Loss of kidney function

Question 1

What happens when the kidneys stop working?

Answer 1

• Loss of excretory function:
  Accumulation of waste products
• Loss of homeostatic function:
  Disturbance of electrolyte balance
  Loss of acid-base control
  Inability to control volume homeostasis
• Loss of endocrine function:
  Loss of erythropoietin production
  Failure of 1 alpha-hydroxylase vitamin D
• Abnormality of glucose homeostasis:
  Decreased gluconeogenesis

Question 2

What are the clinical features from kidney damage determined by?

Answer 2

Rate of deterioration
A slow loss of kidney function may present asymptomatically whereas an acute loss of kidney function could be disastrous (acute kidney injury vs chronic kidney disease)

Question 3

What is reflex nephropathy?

Answer 3

= faulty ureter-bladder valves, so back flow of urine

Question 4

What are the symptoms of kidney damage?

Answer 4

• extreme lethargy
• weakness
• anorexia
• severe hypotension due to volume depletion
• elevated plasma urea and creatinine (diagnostic of renal failure)
• hyperkalaemia
• hyponatremia
• metabolic acidosis
• anaemia

Question 5

What causes the symptoms of lethargy and anorexia?

Answer 5

• Accumulation of waste products
• Acidosis
• Hyponatraemia
• Volume depletion
• Anaemia – decreased erythropoietin
• Chronic neurological damage (maybe by peripheral neuropathy)

Question 6

What causes the symptoms of salt and water imbalance?

Answer 6

• Normally, patients with renal dysfunction have difficulty excreting sodium (and thus retain water)
• Therefore they get hypertension and (pulmonary) oedema
• Sometimes, in patients with tubulointerstitial disorders (this is a more specific renal failure - inner medulla), too much sodium is excreted and thus water

Question 7

What are the implications of acidosis on the patient?

Answer 7

Caused by decreased excretion of H+ ions

• A buffering occurs as H+ passes into cells in exchange for K+ ions -> aggravating hyperkalaemia
• The partially compensated metabolic acidosis tends to make patients tachypnoeic to increase CO2 loss through the lungs – known as Kussmahl respiration OR ‘air hunger’
• The acidosis can exacerbate anorexia and increases muscle catabolism – for the protein buffer mechanism.

Question 8

What are the implications of hyperkalaemia?

Answer 8

• Caused by the failure of the DCT to secrete potassium (and thus retains it)
• Exacerbated by acidosis – causes shift of potassium from intracellular to extracellular (to correct acidosis)
• High blood potassium can cause cardiac arrhythmias (initial loss of p waves and bradycardia -> arrest)
• Can also cause neural and muscular activity
• Clinical features of the effects of hyperkalaemia are dependant on the chronicity (the state of being chronic)

Question 9

Describe the progression of hyperkalaemia into cardiac arrest on an ECG

Answer 9

T-wave peaks -> P-wave disappears -> bradycardia -> broadening of QRS complex -> ARREST

Question 10

Describe some disruptions in metabolic functions of the kidney

Answer 10

• Decreased erythropoietin production -> anaemia
• Low 1, 25-Dihydroxycholecalciferol (1,25-Vitamin D3) -> poor intestinal calcium absorption:
  Hypocalcaemia – Short term
  Hyperparathyroidism – Long term
  Phosphate is retained in CRF and it binds calcium

This all results in an increased CARDIOVASCULAR risk (as low EC calcium)

Question 11

What is a major outcome for a person with chronic kidney disease and why?

Answer 11

Cardiovascular disease; you have the potential to get hypertension, secondary cardiac effects (arrhythmias), endothelial effects, lipid abnormalities etc

Question 12

What causes hyperparathyroidism in CRF?

Answer 12

phosphate retention and low levels of calcitriol lead to hypocalcemia -> hyperparathyroidism

Question 13

How to differentiate between CKD and AKD?

Answer 13

It’s difficult to tell the difference clinically between the two (similar symptoms).
However, certain aspects can be looked out:
- CKD shows shrunken kidneys.
- AKD has a previously normal creatinine level whereas in CKD, creatinine has always been abnormally high

Question 14

How can GFR be assessed via traditional methods?

Answer 14

• urea
• creatinine
• creatinine clearance
• inulin clearance
• radionuclide studies

Question 15

Why is urea a bad indicator of GFR?

Answer 15

Poor indicator – confounded by diet, catabolic state, GI bleeding (bacterial breakdown of blood in gut), drugs, liver function, etc.

Question 16

Why is creatinine a bad indicator of GFR if not used in context of the patient?

Answer 16

Creatinine levels vary fro person to person naturally as it’s affected by; muscle mass, age, race, sex, etc even through people have the same GFR

Question 17

What is normal GFR?

Answer 17

120ml/min

Question 18

Why is creatinine clearance a poor indicator of GFR?

Answer 18

Difficult for the elderly to collect an accurate sample logistically.

24hr urine collection

Overestimates GFR at low GFRs as a small amount of creatinine is secreted into the urine.

Question 19

Why is inulin clearance not used anymore?

Answer 19

Laborious - involves endogenous injections and catheterisation

Question 20

Why is a radionuclide study not used?

Answer 20

reliable but expensive

Question 21

What is the modern method of assessing GFR?

Answer 21

Equation used:

creatinine while taking into account the context of the patient.

Question 22

When does MDRD become unreliable?

Answer 22

Once GFR > 60ml/min.

In very obese or very thin patients.

Question 23

How do NICE guidelines categorise CKD patients?

Answer 23

Based on GFR and their ACR (urine albumin: urine creatinine ratio)