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uro + renal med > 1B CKD and renal failure > Flashcards

1B CKD and renal failure Flashcards

1
Q

What homeostatic functions do the kidneys have?

A
  • Electrolyte balance
  • Acid-base balance
  • Volume homeostasis
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2
Q

What happens to homeostatic function in kidney disease?

A
  • Potassium increases
  • Phosphate increases
  • Bicarbonate decreases
  • pH decreases (metabolic acidosis)
  • Salt and water imbalance
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3
Q

What excretory functions do the kidneys have?

A
  • Nitrogenous waste
  • Hormones
  • Peptides
  • ‘Middle sized molecules’
  • Salt and water
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4
Q

What happens to excretory function in kidney disease?

A
  • Increase in urea
  • Increase in creatinine
  • Decrease in insulin requirement (due to low insulin clearance so more stays in system)
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5
Q

What endocrine functions do the kidneys have?

A
  • Erythropoietin
  • 1-alpha hydroxylase for vitamin D
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6
Q

What happens to endocrine functions in kidney disease?

A
  • Decrease in calcium
  • Anaemia
  • Increase in parathyroid hormone (to compensate for low calcium)
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7
Q

What glucose metabolism functions do the kidneys have?

A
  • Gluconeogenesis
  • Insulin clearance
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8
Q

In kidney disease, what is there an increased overall risk of?

A

Increase in cardiovascular risk

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9
Q

How does rate of deterioration affect clinical presentation?

A
  • If rate of deterioration is slow, body is very good at adapting
    • e.g. some patients present with urea of 50 (which for a normal person is really bad) but their body is used to it since it’s developed over years so they don’t feel unwell
  • Acute renal failure presents quicker because body hasn’t adapted
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10
Q

What acid-base problems can be seen in CKD?

A
  • pH lower
  • pCO2 lower
  • pO2 higher
  • HCO3- lower

Mild metabolic acidosis with respiratory compensation

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11
Q

How would end stage renal failure patients typically present?

A
  • Extreme lethargy
  • Weakness
  • Anorexia
  • Itching because of hyperphosphatemia
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12
Q

What are complications of CKD?

A
  • Elevated plasma urea and creatinine (renal failure)
  • Hyperkalaemia
  • Hyponatraemia
  • Metabolic acidosis
  • Anaemia
  • Shrunken kidneys
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13
Q

What are urea, creatinine, salts and Hb complications of AKI?

A
  • Urea higher
  • Creatinine higher
  • Sodium could be either- it’s normal here
  • Potassium higher
  • Haemoglobin normal (because it’s acute renal failure so there’s still some EPO around)
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14
Q

What are acid-base complications in AKI?

A
  • pH lower
  • pCO2 lower
  • pO2 higher
  • HCO3- lower

Mild metabolic acidosis with respiratory compensation

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15
Q

How does kidney failure affect salt and water balance?

A
  • Kidney failure tends to reduce secretion of salt and water leading to:
    • Hypertension
    • Oedema
    • Pulmonary oedema
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16
Q

In what kind of circumstances can salt and water loss be seen in kidney failure?

A
  • In tubulointerstitial disorders- damage to concentrating mechanism of urine
  • Seen right after kidney transplant- there’s a bit of damage to tubules and they pee out a lot of water
  • Seen also after kidney obstruction is relieved, kidney can’t concentrate urine and you get kidney failure
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17
Q

What may be a cause of AKI?

A

Hypovolemia

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18
Q

What does hyponatremia mean and what does it not mean?

A
  • It does not mean reduced total body sodium
  • It’s to do with how much free water you have- you’ll have more in hyponatremia
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19
Q

What has free water got to do with treatment of hyponatremia?

A

You may not want to give them salt but instead remove the excess free water

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20
Q

Describe how acidosis happens in renal failure

A
  • Reduced secretion of H+ ions which means you become acidotic
  • Cells take up this H+
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21
Q

What does acidosis do to K+?

A

The cells taking up the H+ also forces K+ out of the cells leading to hyperkalaemia

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22
Q

What are the two causes of hyperkalaemia?

A
  • Acidosis
  • Reduced distal tubule potassium secretion
23
Q

What are the symptoms of hyperkalaemia?

A
  • Cardiac arrhythmias
  • Neural and muscular activity
  • Vomiting
24
Q

What does symptom presentation of hyperkalaemia depend on?

A

Chronicity of the disease- if it’s acute hyperkalaemia then these symptoms show but if its chronic then body adapts and they don’t show

25
Q

What ECG changes come up in hyperkalaemia?

A
  • Peaked T waves
  • P waves broaden, have reduced amplitude and disappear
  • QRS widening
  • Heart block
  • Asystole
  • VT/VF (ventricular tachycardia/ventricular fibrillation)
26
Q

What health consequences does acidosis/hyperkalaemia have?

A
  • Anorexia
  • Muscle catabolism
27
Q

What effects does reduced EPO and reduced 1-25 Vit D levels have?

A
  • Reduced EPO → anaemia
  • Reduced 1-25 Vit D levels:
    • Reduced intestinal calcium absorption
    • Hypocalcaemia
    • Hyperparathyroidism
28
Q

How does chronic renal failure affect reduced EPO and 1-25 Vit D levels?

A
  • There’s also phosphate retention in chronic renal failure (phosphate usually excreted by kidneys)
  • This contributes to low levels of 1-25 vit D and hypocalcaemia and therefore hyperparathyroidism
29
Q

What is the major predictor of end stage renal failure?

A

CKD

30
Q

What is the major outcome for a patient with CKD?

A

CVD

This means a patient with CKD is more likely to die from CVD than end stage renal failure

31
Q

What standard cardiovascular risk is there for kidney failure patients?

A
  • Hypertension
  • Diabetes
  • Lipid abnormalities

Additional risks:

  • Inflammation
  • Oxidative stress
  • Mineral/bone metabolism disorder
32
Q

What are the 2 main things we want to treat in initial management of AKI?

A
  • Fluid balance
  • Hyperkalaemia
33
Q

How do we manage hypovolaemia vs hypervolaemia?

A

Hypovolaemia: give fluids
Hypervolaemia: trial of diuretics/dialysis

34
Q

What are the three ways we manage hyperkalaemia?

A
  • drive into cells
    • sodium bicarbonate
    • insulin dextrose
  • drive it out of body
    • diuretics/dialysis
  • reduce gut absorption
    • potassium binders
35
Q

How does sodium bicarbonate work?

A
  • Binds to H+ to push equation to the right
  • H+ come out of cell into blood to equalise this and K+ goes back into cell
36
Q

Why do we need to be careful with insulin dextrose?

A
  • There are fatalities associated with it due to hypoglycaemia
  • We only use it when potassium >6.5 or there are ECG changes
37
Q

What conservative long term management options are there for renal failure?

A
  • EPO injections to correct anaemia
  • 1,25 vit D supplements for hypocalcaemia
  • Diuretics to correct salt water overload
  • Phosphate binders- for hyperphosphataemia so reduces itching
  • Symptom managements e.g. nausea
38
Q

What home therapies are there for renal failure?

A
  • Haemodialysis
  • Peritoneal dialysis/assisted programmes
39
Q

What does in centre therapy include?

A
  • Haemodialysis, 4 hours 3 times a week
40
Q

What is important to keep in mind for managing patients in hospital with kidney disease in terms of taking blood from them?

A

Take it from the back of the hand and not anterior cubital fossa or cephalic vein at wrist level because we need it for the fistula and it can scar up (stenosis) and we can’t do the fistula

41
Q

If a patient is fit for transplantation, why do we need to avoid transfusions?

A

Transfusions sensitise patients to the antigens in the blood of the donor and then if they then get a kidney donation from someone else who shares similar antigens to the blood donor there’s increased risk of transplant failure

42
Q

What different methods are there for assessing kidney function?

A
  • Urea
  • Creatinine
  • Radionuclide studies
  • Creatinine clearance
  • Inulin clearance
  • GFR/eGFR
43
Q

Is urea a good indicator of assessing kidney function?

A

No because it’s confounded by diet, catabolic state, GI bleeding (bacterial breakdown of blood in gut), drugs, liver function etc

44
Q

Is creatinine a good indicator for kidney function?

A
  • It’s affected by muscle mass, age, race, sex etc
  • We need to therefore look at the patient when interpreting the result (if they’re small/big, M/F etc)
  • We look at the trend of creatinine (if we know what normal creatinine is) which is useful
45
Q

Are radionuclide studies good indicators?

A
  • EDTA clearance etc
  • Very reliable but expensive
  • Used for donors
46
Q

Is creatinine clearance a useful indicator for renal failure?

A
  • Difficult for elderly patients to collect an accurate 24 hour urine sample
  • Overestimates GFR at low GFR (as a small amount of creatinine is also secreted into urine)
47
Q

Is inulin clearance a useful indicator for renal failure?

A

Laborious so used for research purposes only

48
Q

What is the main factor in eGFR?

A

Serum creatinine

49
Q

These graphs show difference between actual GFR and eGFR. What does it show?

A

As kidneys get better and actual GFR goes up, the eGFR becomes less accurate

50
Q

Since eGFR becomes less accurate as GFR goes up, what do we do with people with normal/high eGFR in kidney disease patients then?

A

We look at creatinine trend e.g. someone could have increase in creatinine 30 → 60 but still have eGFR >90 so it won’t be picked up

51
Q

What do we use to classify CKD?

A
  • Proteinuria
  • ACR (albumin:creatinine ratio)
  • GFR

More protein means more risk of end stage renal failure

52
Q

What is the kidney failure risk equation?

A

Validated risk prediction tool for kidney replacement therapy in the next two or five years for adults with STABLE chronic kidney disease (CKD) Stages 3A to 5 . NOT to be used in patient with rapidly changing eGFR.

53
Q

What is KFRE calculated from?

A
  • Age
  • Sex
  • CKD-EPI eGFR
  • Urine albumin creatinine ratio (ACR)
54
Q

What is KFRE used for?

A
  • Patient understanding of their CKD diagnosis especially in the context of multi-morbidity
  • Identification of high risk CKD patients:
    • targeted patient engagement/education
    • aggressive risk factor management
    • referral to secondary care

uro + renal med (6 decks)

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