Lecture 14- Chronic Kidney disease and cardiovascular risk Flashcards

1
Q

4 main functions of the kidneys

A

excretory function
homeostatic function
endocrine function
metabolic function

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2
Q

what is CKD?

A

gradual loss of kidney function over time (months/years) related to disease/disorder/damage to kidneys (irreversible)

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3
Q

what is acute kidney injury?

A

sudden episode of kidney injury which occurs over hours/days (potentially reversible)

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4
Q

CKD defined as?

A
  • lost more than half of kidney function (GFR) with or w/o evidence of kidney damage OR
  • normal/abnormal GFR but have evidence of kidney damage e.g. proteinuria
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5
Q

what is the measure for kidney function?

A

GFR

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6
Q

stages 1 and 2 of CKD

A

kidney damage with normal kidney function

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7
Q

stages 3 and 4 of CKD

A

reduced kidney function (moderate and severe)

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8
Q

what stage causes the most problem? higher prevalence?

A

stage 3

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9
Q

stage 5 CKD

A

kidney failure

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10
Q

implications for kidney function at age 80

A

CKD is a disease of ageing

  • therefore kidney function usually declines as you get older
  • if no other factors for kidney damage present, then not CKD
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11
Q

people at risk of CKD

A

> 60
family history
have DM, high BP, established CVD
overweight, smoker, indigenous

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12
Q

2 most common causes of CKD

A

-diabetic nephropathy

renovascular -disease/hypertensive nephrosclerosis

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13
Q

3 less common causes of CKD

A
  • reflux nephropathy- congenital problems (reflex of urine from bladder into kidney, scarring/fibrosis in kidney)
  • glomerulonephritis - intrinsic kidney disease
  • genetic renal disorders (PCKD)
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14
Q

3 tests for detection of CKD

A

BP
dipstick for proteinuria- early marker of kidney disease even when normal kidney function
eGFR

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15
Q

why is it important to do all 3 tests?

A

to maximise likelihood of CKD detection as there is variable overlap of indicators of kidney damage

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16
Q

is CKD asymptomatic?

A

yes- only start to feel non-specific symptoms (tired, unwell, itchy etc) when kidney function is 10-15%

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17
Q

how to manage aspects of CKD to slow deterioration in kidney function?

A

detect people earlier than symptomatic stage, can effectively intervene
-BP control, certain medication, reduce proteinuria will reduce natural progression of disease

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18
Q

ESKD

A

end stage kidney disease

19
Q

generalisation about patients on dialysis in terms of cardiovascular conditions and general population

A
  • earlier age on dialysis, risk of dying from cardiovascular condition is same as someone in their 70s/80s
  • dialysis patients- 200-300x increase of CVD compared to general population
  • 50% of people on dialysis will die from CVD
  • vast majority of people in stage 3 CKD on dialysis die along the way from CVD- which is why they dont progress to next stages
  • patients with CKD are 20 times more likely to die from CV event than survive to reach dialysis
20
Q

kidney and heart disease…

A

very intimately related

21
Q

risk of ESKD related to baseline proteinuria

A

proteinuria= prognostic marker

  • leak protein, more likely to wear kidneys out during the track
  • reduce leaking, reduce wearing out
22
Q

albuminuria and GFR

A

itself a risk factor

- albuminuria and reduced GFR predict morbidity and mortality

23
Q

BP and ESKD

A

target BP

  • salts in western diets lead to BP
  • lower BP, lower kidney wearing out rate
24
Q

traditional CV risk factors in kidney disease

A

HT, DM, lipid status, physical inactivity,

25
Q

cholesterol and dialysis for general population

A

people with high cholesterol will do bad compared to doing good on dialysis

26
Q

cholesterol and dialysis for those on dialysis

A

do better with high cholesterol (Eat better, dialysis needs more protein intake)

  • low cholesterol- malnutrition
  • tried to use statins to reduce cholesterol, makes no difference
27
Q

reverse epidemiology relevant for?

A

cholesterol, obesity, hypertension
e.g. overweight people and higher BP people do better on dialysis
= confounding factors
- therefore traditional CVD risk factors not the whole answer for why people have burden of CVD in kidney disease

28
Q

non-traditional CV risk factors in kidney disease

A
hyperphosphatemia
Ca x P
PTH
inflammation
uremic retention solutes 
anaemia
29
Q

mechanisms of Ca/PO4 disturbance

A
  1. phosphate retention- with reduced GFR results in increased serum phosphate and suppresses vitD production
  2. reduced vitamin D- leads to reduced calcium absorption; this plus high serum phosphate–>low serum calcium
  3. PTH- stimulated by low calcium, high phosphate and low vitD
30
Q

enzyme hydroxylase

A

produced by kidney

converts inactive vitD to active vitD

31
Q

development of hyperparathyroidism

A

low calcium due to phosphate retention and vitD deficiency

32
Q

Ca/PO4 disturbance causes

A
bone disease
soft tissue calcification
pruritus 
proximal myopathy
premature death
33
Q

when do patients develop Ca/PO4 disturbances?

A

in CKD stages 3-5

34
Q

CKD-MBD and CVD

A

bone disease people more likely to have CVD

- minerals not going into bone (building up in vessel wall)

35
Q

vascular calcification

A
  • clinical consequence of hyperphosphatemia in CKD
    build up of calcium form bone in blood vessels–>makes it stiff
  • blood vessels in endothelial layer disrupts function of kidney–>contributing to arterial stiffness
36
Q

two types of vascular calcification

A

intimal- measure of atherosclerotic load within intimal layer
medial- stiffness- more related to bone and mineral abnormalities
-doesnt lead to occlusive atherosclerotic problems
- have increased arteriosclerosis (vascular stiffness–>LVH–>sudden death)

37
Q

pathogenesis of vascular calcification

A

active process
we have promoters and inhibitors of vascular calcification
- normally so many inhibitors that we dont calcify
- on dialysis and kidney disease- more promoters- therefore pro calcific state

38
Q

FGF-23 (fibroblast growth factor 23)

A
  • phosphotonin, produced by bone
  • maintains phosphate homeostasis, binds to FGF receptor
  • acts on vitD to reduce its levels (people become vitD deficient, low levels of phosphate absorption as well)
  • kidney disease- have greater levels of FGF-23, even more in dialysis
  • higher levels- increase mortality
39
Q

2 pathways for intestinal phosphate absorption

A
  • paracellular pathway- passive diffusion down an electrochemical potential gradient (important following a meal, when intraluminal conc is high)
  • transcellular Na dependent carrier-mediated pathway- under control of active vitD and other regulatory signals
40
Q

phosphate and CVD

A

poor outcomes in CVD with high rates of phosphate

41
Q

organic vs inorganic phosphate and implication

A

organic- incompletely hydrolysed and absorbed (phytin, casein)
inorganic- readily hydrolysed and absorbed (food additives)
implication- phosphate burden from food additives disproportionately high relative to their dietary content and relative to protein-based phosphate

42
Q

phosphate levels in CKD

A

dont seem to increase until you get to CKD3

- until then, levels are normal

43
Q

phosphate and CVD in general population

A

high normal phosphate compared to ‘normal normal’ or ‘low normal’ are at increased risk of CVD and mortality

44
Q

key CKD management tasks

A
  • lifestyle- healthy diet, exercise, no smoking, weight control
  • reduce CV risk
  • BP at target
  • reduce proteinuria (with ACE or ARB)
  • optimise calcium/phosphate