine (5%) is secreted by the tubules
How is eGFR estimated?
Using: • Serum creatinine • Age • Sex • Race
What is creatinine?
Product of muscle breakdown, i.e: muscular people produce more creatinine
E.g: women are less muscular than males, black males more muscular than white/Asian males
When is eGFR accurate?
For most people if it is <60 ml/min
Problems with eGFR measurement?
However, it:
• Over-estimates GFR is muscle mass is low
• Under-estimates if muscle mass is high
• Only valid if the serum creatinine is stable, i.e: not useful in acute kidney injury
Stages of CKD?
Stage 1 - GFR >90 ml/min WITH evidence of kidney damage
Stage 2 - GFR 60-90 ml/min WITH evidence of kidney damage
The above cannot be diagnosed on the basis of GFR alone, i.e: GFR of 80 ml/min without kidney damage is not stage 2 CKD
Stage 3 - GFR 30-60 ml/min:
• 3A - 45-60 ml/min
• 3B - 30-44 ml/min
Stage 4 - GFR 15-30 ml/min
Stage 5 - GFR <15 ml/min OR if on renal replacement therapy
Progression of early CKD?
Some people will progress to advanced CKD, which increased CV risk
Patients with proteinuria are more likely to progress and more proteinuria correlates to a faster progression
Younger patients have longer to progress, i.e: they are more likely to reach stage 5
Normal decline in GFR with age?
Normally, there is a slow decline in GFR >40 years
Common causes of CKD?
Diabetes (most common reason for dialysis)
Hypertension
Vascular disease (reduces blood flow and causes ischaemic of the kidneys)
Chronic glomerulonpehritis
Reflux nephropathy - damage begins in childhood due to incompetent valves and urine reflux leading to scarring
Polycystic kidneys
Idiopathic - many patient present late with small, scarred kidneys
Symptoms of reduced GFR?
Do not occur until late (GFR <20 ml/min)
Non-specific symptoms are common: • Tiredness • Poor appetite • Itch • Sleep disturbance
Impaired urine conc. ability (symptoms may occur earlier):
• Nocturia
4 principles of managing CKD?
- Slow progression
- Reducing CV risk
- Identify and treat complications of CKD
- Prepare for renal replacement therapy
Methods of slowing progression of CKD?
ACEIs and ARBs reduce BP and proteinuria:
• Proteinuria is assoc. with progression so reducing this slows progression
• Control BP
There is some evidence for spironolactone
Good glycaemic control in diabetics
Smoking cessation
Cautions with ACEIs and ARBs?
Reduced BP results in less pressure at the glomerulus so there is an initial fall in GFR; with renal artery stenosis, there may be a sharp fall in GFR and drugs should be stopped
Hyperkalaemia is a risk
Methods of reducing CV risk in CKD?
BP and proteinuria
Smoking cessation
Statins
Complications of CKD?
Anaemia - erythropoietin (Epo) production decreases; there may be other causes for the anaemia, e.g: Fe deficiency
Bone disease - impaired vit D hydroxylation in the kidneys results in reduced Ca absorption, leading to secondary hyperparathyroidism; in advanced CKD, serum phosphate rises and this also increases PTH secretion
Ix for anaemia in CKD?
Check Fe status and, if deficient, they may need further Ix; also check for vit B12 and folate deficiency
Treatment of anaemia in CKD?
Use IV Fe; if still anaemia, Epo may be indicated (administer via injection every week/fortnight)
Target Hb: 105 - 125 g/l
As Epo works, the Fe stores become depleted so regular top-ups are required
Describe secondary hyperparathyroidism
Can maintain normal serum Ca at the expense of the bones; result is hyperplasia of all the glands and 1 gland may autonomously produce PTH (not suppressed by Ca) and this is tertiary hyperparathyroidism
This can lead to hypercalcaemia
Presentation of bone disease in CKD?
Severe bone disease, with pain and radiological changes, is uncommon
However, high phosphate and high Ca can cause vascular calcification (stiff vessels) and heart valve calcification
Management of bone disease in CKD?
Alfacalcidol (hydroxylated vit D that does not require activation by the kidneys)
Phosphate (dietitian advice)
Phosphate binders (prescribed to most patients on dialysis)
What are phosphate binders?
E.g: calcium carbonate, calcium acetate and sevelamer
Bind to phosphate in the gut to reduce absorption
Treatment options for established (AKA end stage) renal failure, i.e: renal replacement therapy?
Haemodialysis
Peritoneal dialysis
Transplantation
Conservative management
