CKD Flashcards

0
Q

What range does a normal GFR have?

A

~ 90-120ml/min (in 1.73m person)

note: using 100ml/min allows % values to be used

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1
Q

What are some of the signs and symptoms of chronic kidney disease?

A

Slow, progressive renal impairment: no symptoms until GFR falls below 30ml/min

Dialysis required at 8-10ml/min

  • tiredness & lethargy
  • breathlessness
  • nausea & vomiting
  • aches and pains
  • sleep reversal
  • nocturia
  • restless legs
  • itching
  • chest pains
  • seizures & coma
  • pale
  • pruritis
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2
Q

Define chronic kidney disease.

A

Irreversible and sometimes progressive loss of renal function over a period of months to years

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3
Q

What are some of the causes of CKD?

A

COMMON:

  • vascular
  • systemic disease e.g. diabetes, myeloma
  • idiopathic (most common in those who require dialysis)
  • immunological e.g. glomerulonephritis
  • polycystic kidney disease
  • obstruction reflux nephropathy
  • hypertension
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4
Q

What are some of the histological features of CKD?

A

Atrophy of cortex

Shrunken kidney

Irregular outline

Kidney scarring

note: renal injury causes renal tissue to be replaced by fibrin

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5
Q

How can CKD be classified?

A

GFR (ml/min/1.73m^2):
G1 = >90ml/min (therefore it is possible to have kidney disease but have a normal GFR)
G2-G4 = decreased GFR relative to young adult level
G5 = kidney failure

ACR (albumin:creatinine) (mg/mmol):
A1-A3 = increased ACR relative to young adult level

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6
Q

What proportion of the population have CKD?

A

~12% have CKD G1-G3

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7
Q

Outline the prognosis of CKD.

A
  • associated with substantial cardiovascular morbidity & mortality (often before requiring dialysis)
  • some patients inevitably lose renal function despite treatment
  • greatly shortened life expectancy with renal failure (renal transplant > dialysis)
  • at ~75% GFR renal function decline accelerates
  • dialysis required at ~2%-10% GFR
  • proteinuria indicates worse prognosis/increased risk of CVD
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8
Q

What are some of the problems in measuring GFR?

A

Serum creatinine = ~80-120umol/l

INACCURATE - GFR can decline to 60% before [creatinine]serum is abnormal

eGFR (applies modifiers for age, sex, race)

  • only accurate in adults
  • not useful in AKI, intermittent illness, haemodynamic problems (as eGFR relies on the GFR being stable)
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9
Q

How can the cause of CKD be assessed?

A

Blood e.g. autoantibody screen, complement, Ig, ANCA, CRP, etc. (if glomerulonephritis is suspected)

Imaging - ultrasound (size, ?hydronephrosis), CT, MRI (structural abnormalities)

Angiography (?renal artery stenosis)

Renal biopsy (if kidneys are normal size & cause of CKD is not obvious)

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10
Q

What is polycystic kidney disease?

A

Can be autosomal dominant or recessive

Multiple cysts develop on the kidney, eventually replacing normal kidney tissue

Do not develop kidney failure until ~50-60yrs

note: one or two cysts on kidneys normal and usually harmless

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11
Q

What are some of the complications of CKD?

A

Acidosis = affects muscle, bone, renal function (treat with NaHCO3 tablets)

Anaemia due to:

  • reduced EPO production
  • resistance to EPO (uraemic environment)
  • reduced RBC survival (releases urea -> uraemic environment)
  • blood loss (reduced platelet function)

Bone disorders due to reduced GFR:

  • reduces active vit. D (kidney cannot hydroxylate) —> osteomalacia
  • increases phosphate (reduced excretion) —> reduces calcium (maintenance of calcium phosphate product)
  • reduced calcium & reduced active vit. D —> increases PTH —> osteitis fibrosa cystica

+ abnormal bone turnover, mineralisation, volume, linear growth, and strength of bones (renal osteodystrophy)
+ bone cysts, erosion to terminal phalanges, sclerosis of end plates (“rugger jersey spine”)
+ vascular/soft tissue calcification e.g. aorta, extra-articular, calciphylaxis (calcification of vessels & skin necrosis)

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12
Q

What are some considerations which need to be made in giving drugs to CKD patients?

A

Dose alteration required due to reduced metabolism/elimination

Drug sensitivity can be increased even if elimination is unaffected ——–> side-effects more likely

e.g. statins (even though they are metabolised by the liver)

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13
Q

How is CKD treated?

A
  • lifestyle (to reduce CVD risk) e.g. stop smoking, lose weight, exercise
  • treat diabetes if present (to reduce CVD risk)
  • treat hypertension if present (to reduce CVD risk)
  • ACE inhibitors/angiotensin receptor blockers in proteinuria (reduces CVD risk, reduces proteinuria, slows renal function decline)
  • renal therapy (dialysis/transplant) = indicated when eGFR <8-10ml/min
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14
Q

When is dialysis indicated?

A

eGFR =< 8-10ml/min

  • uraemic symptoms e.g. reduced appetite, nausea/vomiting, pruritis
  • acidosis —> bone disease/muscle wasting
  • pericarditis
  • fluid overload
  • hyperkalaemia
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15
Q

What is the definition of end stage renal failure?

A

Death is likely without renal replacement therapy

eGFR =< 15ml/min

16
Q

How does CKD effect the kidney’s ability to modify the water and salt concentration in the blood?

A

Reduced GFR —> lose ability to maximally dilute/concentrate urine

Small glomerular filtrate (28.8l/day) with same solute load —> osmotic diuresis —-> nocturia (reduced response to ADH, reduced concentrating ability)

Low volume of filtrate reduces maximum excretion (so maximum volume of urine is reduced)