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3/ REN > Chronic Kidney Disease > Flashcards

Chronic Kidney Disease Flashcards

1
Q

What are the 3 general functions of the kidney?

A

homeostasis
metabolic/endocrine
excretion of drugs and drug metabolites

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2
Q

What are the metabolic/endocrine functions of the kidneys?

A

Vitamin D
EPO
RAAS

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3
Q

What are the homeostatic functions of the kidneys?

A 
elimination of waste
water volume
electrolytes
acid-base
blood pressure
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4
Q

How is kidney function measured?

A

traditionally via serum creatinine

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5
Q

What is serum creatinine influenced by?

Is it sensitive to small changes in function?

A

sex, ethnicity, age, body mass, diet, exercise

No

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6
Q

What is eGFR?

A

calculated from creatine, age, sex, ethnicity,
better reflection of kidney function
best measure for use in stable renal function

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7
Q

What is the definition of chronic kidney disease (CKD)?

A

irreveserrible and progress kidney disease

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8
Q

What are the stages of CKD, defined by eGFR?

A 
Stage 1 >90
Stage 2 >60
Stage 3 >25
Stage 4 >15
Stage 5 <15
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9
Q

What is the prognosis of Stage 5 CKD without treatments?

What are the treatments?

A

Insufficient renal function to sustain life/health
–> death
haemodialysis, peritoneal dialysis, kidney transplantation

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10
Q

What patients are likely to have CKD?

A

diabetes, hypertension, multiple drugs especially NSAIDs, elderly
- other causes are genetic e.g. polycystic kidney disease or rare e.g. vasculitis or both

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11
Q

How is CKD related to socio-economic status?

A

mean GFR decreases with increased deprivation

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12
Q

What are the risk factors associated with CKD?

A

age, hypertension, diabetes, smoking and poor education

black and into-asian populations

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13
Q

What are the 6 classifications of CKD causes?

A
  1. systemic diseases - diabetes, hypertension
  2. immune mediated diseases - membranous nephropathy, igA nephropathy
  3. infectious diseases - HIV, HBV, HCV, TB
  4. genetic diseases - polycystic kidneys, cystinosis
  5. arterial diseases - atherosclerosis
  6. obstruction - tumours, stones, fibrosis
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14
Q

What are the histological signs of CKD?

A

chronic glomerulorephritis

sclerosed glomeruli, atrophied tubules, replaced by scar tissue

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15
Q

What is the pathology of diabetic nephropathy?

A
  • thickening of basement membrane
  • mesangial expansion: hyperglycaemia stimulates increased metric production by mesangial cells, stimulation of TGF-b release
  • glomerulosclerosis: due to intraglomerular hypertension or ischaemic damage
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16
Q

What are 9 complications of chronic kidney disease?

A 
anaemia
hypertension
disturbed calcium/phosphate homeostasis
cardiovascular disease
bone disease
abnormal handling of drugs
immune suppression
bleeding tendency
complications of treatment
17
Q

What are the two aspects to failure of fluid homeostasis and what does this lead to?

A 
Inability to concentrate urine
- loss of diurnal rhythm of urine excretion
- osmotic diuresis of surviving glomeruli
- limited rate of water excretion 
Inability to excrete water load
- dilution hyponatraemia
- oedema 
- hypertension
18
Q

What is the treatment for fluid overload?

A

diuretics
salt restriction
fluid restriction

dialysis
transplantation

19
Q

How is sodium affected and what are the consequences of this?

A
  • loss of nephrons reduces ability to excrete salt and water
  • major cause of hypertension and fluid overload
  • sodium must be within normal range for normal neurological function
  • high or low sodium levels leads to confusion, fits and coma (CNS dysfunction)
20
Q

How is potassium affected and what are the consequences of this?

A
  • enormous functional reserve to excrete potassium
  • severe hyperkalaemia when GFR <10ml/min
    Due to:
  • excessive load
  • interference with potassium excretion
  • acidosis with volume contraction
  • diabetic nephropathy
21
Q

What are the consequences of hyperkalaemia?

How does the ECG trace change?

A
  • alterations in membrane excitability
  • cardiac arrhythmias
    ECG changes
  • tall T waves
  • long QRS interval
  • long PR interval
  • cardiac arrest
22
Q

What is the treatment to prevent hyperkalaemia and hypernatraemia?

A

salt restricition
potassium restriction

dialysis
tranplant

23
Q

What are the symptoms of metabolic acidosis?

A 
increased respiratory drive --> SOB
chest pain
confusion
bone pain
demineralisation of bone
24
Q

What is the treatment for metabolic acidosis?

A

sodium bicarbonate

dialysis/transplant

25
Q

What 3 hormones are produced in the kidney and what are they responsible for?

A

vitamin D - calcium metabolism
erythropoietin - RBC production
renin - blood pressure control

26
Q

When is PTH released?

What are its effects?

A

Low Ca2+
PTH release
activates Vit D in kidneys
increases bone resorption

27
Q

What classical cases are there for hyperparathyroidism and hyperphosphataemia?

A

brown tumours
rugger jersey spine
both due to demineralisation of bone

28
Q

What is ectopic calcification?

A

calcium deposits in soft tissue due to high PTH levels in kidney disease

29
Q

What treatment prevents bone disease and ectopic calcification?

A

active Vit D replacement
phosphate restriction
phosphate binders
calcimimetics

parathyroidectomy

30
Q

What is the impact of renal anaemia?

A 
impaired quality of life
- reduced exercise capacity
- impaired cognition
transfusion requirement
- iron overload 
- blood-borne infection
risk of left ventricular hypertrophy
increased CV disease in patients with CKD and anaemia vs those with CKD without anaemia
31
Q

What is the treatment more renal anaemia?

A

recombinant EPO

32
Q

What are the mechanisms for renal hypertension?

A 
sodium retention
volume expansion
RAS activation
sympathetic NS activity
endothelial dysfunction
33
Q

What are the consequences of hypertension?

A

accelerates decline of kidney function

contributes to cardiovascular risk (stroke, MI, heart failure)

34
Q

What is the treatment for hypertension in CKD?

A

salt restriction
diuretics
RAS blockade
other antihypertensives

35
Q

What are the consequences of failure in excretory function?

A

accumulation of toxic waste products

  • creatinine rises only after significant renal damage
  • retention of nitrogenous waste
  • retention of urate
  • retention of phosphate
36
Q

What is the treatment for uraemia?

A

dialysis or transplantation

why not protein restriction? –> malnutrition

37
Q

What are the consequences of the accumulation of the following?

  1. insulin
  2. opiates
  3. antibiotics
  4. sedatives
  5. digoxin
A
  1. hypoglycaemia
  2. confusion/narcosis
  3. affect brain function, encephalopathy
  4. respiratory arrests
  5. cardiac glycoside used to treat AF –> causes arrythmias
38
Q

What is the treatment to prevent drug toxicity?

A

modify prescription

change drug type/dose

39
Q

What are the major modifiable risk factors in CKD?

A

uncontrolled underlying disease
hypertension
proteinuria
smoking

3/ REN (19 decks)

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