CKD & renal failure Flashcards

1
Q

What are homeostatic functions of the kidney?

A
  • Electrolyte balance,
  • acid-base balance
  • volume homestasis
  • EPO production
  • 1-alpha hydroxylase for vitamin D
  • excretes nitrogenous waste, hormones, peptides, middle sizes molecules, salt & water.
  • Glucose metabolism: gluconeogenesis (filter/reabsorb glucose) & insulin clearance
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2
Q

What does kidney failure lead to and why?

A
  • Increased potassium & phosphate (not excreted),
  • decreased bicarbonate so low pH (metabolic acidosis),
  • salt & water imbalance
  • low EPO so anaemia
  • low calcium because low vitamin D, high PTH to compensate.
  • Increased waste products: urea, creatinine.
  • Insulin not cleared so insulin diabetics need less.
  • Increased CV risk
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3
Q

How might chronic and acute kidney failure present?

A
  • Chronic may present with abnormal blood results but feel ok because body adapted.
  • Acute may present worse (skin rash, haemoptysis etc)
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4
Q

In case of kidney failure why metabolic acidosis? How will the body react to compensate for this?

A
  • Less H+ ions excreted, less bicarbonate reabsorbed/produced so get metabolic acidosis.
  • To compensate hyperventilation to get rid of CO2 (decrease)
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5
Q

What happens to urea, creatinine, sodium, potassium and haemoglobin in kidney failure?

A
  • Urea, creatinine increase.
  • Sodium can increase or decrease.
  • Potassium increases.
  • Heamoglobin decreases
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6
Q

Why anaemia in kidney failure?

A

less EPO production

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7
Q

What can cause acute kidney failure? How can this present?

A

Eating wild mushrooms.

  • Can present with nausea/vomiting/reduced urinary output.
  • Waste products increased, sodium/potassium/hb stay kind of in range (because acute).
  • Acidosis so PCO2 decreases to compensate
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8
Q

What does kidney failure tend to do with salt and water?what does this elad to?

A

-Tend to get reduced secretion of salt & water (increased retention) leading to hypertension, oedema, pulmonary oedema.

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9
Q

When is salt and water loss seen?

A

In tubulointerstisial disorders (damage to concentrating mechanism)

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10
Q

Why do we get kidney failure acidosis and what can this cause?

A
  • Reduced excretion of H+ ions, less bicarbonate so metabolic acidosis.
  • Leads to anorexia & muscle catabolism.
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11
Q

Why do we get hyperkalaemia in kidney failure? What can cause this?

A

Decreased distal tube potassium secretion. acidosis

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12
Q

What are the symptoms associated with hyperkalaemia?

A

Cardiac arrhythmias, neural & muscular activity, vomiting to get rid of it

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13
Q

What are the ECG changes seen in hyperkalameia?

A

Broad P wave (reduced amplitude, disappears), peaked T wave, QRS widening, heart block, asystole, VT/VF (can lead to irregular heartbeat)

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14
Q

How does kidney failure cause hypocalcaemia? What is seen to compensate? What can this lead to?

A

Low vitamin D because of decreased 1-alpha hydroxylase activity, so leads to hypocalcaemia.
-to compensate hyperparathryoidism (inc PTH)

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15
Q

What does chronic renal failure do to phosphate?

A

Phosphate retention (hyperphosphataemia). Can cause itch

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16
Q

What do end-stage renal failure patients usually die from?

A

CV disease

17
Q

What causes CV risk?

A

Hypertension, diabetes, lipid abnormalities, inflammation, oxidative stress, mineral/bone metabolism disorders

18
Q

What is initial management for kidney failure? What do you do if they are hypovolaemic/hypervolaemic?

A
  • If hypovolaemic - give fluids.

- If hypervolaemic - diuretics/dialysis trial

19
Q

What do you do to fix the hyperkalaemia?

A
  1. To drive potassium into cell: sodium bicarbonate, insulin dextrose (caution).
  2. To drive out of body - diuretics/dialysis.
  3. To decrease gut absorption - potassium binders
20
Q

What to do for long term management of kidney failure?

A

EPO injections for anaemia, diuretics for salt/fluid overload, phosphate binders, 1,25 Vit D supplements, symptom management.

  • Home therapy: haemodialysis, peritoneal dialysis/assisted programmes.
  • In centre therapy: haemodialysis 4 hours 3x a week for transplantation
21
Q

What do you need to avoid in transplantable patients with kidney disease and why?

A

Transfusions.

Prevent sensitisation to prevent transplant failure

22
Q

What kidney size in chronic kidney failure? What kidney size in acute kidney failure?

A

Chronic - small kidneys.

Acute - normal sized kidneys

23
Q

What are traditional methods of assessing GFR and their disadvantages?

A
  1. urea: poor indicator confounded by diet, catabolic state, GI bleeding, drugs, liver function.
  2. creatinine: affected by muscle mass, age, race, sex.
  3. radionuclide studies - eg. EDTA clearance, reliable but expensive.
  4. creatinine clearance: hard for elderly to collect accurate sample, overestimates GFR at low GFR (small amount creatinine secreted into urine)
  5. insulin clearance: laborious, for research purposes only
24
Q

When cant we see a trend for creatinine?

A

CKD-EPI . when EGFR above 90 cant see trend

25
Q

What does NICE classification classify as kidney failure? What does it look at?

A

Looks at albumin creatinine ration ACR for proteinuria & GFR.
ACR <3 normal. 3-30 moderate increased. >30 very increased.
GFR >90 normal and high. <15 kidney failure