Chronic Kidney Disease Flashcards

1
Q

Define CKD?

A

Reduced GFR and/or evidence of kidney damage

This MUST be chronic, i.e: CKD cannot be diagnosed on the basis of 1 measurement

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2
Q

Methods of measuring GFR?

A

Can be measure in nuclear medicine (impractical, time-consuming and expensive)

Estimation by creatinine clearance

24 hour urine collection (often inaccurate)

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3
Q

Disadvantage of estimating GFR by creatinine clearance (most common method)?

A

Over-estimates GFR as creatinine (5%) is secreted by the tubules

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4
Q

How is eGFR estimated?

A
Using:
• Serum creatinine
• Age
• Sex
• Race
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5
Q

What is creatinine?

A

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

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6
Q

When is eGFR accurate?

A

For most people if it is <60 ml/min

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7
Q

Problems with eGFR measurement?

A

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

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8
Q

Stages of CKD?

A

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

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9
Q

Progression of early CKD?

A

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

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10
Q

Normal decline in GFR with age?

A

Normally, there is a slow decline in GFR >40 years

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11
Q

Common causes of CKD?

A

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

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12
Q

Symptoms of reduced GFR?

A

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

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13
Q

4 principles of managing CKD?

A
  1. Slow progression
  2. Reducing CV risk
  3. Identify and treat complications of CKD
  4. Prepare for renal replacement therapy
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14
Q

Methods of slowing progression of CKD?

A

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

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15
Q

Cautions with ACEIs and ARBs?

A

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

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16
Q

Methods of reducing CV risk in CKD?

A

BP and proteinuria

Smoking cessation

Statins

17
Q

Complications of CKD?

A

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

18
Q

Ix for anaemia in CKD?

A

Check Fe status and, if deficient, they may need further Ix; also check for vit B12 and folate deficiency

19
Q

Treatment of anaemia in CKD?

A

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

20
Q

Describe secondary hyperparathyroidism

A

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

21
Q

Presentation of bone disease in CKD?

A

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

22
Q

Management of bone disease in CKD?

A

Alfacalcidol (hydroxylated vit D that does not require activation by the kidneys)

Phosphate (dietitian advice)

Phosphate binders (prescribed to most patients on dialysis)

23
Q

What are phosphate binders?

A

E.g: calcium carbonate, calcium acetate and sevelamer

Bind to phosphate in the gut to reduce absorption

24
Q

Treatment options for established (AKA end stage) renal failure, i.e: renal replacement therapy?

A

Haemodialysis

Peritoneal dialysis

Transplantation

Conservative management

25
Q

When should preparation for dialysis commence?

A

When GFR ~20 ml/min (earlier if they have fast progression)

If patient opts for haemdialysis, vascular access via an arteriovenous (AV) fistula is the best form of access

If patient opts for peritoneal dialysis. operation is required to insert the catheter (can be used after 1-2 weeks)

26
Q

When should AV fistulas be made?

A

Require 6 weeks to mature after formation so refer to vascular surgeons when GFR ~15 ml/min

27
Q

Transplantation options for patients?

A

They are placed on the cadaveric transplatation list when they are within 6 months of dialysis; they require careful assessment to ensure they are “fit enough”

Identify potential live donors

28
Q

Conservative management of established (AKA end-stage) renal failure?

A

Chosen by many older patients with multiple co-morbidities; they can choose not to have dialysis

Other care is still provided, i.e: Epo and symptom control