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Charis & Ellie vs Renal > Chronic Kidney Disease > Flashcards

Chronic Kidney Disease Flashcards

1
Q

What is CKD?

A

Chronic reduction in kidney function as a result of damage to the kidneys, their vessels or pathology in lower urinary tract

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2
Q

Clinical definition of CKD?

A

Reduction in GFR to <60mL/min for at least 3 months
OR
Persistent proteinuria/haematuria

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3
Q

Causes of CKD?

A
  • Diabetes
  • HT
  • Age-related decline
  • Glomerulonephritis
  • Polycystic kidney disease
  • Medications eg NSAIDs, PPI, Ciclosproin, lithium
  • SLE
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4
Q

Risk factors for CKD?

A
  • Older
  • HT
  • Diabetes
  • Smoking
  • Use of kidney affecting meds
  • Renal tract infections
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5
Q

Who gets CKD?

A
  • African-Carribean
    -South Asian
    (probably because of prevalence of HT/T2DM)
    -Acute kidney injury
    -Hereditary diseases
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6
Q

Presentation of CKD?

A

Asymptomatic usually diagnosed on routine screening

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7
Q

Signs which suggest CKD?

A
  • Pruritus
  • Loss of appetite
  • Nausea
  • Oedema
  • Muscle cramps
  • Peripheral neuropathy
  • Pallor
  • HT
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8
Q

Complications arising from CKD?

A
  • Anaemia
  • Renal bone disease
  • CVS
  • Peripheral neuropathy
  • Dialysis related problem
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9
Q

Investigation for CKD?

A
  • U&E blood test (Find eGFR)
  • Albumin: creatinine ratio to check for Proteinuria
  • Urinalysis dip stick: check for haematuria
  • Renal USS
  • Urine microscopy: WBC, RBC
  • Urine electrolytes
  • FBC
  • Biopsy if cause unclear
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10
Q

What is checked in a blood test for CKD?

A
  • Urea, creatinine, eGFR
  • Electrolytes
  • Calcium
  • Phosphate
  • PTH
  • FBC
  • Complement components
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11
Q

2 aspects of staging CKD?

A 
G score (based on eGFR)
A score (based on albumin: creatinine ratio)
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12
Q

What is G score?

A 
G1: eGFR= >90
G2: eGFR = 60-89 
G3A: eGFR = 45-59
G3b: eGFR = 30-44
G4: eGFR 15-29
G5: eGFR <15
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13
Q

What is G5 also known as?

A

End stage renal failrue

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14
Q

What is A score?

A

A1: <3mg/mmol
A2: 3-30mg/mmol
A3: >30mg/mmol

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15
Q

What must a patient have for a diagnosis of CKD?

A

eGFR of <60
OR
Proteinuria

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16
Q

NICE suggest to refer to a specialist when?

A
  • eGFR < 30
  • ACR > 70mg/mmol
  • ACR 30mg/mmol or more + haematuria
  • Accelerated progression defined as a decrease in eGFR of 15 or 25% or 15ml/min in 1 year
  • Uncontrolled HT despite 4 or more anti-HTs
  • rare/genetic causes of CKD suspected or suspected renal artery stenosis
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17
Q

Reducing risk of complications with CKD?

A
  • Exercise, diet, stop smoking, weight loss
  • Special dietary advice about Phosphate, sodium, potassium and water intake
  • Offer atorvastatin 20mg for primary prevention of CVD to people who have CKD
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18
Q

Treating complication: metabolic acidosis?

A

-Oral sodium bicarbonate

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19
Q

Treating complications: anaemia?

A
  • Iron supplementation

- Erythropoietin

20
Q

Treating complications: Renal bone disease?

A

Vit D

21
Q

Treating HT?

A 
1st line = ACEis 
However monitor serum K+
ONLY modify dose if 
- GFR decrease >25% 
or 
- serum creatinine increase>30% 
if less than these don't modify
22
Q

What do healthy kidney cells produce?

A

Erythropoietin

23
Q

What is erythropoietin?

A

Hormone which stimulates production of RBCs

24
Q

What can anaemia be treated with?

A

Erythropoiesis stimulating agents such as exogenous erythropoietin

25
Q

What is renal bone disease AKA?

A

Chronic kidney disease- Mineral and bone disorder (CKD MBD)

26
Q

Features of renal bone disease?

A
  • Osteomalacia
  • Osteoporosis
  • Osteosclerosis
27
Q

X-ray changes in renal bone disease?

A

Rigger jersey spine

  • Sclerosis of both ends of vertebra (denser white)
  • Osteomalacia in centre of vertebra (less white)
28
Q

Why does high serum phosphate happen in CKD?

A

Occurs due to reduced phosphate excretion

  • Low active Vit D occurs because kidney is essential in metabolising Vit D to active form
  • Vit D also regulates bone turnover
29
Q

What can be caused by CKD?

A
  • High serum phosphate
  • Secondary hyperparathyroidism
  • Osteomalacia
  • Osteosclerosis
  • Osteoporosis
30
Q

Why does secondary hyperparathyroidism happen in CKD?

A

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

  • This leads to increased osteoclast activity
  • Osteoclast activity leads to absorption of calcium from bone
31
Q

What can be used to treat osteoporosis?

A

Bisphosphonates

32
Q

what is the pattern of CKD?

A

frequently unrecognised
often co-exists with other conditions e.g. CVD, DM
moderate to severe CKD - increased risk of
- AKI
- falls
- fragility
- mortality
risk of developing CKD increases with age

33
Q

aim of CKD treatment?

A

prevent/delay progression
reduce/ prevent complications
reduce risk of CVD

34
Q

As people with AKI have an increased risk of CKD how should AKI patients be managed?

A

monitor people for development/ progression of CKD for 2-3 years after AKI even if serum Cr has returned to normal

35
Q

when should atorvastatin be increased in patient with CKD to prevent CVD?

A

increase dose if
- non-HDL cholesterol is not decreased by >40%
and
- eGFR is > 30ml/min/1.73m2 or more
higher doses need to be agreed with renal specialist if eGFR <30ml/min/1.73m2

36
Q

what is eGFRcystatinC used for?

A

at initial diagnosis - confirms/rules out CKD in people with eGFR creatinine 45-59 sustained for at least 90 days
no proteinuria (ACR <3mg/mol)/other marker of kidney disease
CKD if <60ml/min/1.73m2

37
Q

what are the possible conditions/possible pathogenesis that lead to CKD?

A 
diabetes mellitus 
hypertension 
glomerulonephritis 
- primary - membranous/IgA/FSGS 
- secondary - membranous/lupus/FSGS due to HIV/heroin/obesity 
vascular (macro and micro) 
- RAS
- ischaemic/hypertensive nephrosclerosis 
- microangiopathic - HUS/TTP
- SVV - GPA/MPA/EGPA
tubulointerstitial 
- acute interstitial nephritis 
- tubulointerstitial nephritis 
- ADPKD 
- Reflux nephropathy 
post-renal (obstructive) 
- calculi: renal/ureteric/bladder 
- prostatic: BPH, cancer 
- bladder: malignancy, bladder wall thickening 
- urethral stricture
38
Q

how does CKD present?

A 
anaemia - conjunctival and palmar pallor, fatigue, muscle weakness
signs of weight loss 
advanced uraemia 
uraemic symptoms 
- N&V
- anorexia 
- weight loss 
- fatigue 
- itch 
- altered taste
- restless legs 
- muscle twitching 
- difficulties concentrating 
- confusion 
pain 
- bony 
- neuropathic 
- ischaemic 
- visceral 
oedema 
- swelling 
- breathlessness
39
Q

what is accelerated progression of CKD?

A

sustained decrease in GFR of 25% or more and change in GFR category within 12 months
or
sustained decrease in GFR of 15ml/min/1.73m2/year

40
Q

risk factors for accelerated progression of CKD

A 
CVD
proteinuria 
AKI
hypertension 
diabetes 
smoking 
African, African-Caribbean, Asian 
chronic NSAID use 
untreated urinary outflow tract obstruction
41
Q

renal consequences of CKD

A

local - pain, stones, haemorrhage, infection
urinary - haematuria, proteinuria, nocturia, oliguria
impaired salt and water handling - pee at night, difficulty concentrating
hypertension
electrolyte abnormalites
acid-base disturbance
ESRD

42
Q

extra renal consequences of CKD

A

cardiovascular disease - 10-20 fold higher risk of death than general population for ESRD. It starts early: eGFR <50ml/min. The risk is increased with microalbuminuria
mineral and bone disease
anaemia - less common if eGFR >45, diabetics are more at risk

43
Q

how is the risk of CV disease managed?

A
  • smoking cessation
  • weight loss
  • aerobic exercise
  • limiting salt intake
    control of hypertension
    other prophylaxis
  • lipid-lowering therapy
  • consider aspirin for secondary prevention (bleeding :( )
44
Q

what causes the mineral and bone disease related to CKD?

A 
different adaptive changes in 
- calcium 
- phosphate 
- PTH
- Vitamin D 
- FG-23 
seriously compromised homeostatic mechanisms 
bone abnormalities and vascular calcification and laboratory abnormalities
45
Q

what are the consequences of the bone and mineral abnormalities associated with CKD?

A 
secondary/ tertiary HPT
vascular calcification 
bone pain 
fractures 
CV events 
lower QoL
higher morbidity and mortality
46
Q

how are bone and mineral abnormalities associated with CKD managed?

A 
phosphate restriction 
also consider 
- salt reduction 
- potassium restriction (if persistentily >5.5 mmol/L) 
- fluid restriction: 1-1.5L/day 
- dietary restrictions also - DM/coeliac disease 
correct metabolic acidosis: NaHCO3 can result in Na overload 
medications 
alfacalcidol - active vitamin D 
phosphate binders 
- calcium based 
- aluminium 
- non-calcium based 
calcimimetic = cinacalcet
47
Q

how is anaemia managed?

A

target Hb:100-12 g/L
- lower level acceptable if Hb fails to rise despite adequate iron replacement & epoetin therapy
investigation
- exclude other causes: B12/folate deficiency
- check ferritin & iron stores: ferritin >100, T Sats > 20%
- consider MDS/ other haematological causes
management
- ferinject - ferric carboxymaltose
- venofer - iron sucrose
- if oral fails - IV iron

Charis & Ellie vs Renal (40 decks)

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