CKD Flashcards

1
Q

What is CKD?

A

A chronic reduction in kidney function that tends to be permanent and progressive.

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2
Q

What are the risk factors of CKD?

A
  • Older age
  • Hypertension
  • Diabetes
  • Smoking
  • Use of nephrotoxins
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3
Q

What are the causes of CKD?

A
  • Diabetic nephropathy
  • Hypertension
  • Age related decline
  • Glomerulonephritis
  • Polycystic kidney disease
  • Medications such as NSAIDS, ACEi, PPIs and lithium
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4
Q

How does CKD usually present?

A

Usually asymptomatic

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5
Q

What symptoms may CKD present with if not asymptomatic?

A
  • Pruritis
  • Lack of appetite
  • Nausea
  • Oedema
  • Peripheral neuropathy
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6
Q

What bedside test is important in CKD?

A

Urine dip

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7
Q

How is G score calculated?

A

Using eGFR

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8
Q

What gives a G score of 1?

A

eGFR 90+

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9
Q

What gives a G score of 2?

A

eGFR 60-89

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10
Q

What gives a G score of 3a?

A

eGFR 45-59

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11
Q

What gives a G score of 3b?

A

eGFR 30-44

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12
Q

What gives a G score of 4?

A

eGFR 15-29

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13
Q

What gives a G score of 5?

A

eGFR<15

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14
Q

What is G5 better known as?

A

End-stage renal failure

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15
Q

How is A score calculated?

A

Urine albumin:creatinine ratio (ACR)

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16
Q

What gives an A score of 1?

A

Albumin:creatinine ratio <3mg/mmol

17
Q

What gives an A score of 2?

A

Albumin:creatinine ratio 3-30mg/mmol

18
Q

What gives an A score of 3?

A

Albumin:creatinine ratio 30+mg/mmol

19
Q

What G score and eGFR is needed to diagnose CKD?

A

G3 (eGFR<60) or proteinuria

20
Q

What are the complications of CKD?

A

RC PAD

  • Renal bone disease
  • Cardiovascular disease
  • Peripheral neuropathy
  • Anaemia (lack of EPO)
  • Dialysis related problems
21
Q

When do NICE suggest a specialist referral?

A
  • eGFR<30
  • ACR 70+ mg/mmol
  • Decrease in eGFR of 15 or 25% in 1 year
  • HTN not controlled on 4 medications
22
Q

What are the aims of CKD management?

A
  • Slow disease progression
  • Reduce CVS risk
  • Prevent/treat complications
23
Q

How can disease progression be slowed?

A
  • Optimise diabetic control
  • Optimise hypertensive control
  • Treat glomerulonephritis
24
Q

How can complications be prevented?

A
  • Exercise/Healthy weight
  • Stop smoking
  • Special dietary advice about phosphate, sodium, potassium and water intake
  • Atorvastatin 20mg for primary prevention of cardiovascular disease
25
Q

How can a metabolic acidosis be treated?

A

Oral sodium bicarbonate

26
Q

How can anaemia be treated?

A
  • Iron supplementation

- EPO

27
Q

How can renal bone disease be treated?

A

Vitamin D

28
Q

How can end stage renal failure be treated?

A
  • Transplant

- Dialysis

29
Q

Describe the pathophysiology of anaemia of chronic renal disease.

A
  • CKD damages cells in the kidney
  • Fibroblasts cannot produce as much EPO
  • Less EPO so less RBCs produced
30
Q

Why should regular transfusion be avoided?

A

Regular transfusions sensitise the immune system, so transplanted organs are more likely to be affected

31
Q

What should always be offered before EPO?

A

Iron (IV or PO)

32
Q

What are the features of renal bone disease?

A
  • Osteomalacia (softened bones)
  • Osteoporosis (brittle bones)
  • Osteosclerosis (hardened bones)
33
Q

What will a spinal XR show in renal bone disease?

A

‘Rugger Jersey’

- Sclerosis of both ends of the vertebra (denser white) - - Osteomalacia in the centre of the vertebra (less white)

34
Q

Describe the pathophysiology of renal bone disease.

A
  • High serum phosphate due to reduced phosphate excretion
  • Low active vitamin D since the kidney metabolises it to its active form
  • Active vitamin D drives Ca2+ absorption in the intestines and kidneys
  • It also regulates bone turnover
35
Q

How does a secondary hyperparathyroidism occur in CKD?

A

Parathyroid glands react to the low calcium and high phosphate by excreting more PTH

36
Q

What does a secondary hyperparathyroidism cause?

A
  • High PTH increases osteoclasts
  • Calcium absorbed from bones
  • Decreased bone density (osteomalacia)
37
Q

How does osteosclerosis occur?

A
  • Osteoblasts increase activity to match osteoclasts

- Due to lack of calcium, this bone isn’t properly mineralised

38
Q

Summarise renal bone disease.

A
  • Low active VitD= low calcium and high phosphate
  • PTH increases to increase osteoclast activity
  • Osteoclasts cause osteomalacia
  • Osteoblasts increase activity, causing osteosclerosis
39
Q

How is renal bone disease treated?

A
  • Active forms of vitamin D (alfacalcidol and calcitriol)
  • Low phosphate diet
  • Bisphosphonates for osteoporosis