Complications of Chronic Renal Failure Flashcards

1
Q

What is target blood pressure for hypertensive patients?

A

140/90 - if above then unhappy

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2
Q

What is the kidney’s role with bicarbonate?

A
  • Carbonic anhydrase present at PCT
  • Within cell, H+ and HCO3- produced in a rxn catalysed by CA
  • The H+ is secreted into tubular fluid
  • Whereas HCO3- exits cell across basolateral membrane and returns to peritubular blood

Summary: carbonic anhydrase in brush border of PCT facilitates reabsorption of HCO3-, which is a buffer in acid-base balance.

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3
Q

What is the definition of chronic kidney disease?

A
  • Slow process (>3 months)
  • of inexorable attrition of nephron number and function
  • due to multiple aetiologies
  • resulting and frequently leading to end stage renal failure
  • low eGFR (<60) OR haematuria/proteinuria OR radiological abnormality
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4
Q

What complications arise in stage 1 CKD?

A

No complications

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5
Q

What complications arise in stage 2 and 3 CKD?

A
  • Stage 2 - increased CVD
  • Stage 3 - increased CVD; bone disease (raised PTH)
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6
Q

What additional complication arises in stage 4 CKD?

A

Anaemia

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7
Q

What additional complications arise in stage 5 of CKD?

A
  • Pruritus
  • Bleeding
  • Malnutrition

All on top of CVD, anaemia and bone disease

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8
Q

How does CKD result in anaemia?

A
  • EPO released by interstitial cells in kidney
  • EPO for haemoglobin production
  • Sensitive to oxygen
  • Lack of oxygen -> haemoglobin production goes up
  • Kidney disease -> cells don’t work v well -> don’t make EPO
  • Present with tiredness
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9
Q

Don’t jump to conclusion of renal anaemia due to impaired EPO. What are additional/other causes of anaemia in CKD that you must consider before giving EPO?

A
  • Iron deficiency
  • Hypothyroidism
  • Active blood loss
  • Hemoglobinopathies
  • Haemolysis
  • Hyperparathyroid
  • Folic acid deficiency
  • Vit B12 deficiency
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10
Q

Describe the pathway of management of anaemia in CKD?

A
  1. Exclude other causes (iron def, vit B12 def, blood loss etc)
  2. Give IV iron if ferritin <200
  3. EPO 30 ug/week
  4. Monitor Hb every 2 weeks
  5. Adjust EPO 25% increase
  6. Target Hb = 10.5-12.0g/dl
  7. Target ferritin 200-500 ng/ml
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11
Q

Why do we give IV ferritin (iron) instead of oral tablets?

A

Iron supplements at doses of 60 mg Fe as FeSO4 or higher increase hepcidin for up to 24 hours and are associated with lower iron absorption on the following day.

Hepcidin prevents iron absorption, no matter how much iron you give as a tablet it causes constipation and problems for patient. Bypassed by bolus injection of 500mg (a large dose) - build up immediately high.

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12
Q

Target Hb is 10.5-12.0 g/dl - Why do we keep it just under 12 and not over?

A

Increase over 12 g/dl of Hb is linked to more strokes less survival

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13
Q

What are the biochemical abnormalities in CKD in relation to bone disease?

A
  • Calcium (low)
  • Phosphate (high)
  • Vitamin D (low-normal)
  • PTH (high)

The plasma calcium is a v important thing for us, as balance between plasma and IC calcium causes triggering of brain/muscle/gut wall cells. So plasma calcium has to remain in a tight range.

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14
Q

How does abnormality of calcium come about?

A
  • Low vit D from kidneys (less hydroxylation)
  • Less absorption of calcium
  • Stimulation of PTH
  • Mobilisation of calcium from bone
  • Low normal serum calcium
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15
Q

Why can you not only work on the calcium levels to bring PTH down to normal?

A

As there is PO4 (phosphate) retention, which needs to be excreted by kidney but isn’t due to abnormal kidney function

Phosphate retention also stimulates PTH

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16
Q

What hormone rises with phosphate retention and what negative physiological effect does this exert?

A
  • Phosphate retention
  • -> increase in FGF-23 (which helps to reduce phosphate)
  • But FGF-23 is cardiotoxic
17
Q

How does PTH increase in relation to low calcium?

A
  • Calcium sensing receptor (CSR) on parathyroid glands
  • Parathyroid glands detect low calcium
  • Release PTH
18
Q

What are types of bone diseases in CKD?

A
  • Osteitis fibrosa: inc PTH
  • Osetomalacia: defective mineralisation
  • Osteoporosis: defective bone formation
  • Adynamic bone: low bone turnover

Osteomalacia and osteoporosis seen more often, osteitis fibrosa not seen v often.

Adynamic bone is a dreadful disease as shit prognosis

19
Q

What bone changes occur (signs/symptoms)?

A
  • Bone pain - backs, hips, legs
  • Joint pain
  • Fractures
  • Poor mobility
  • Children - growth retardation, deformities
20
Q

It’s not just the bone that suffers in bone disease, what changes happen in other tissues?

A
  • Periarticular calcification
  • Blood vessel wall calcification
  • Muscle weakness
  • Calciphylaxis
  • Calcification of the heart
21
Q

What are the types of vascular calcification in CKD?

A
  • Intimal calcification
  • Medial calcification
  • Valvular calcification
  • Calciphylaxis
22
Q

What is the management of bone disease in CKD 3/4? (Algorithm)

A
23
Q

What is the trend of cardiovascular events in CKD patients?

A

As GFR worsens (CKD progresses), the CVS events increase and are linked to greater mortality. Often, renal patients will not die of renal failure but from cardiovascular events (eg stroke, MI)

24
Q

Why is it important to watch weight of CKD patients?

A
  • By stage 4 malnutrition often comes around due to bloating, loss of appetite, nausea, vomiting, nutrient loss and protein catabolism
  • It’s important to monitor and maintain weight as lower muscle mass is linked to failure in dialysis
25
Q

Describe platelet and coagulation abnormalities in CKD

A
  • Platelet dysfunction + haemorrhage
    • inhibition of platelet adhesion
    • defective vWF receptor ligand
    • bleeding time is useful
  • Prothrombotic tendency
    • protein C/S functional deficiency
    • increased hymocysteine
    • inadequate tPA
26
Q

What are neurologic complications in CKD?

A
  • Uraemic encephalopathy
  • Autonomic neuropathy
  • Peripheral neuropathy