Chronic Kidney Disease Flashcards

(42 cards)

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
  • bone 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
  • blood pressure
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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
  • offer statin to reduce CVD risk
  • 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

Iron supplements
EPO injection
Target Hb levels (10-12g/dL)
.
check iron levels before starting EPO

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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
  • reduce dietary phosphate first line
  • phosphate binders to control the amount of phosphate in blood
  • vitamin D supplements: suppresses PTH production + increases calcium absorption e.g. calcitriol
  • 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
How does renal function affect calcium and phosphate levels? What does this cause?
- 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
Describe hyperfiltration in diabetes mellitus
- 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
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?
Normal: <140 High: <130
28
Why is uraemia a complication of CKD?
Damage to filtration > can’t excrete in urine properly
29
Presentation of polycystic kidney disease
- 30-40 years - hypertension - loin pain - haematuria - bilateral palpable kidneys - large kidneys with yellow fluid filled cysts - recurrent UTIs
30
Inheritance of polycystic kidney disease
Autosomal dominant (more common) Autosomal recessive
31
How does polycystic kidney disease present with macroscopic haematuria?
- cysts can form in childhood - cysts fill with blood following trauma - cysts burst > haematuria + abdominal pain
32
What can polycystic disease cause?
Hypertension CKD
33
How does high levels of PTH cause bone resorption?
Activation of oestoclasts causes increased bone breakdown
34
Extra renal manifestations of autosomal dominant polycystic kidney disease
- mitral regurgitation - cerebral aneurysms - colonic diverticula - hepatic, splenic, pancreatic, ovarian + prostatic cysts
35
When is autosomal recessive polycystic kidney disease often noticed?
On antenatal scans with oligohydramnios
36
Management of polycystic kidney disease
- 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
What drug can be used in management of autosomal dominant polycystic kidney disease + why?
**tolvaptan** - vasopressin receptor antagonist - slows development of cysts + progression of renal failure
38
What should people with polycystic kidney disease avoid?
- contact sports due to risk of rupture - NSAIDs - anticoagulants
39
Follow ups for CKD
- frequency of monitoring depends on the stage of disease + individual risk factors for progression - measure GFR + ACR - FBC - bone profile
40
What type of parathyroidism can CKD cause?
**Secondary hyperparathyroidism** Due to low calcium, high phosphate + low vitamin D Parathyroid gland produces PTH
41
Management of proteinuria in CKD
ACE inhibitors SGLT-2 inhibitors
42
What will USS KUB show in CKD?
Bilateral small kidneys