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Urinary > Chronic Kidney Disease > Flashcards

Chronic Kidney Disease Flashcards

1
Q

What is chronic kidney disease?

A

Permanent + progressive kidney damage - manifested by abnormal albumin excretion or decreased kidney function that persists for more than 3 months

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2
Q

Why is chronic kidney disease normally irreversible?

A

Renal tissue is replaced by extracellular matrix in response to damage

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3
Q

How is chronic kidney disease measured?

A

eGFR

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4
Q

Primary causes of chronic kidney disease

A

Directly affect kidneys
- Polycystic kidney disease
- Acute tubular necrosis
- Recurrent pyelonephritis (regular infections)
- Glomerulonephritis

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5
Q

Secondary causes of chronic kidney disease

A

Diabetes mellitus (diabetes nephropathy)
Hypertension
Renovascular disease
Autoimmune

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6
Q

Presentation of CKD

A
  • most are asymptomatic
  • oedema
  • foamy urine
  • pruritus
  • hypertension
  • loss of appetite
  • pallor (due to anaemia)
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7
Q

Investigations of CKD

A
  • eGFR
  • ACR
  • urinedipstick + microscopy
  • USS KUB
  • HbA1c
  • blood pressure
  • lipid profile
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8
Q

What investigations could you do to work out the cause of CKD?

A
  • urinalysis (protein/blood)
  • USS KUB
  • kidney biopsy
  • HbA1c - diabetes
  • ANCA - vasculitis
  • anti-GBM + ANA - lupus
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9
Q

How do you stage chronic kidney disease?

A

using eGFR
- stage 1: >90
- stage 2: 60-89
- stage 3a: 45-59
- stage 3b: 30-44
- stage 4: 15-29
- stage 5: <15 (kidney failure)

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10
Q

How do you stage chronic kidney disease using ACR?

A

Albumin-creatinine ratio
- stage 1: <3
- stage 2: 3-30
- stage 3: >30

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11
Q

Why are the kidneys smaller in kidney damage?

A

Loss of kidney tissue (cortex)

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12
Q

Management of CKD

A
  • treat underlying disease
  • treat complications e.g. EPO, dietary advice, vitamin replacement
  • ACEi/ARBs - hypertension + proteinurai
  • statin
  • weight loss advice + exercise
  • smoking cessation
  • plan for future - discuss options for if they reach ESRF (RRT)
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13
Q

How do we control blood pressure in chronic kidney disease?

A

Patients with CKD will almost always mean hypertension
- antihypertensives e.g. ACEi, angiotensin receptor blockers
- diuretics
- fluid restriction

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14
Q

Complications of chronic kidney disease

A
  • anaemia: EPO not produced by kidneys
  • fluid overload + oedema
  • metabolic acidosis
  • bone mineral disease: lack of active form of vit D > reduced calcium absorption
  • non-bone calcification
  • uraemia > uraemic pericarditis + encephalopathy
  • hyperphosphatemia + hypocalcaemia (secondary hyperparathyroidism)
  • hypertension
  • accelerated atherosclerosis | cardiovascular disease
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15
Q

Why is anaemia a complication of CKD?

A
  • decreased EPO produced by kidneys
  • decreased erythropoiesis
  • decreased RBC production
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16
Q

Treatment of anaemia in CKD

A

EPO injection
Iron supplements
Target Hb levels (10-12g/dL)

17
Q

Why is bone mineral disease a complication of CKD?

A
  • decreased active vitamin D
  • less calcium reabsorption > lower plasma [Ca2+]
  • hypocalcaemia
    .
  • decreased phosphate excretion
  • increased plasma [PO4]
  • hyperphospatemia
    .
  • stimulates parathyroid glands
  • hyperparathyroidhormone
  • increases parathyroid hormones
  • increases bone resorption (bone breakdown by osteoclasts)
  • bone mineral disease
18
Q

Management + treatment of bone mineral disease in those with ESRD

A
  • phosphate binders to control the amount of phosphate in blood
  • vitamin D supplements: suppresses PTH production + increases calcium absorption
  • calcimimetic agents: enhances sensitivity of parathyroid gland to calcium > reducing PTH secretion
  • regular monitoring of calcium, phosphate + PTH levels
19
Q

What is uraemia?

A

Raised levels of urea in blood

20
Q

Symptoms of ureamia

A
  • muscle cramps
  • itch
  • stroke
  • swelling
  • high BP
  • nausea + vomiting
  • anaemia
  • easy bleeding
  • constipation + diarrhoea
21
Q

What is end stage renal failure?

A

When death is likely without renal replacement therapy
eGFR <15

22
Q

When is renal replacement therapy needed?

A

When renal function declines to a level no longer adequate to support health
eGFR 8-10

23
Q

Types of renal replacement therapy

A

Haemodialysis
Peritoneal dialysis
Renal transplant

24
Q

Relationship between calcium and phosphate

A

Inversely proportional
If one goes up, the other goes down

25
Q

How does renal function affect calcium and phosphate levels?
What does this cause?

A
  • decreased active vitamin D
  • less calcium reabsorption > lower plasma [Ca2+]
  • hypocalcaemia
    .
  • decreased phosphate excretion
  • increased plasma [PO4]
  • hyperphospatemia
    .
  • stimulates parathyroid glands
  • hyperparathyroidhormone
  • increases parathyroid hormones
  • increases bone resorption
  • bone mineral disease
26
Q

Describe hyperfiltration in diabetes mellitus

A
  • blood is filtered
  • blood glucose remains elevated as the SGLT2 transporters are all occupied
  • sodium reabsorbed coupled with glucose
  • less Na+ delivered to macula densa
  • RAAS is activated
  • more Na+ absorbed > increased BP
  • afferent arteriole vasodilation
  • increased GFR > increased glomerular capillaries
27
Q

What do you want the normal systolic BP to be in a patient with a normal albumin:creatinine ratio compared to a patient with a high AC ratio?

A

Normal: <140
High: <130

28
Q

Why is uraemia a complication of CKD?

A

Damage to filtration > can’t excrete in urine properly

29
Q

Presentation of polycystic kidney disease

A
  • 30-40 years
  • hypertension
  • loin pain
  • haematuria
  • bilateral palpable kidneys
  • large kidneys with yellow fluid filled cysts
  • recurrent UTIs
30
Q

Inheritance of polycystic kidney disease

A

Autosomal dominant (more common)
Autosomal recessive

31
Q

How does polycystic kidney disease present with macroscopic haematuria?

A
  • cysts can form in childhood
  • cysts fill with blood following trauma
  • cysts burst > haematuria + abdominal pain
32
Q

What can polycystic disease cause?

A

Hypertension
CKD

33
Q

How does high levels of PTH cause bone resorption?

A

Activation of oestoclasts causes increased bone breakdown

34
Q

Extra renal manifestations of autosomal dominant polycystic kidney disease

A
  • mitral regurgitation
  • cerebral aneurysms
  • colonic diverticula
  • hepatic, splenic, pancreatic, ovarian + prostatic cysts
35
Q

When is autosomal recessive polycystic kidney disease often noticed?

A

On antenatal scans with oligohydramnios

36
Q

Management of polycystic kidney disease

A
  • antihypertensives
  • analgesia
  • antibiotics
  • drainage by aspiration or surgery
  • dialysis or renal transplant for end stage renal failure
  • avoid contact sports to reduce risk of rupture
  • avoid NSAIDs + anticoagulants
  • MR angiography to screen for cerebral aneurysms
37
Q

What drug can be used in management of autosomal dominant polycystic kidney disease + why?

A

tolvaptan - vasopressin receptor antagonist
- slows development of cysts + progression of renal failure

38
Q

What should people with polycystic kidney disease avoid?

A
  • contact sports due to risk of rupture
  • NSAIDs
  • anticoagulants

Urinary (24 decks)

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