CKD Flashcards

1
Q

Causes of CKD [5]

A
  • Diabetic nephropathy (20%)
  • GN: usually IgA nephropathy (but also mesangiocapillary GN, SLE or vasculitis)
  • Hypertensive nephropathy or renovascular disease
  • Pyelonephritis and reflux nephropathy
  • Adult polycystic kidney disease
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2
Q

Causes of CKD

Name 2 rare causes

A

Obstructive uropathy

Chronic interstitial nephritis 2* to MM, amyloidosis

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3
Q

Pathogenesis [4]

A
  1. Renal injury causes the kidney to adapt to nephron loss by increasing intraglomeular pressure with glomerular hypertrophy to maintain filtration.
  2. The glomerulus becomes more permeable to macromolecules such as proinflammatory markers>
  3. Mesangial cell expansion, fibrosis and glomerular scarring.
  4. All forms of CKD are also associated with:
    - tubulointerstitial disease
    - a reduction in blood supply
    - lymphocytic and inflammatory mediator infiltration > interstitial fibrosis and tubular atrophy
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4
Q

The CKD syndrome - associated conditions [5]

A
Anaemia
Renal osteodystrophy
Cardiovascular risk
Hyperlipidemia
Malnutrition
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5
Q

Explain why anaemia occurs in CKD

Explain why renal osteodystrophy occurs [4]

A

Anaemia: decreased erythropoietin production by kidney interstitial fibroblasts [1] leads to lack of RBC growth and differentiation in bone marrow [1]

Renal osteodystrophy:

  • kidney is the primary site of phosphate excretion and 1-alpha-hydroxylation of vitamin D
  • Reduced levels of 1,25 dihydroxyvitamin D occurs due to renal scarring and reduced phosphate excretion leads to hyperphosphatemia.
  • This causes hypocalcaemia which parathyroid gland responds to by producing secondary hyperparathyroidism.
  • This promotes calcium resorption causing changes to bony architecture (pre-dialysis have a high turnover and post-dialysis have a low turnover)
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6
Q

Explain why hyperlipidemia occurs in CKD [2]

Explain why cardiovascular risk increases in CKD [5]

A

Hyperlipidaemia: reduced lipoprotein lipase and hepatic triglyceride lipase [1] means less uptake of lipids by the liver and more in circulation [1]

Cardiovascular risk: due to hypertension, hyperlipidaemia, hyperphosphatemia, calcium-ion phosphate product and PTH

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7
Q

Explain why malnutrition occurs in CKD

A

altered metabolism of protein, water, salt and potassium

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8
Q

How does CKD usually present? [4]

A
  1. Asymptomatic until CKD Stage 4, 5
  2. Uraemia: anorexia, vomiting, restless legs, fatigue, weakness, pruritus, bone pain
  3. Impotence
  4. Amenorrhea
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9
Q
What signs will CKD show in the:
Periphery [4]
Face [4]
Neck [2]
Abdomen [3]
A
  • Periphery: HTN, AV fistula (thrill, bruit, recently needled?), signs of previous transplant (bruising (steroids), skin malignancy (immunosuppression)
  • Face: pallor (anaemia), yellow tinge (uraemia), gum hypertrophy (ciclosporin), cushingoid appearance (steroids)
  • Neck: tunnel line (current or previous small scar over IJV and larger scar in breast pocket area from exit site), parathyroidectomy scar
  • Abdomen: PD scar (small midline scar just below umbilicus and small round exit site scar to side of midline), previous transplant (hockey stick scar, ballotable mass), ballotable polycystic kidneys
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10
Q

Investigations
Bloods [5]
Urine [3]
Imaging [3]

A

Bloods

  • FBC normochromic, normocytic anaemia
  • U&E, Cr low
  • Glucose DM
  • Bone profile: hypocalcemia, hyperphosphatemia, elevated PTH
  • Elevated ALP in osteodystrophy

Urine

  • Urinalysis proteinuria, hematuria
  • C&S exclude recurrent UTI
  • Urine albumin: Cr ratio

Imaging

  • Renal ultrasound showing bilateral enlargement in APKD, DM, MM
  • MAG3 renogram showing asymmetrical kidney size

Renal biopsy

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11
Q

Renal biopsy
What will you see if its rapidly progressive disease? [2]
Complications

A

Rapidly progressive disease will show normal sized kidneys with unclear cause
Complications: bleeding, pain

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12
Q

What are 3 modalities of management

A
  1. Identify and treat reversible causes
  2. Limit and prevent complications
  3. Symptom control
  4. RRT
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13
Q

What are the 4 components to limitation of CKD complication

A

Limit and prevent complications:

  • BP
  • Renal bone disease
  • CVD risk
  • Diet
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14
Q

Symptom control in CKD mx

Anaemia [4]

A

Anaemia

  • monitor RBC, replace Fe, folate, B12
  • Dardepoetin if anaemia is unresponsive
  • Haem referral if suspect red cell aplasia due to anti-EPO ab
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15
Q

When would you suspect red cell aplasia in CKD patient? [3]

Side effects of dardepoeitin [4]

A

if Hb continues to fall and no infection, haemolysis or blood loss

SE (dardepoietin):

  • Accelerated HTN > encephalopathy, seizures
  • Bone aches
  • Flu-like sx, rash, urticaria
  • Increased risk of thrombosis
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16
Q

Symptom control in CKD mx:
Acidosis management [3]
Edema management [3]

A

Monitor bicarbonate; SODIUM BICARBONATE supplements if low

  • slows CKD progression and improves symptoms
  • but CAUTION in HTN as sodium loading can worsen HTN

Edema

  • High dose furosemide (morning)
  • +/- metolazone
  • Fluid and Na restriction
17
Q

Symptom control in CKD mx:
Cramps [2]
Restless legs [2]

A

o Cramps: check ferritin (may exacerbate symptoms if low); QUININE SULFATE at night
o Restless legs: CLONAZEPAM or GABAPENTIN