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Renal YR3 > Case 2 - CKD > Flashcards

Case 2 - CKD Flashcards

1
Q

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Define CKD

A
  • Presence of kidney damage
  • Abnormal albumin excretion or decreased kidney function
  • Quantified or measured by eGFR that persists for more than three months
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2
Q

How is CKD staged?

A

eGFR with associated albumin (ACR) score

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3
Q

eGFR CKD stage G1

A
  • eGFR 90 or more but signs of kidney damage
  • Normal and high
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4
Q

eGFR stage G2

A
  • 60-89 with markers of kidney damage
  • Mild reduction related to normal range for young adult
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5
Q

eGFR stage G3a

A
  • 45-59
  • Mild-moderate reduction
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6
Q

eGFR stage 3b

A
  • 30-44
  • Moderate to severe reduction
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7
Q

eGFR stage 4

A
  • 15-29
  • Severe reduction
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8
Q

eGFR stage 5

A
  • eGFR <15
  • Kidney failure
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9
Q

ACR score A1

A
  • Less than 3 mg/mmol
  • Normal to mildly increased
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10
Q

ACR score A2

A
  • 3-30mg/mmol
  • Moderately increased
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11
Q

ACR score A3

A
  • More than 30mg/mmol
  • Severely increased
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12
Q

Causes of CKD

A
  • Diabetes
  • HTN
  • Glomerulonephritis
  • Renovascular disease
  • PCKD
  • Obstructive nephropathy - urological problems
  • Chronic/recurrent pyelonephritis
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13
Q

Complications of CKD

A
  • Anaemia of chronic disease
  • CKD mineral and bone disease
  • Secondary and tertiary hyperparathyroidism
  • HTN
  • Cardiovascular disease - no1 cause of death
  • Malnutrition/sarcopenia
  • Dyslipidaemia
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14
Q

Complications of CKD as it progressess

A
  • Electrolyte distubances
  • Fluid overload
  • Metabolic acidosis
  • Uraemic pericarditis
  • Uraemic encephalopathy
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15
Q

Who is involved in renal management?

A

MDT eg renal physicians, GPs, renal specialist nurse, dieticians, pharmacists, vascular surgeons

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16
Q

Management of CKD - general

A
  • Treat underlying disease
  • Reduce CV risk
  • Reduce progression of CKD
  • Prevent complications
  • Plan for future - RRT?
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17
Q

How do we treat underlying disease in CKD?

A
  • Treat and monitor diabetic control
  • Treat HTN
  • Treat infections promptly
  • Tolvaptan if meeds criteria for PCKD
  • Immunosupression for glomerulonephritis if needed
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18
Q

How do we reduce CV risk to patients with CKD?

A
  • Statin
  • BP control -<130/80
  • Improve diabetes control
  • Weight loss
  • Exercise
  • Stop smoking
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19
Q

How do we reduce progression of CKD

A
  • Reduce proteinuria - ACEi/ARBs
  • Monitor bloods
  • Control BP
20
Q

How do we prevent/treat complications in management of CKD?

A
  • Dietary advice re low phosphate and low K+ diet
  • Phosphate binders
  • IV iron/folate/Vit B12 replacement
  • EPO
  • Replace Vitamin D deficiency
  • Calcimimetics for tertiery hyperparathyroidism
  • Dietician help
21
Q

What do we discuss in plan for future for management of CKD?

A
  • Options if reach end stage renal failure
  • Home care team input
  • Discuss advantages and disadvantages of types of RRT

Depending on choice:
* Fistula referal - venous mapping?
* Refer for PD tube insertion?
* Work up for transplant? - tests and transplant clinic

22
Q

Which diabetes causes diabetic nephropathy?

A

Type 1 DM or long duration of Type 2

23
Q

What is diabetic nephropathy often associated with?

A

Other microvascular diabetes complications eg
* Retinopathy
* Peripheral neuropathy

24
Q

How is diabetic nephropathy often diagnosed?

A
  • Screening for it if have diabetes
  • Raised urine albumin:creatinine ratio/PCR raised
  • Evidence of long standing/poorly controlled DM
  • Evidence of other microvascular disease
25
Q

Treatment of diabetic nephropathy

A
  • ACEi/ARB - reduce proteinuria
  • Anti-hypertensives for BP control
  • CV risk modification
  • Continue screens for microvascular complications eg eye and foot checks
26
Q

What is hypertensive nephropathy?

A
  • Chronic raised BP causes nephrosclerosis
  • Difficult to tell at advanced presentation whether HTN caused renal problems or the other way around
27
Q

Investigations to identify primary or secondary HTN

A
  • 24hr metanephrines (Phaechromocytoma)
  • Aldosterone:renin ratio (primary aldosteronism)
  • Cortisol and dexamethasone supression test (Cushing syndrome)
  • TSH (hyperthyroidism)
  • MRA (renal artery stenosis)
28
Q

Treatment for hypertensive nephropathy

A

Anti-hypertensives

29
Q

What is polycystic kidney disease?

A

Autosomal dominant condition resulting in cysts within kidney which can rupture and/or become infected

30
Q

Two types of PCKD

A
  • Type 1 - PDK1 mutation on chromosome 16 (85%)
  • Type 2 - PDK2 mutation on chromosome 4 (15%)
31
Q

Symptoms of PCKD

A

Related to size/infection of cysts eg
* Flank pain
* Haematuria
* Fever
* Or can be asymptomatic

32
Q

Diagnosis for PCKD

A

USS
Family history is KEY

33
Q

Treatment for PCKD

A
  • Control BP
  • Tolvaptan (vasopressin receptor 2 antagonist) available if slow progression of CKD
  • Genetic counselling and testing
34
Q

2 common complications of CKD

A
  • Anaemia of chronic disease
  • Mineral bone disease
35
Q

What factors contribute to cause anaemia of chronic disease in CKD?

A
  • Decreased EPO production
  • Absolute iron deficiency - poor absorption/malnutrition
  • Functional iron deficiency - inflammation/infection
  • Blood loss
  • Shortened RBC survival
  • Bone marrow supression - uraemia
  • Medication induced
  • VitB12/folate deficiency
36
Q

Managment of anaemia of CKD

A
  • Measure haematinics - Vitamin B12, folate, folate, ferritin, iron, transferrin saturation, CHr
  • If deficient - replace first
  • IV iron may be better tolerated than PO
  • Discuss with renal team re starting ESA (erythropoesis stimulating agent)
  • Aim for Hb 100-120
37
Q

How can CKD mineral bone disease be diagnosed - criteria?

A
  • Abnormalities of calcium, phosphate, alkaline phosphatase, PTH or Vit D metabolism
  • Vascular +/- soft tissue calcification
  • Abnormal bone turnover, metabolism, volume, linear growth/strength
38
Q

Low turnover bone states in CKD

A
  • Adynamic bone disease
  • Osteomalacia - low Vit D usually
39
Q

High bone turnover states CKD

A

Osteitis Fibrosa - usually due to high PTH

40
Q

What does CKD lead to in terms of causing mineral bone disease?

A
  • Increased fibroblast GF23
  • Increased alkaline phosphatase and PTH
  • Increased phosphate
  • Decreased serum calcium
  • Decreased 1,25 Vitamin D
41
Q

What is tertiary hyperparathyroidism?

A

PTH is released despite raised Ca2+ levels (independently)
As a result of PT gland nodular hyperplasia
Consequence of advanced CKD

42
Q

Management of CKD mineral bone disease

A
  • Reduce occurance and or severity of bone disease
  • Reduce CV morbidity and mortality caused by elevated PTH and high phosphate and calcium overload
43
Q

Signs of CKD

A
  • Jaundice
  • Raised JVP
  • Pallor
  • Excoriation of pruiritis
  • Bruising
  • AV fistula for dialysis
  • Brown line pigmentation of nails
  • Central venous catheter for dialysis access
  • Scar of kidney transplant
  • Tenckoff catheter for peritoneal dialysis
  • Crackles lung bases - pulmonary oedema
44
Q

Tests to confirm cause of CKD

A
  • Urine ACR
  • Urine dipstick - haematuria
  • BP
  • Serum HbA1C
  • Renal USS - PCKD? Obstruction?
  • Renal angiogram - renal artery stenosis?
  • Autoimmune screen - ANA/anti-dsDNA, C3, C4 (SLE), anti-GBM (goodpastures) ANCA (vasculitis)
  • CV disease - echo? lipids?
45
Q
A

Renal YR3 (11 decks)

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