Case 2 - CKD Flashcards

(45 cards)

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
Treatment of diabetic nephropathy
* ACEi/ARB - reduce proteinuria * Anti-hypertensives for BP control * CV risk modification * Continue screens for microvascular complications eg eye and foot checks
26
What is hypertensive nephropathy?
* Chronic raised BP causes nephrosclerosis * Difficult to tell at advanced presentation whether HTN caused renal problems or the other way around
27
Investigations to identify primary or secondary HTN
* 24hr metanephrines (Phaechromocytoma) * Aldosterone:renin ratio (primary aldosteronism) * Cortisol and dexamethasone supression test (Cushing syndrome) * TSH (hyperthyroidism) * MRA (renal artery stenosis)
28
Treatment for hypertensive nephropathy
Anti-hypertensives
29
What is polycystic kidney disease?
Autosomal dominant condition resulting in cysts within kidney which can rupture and/or become infected
30
Two types of PCKD
* Type 1 - PDK1 mutation on chromosome 16 (85%) * Type 2 - PDK2 mutation on chromosome 4 (15%)
31
Symptoms of PCKD
Related to size/infection of cysts eg * Flank pain * Haematuria * Fever * Or can be asymptomatic
32
Diagnosis for PCKD
USS Family history is KEY
33
Treatment for PCKD
* Control BP * Tolvaptan (vasopressin receptor 2 antagonist) available if slow progression of CKD * Genetic counselling and testing
34
2 common complications of CKD
* Anaemia of chronic disease * Mineral bone disease
35
What factors contribute to cause anaemia of chronic disease in CKD?
* 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
Managment of anaemia of CKD
* 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
How can CKD mineral bone disease be diagnosed - criteria?
* Abnormalities of calcium, phosphate, alkaline phosphatase, PTH or Vit D metabolism * Vascular +/- soft tissue calcification * Abnormal bone turnover, metabolism, volume, linear growth/strength
38
Low turnover bone states in CKD
* Adynamic bone disease * Osteomalacia - low Vit D usually
39
High bone turnover states CKD
Osteitis Fibrosa - usually due to high PTH
40
What does CKD lead to in terms of causing mineral bone disease?
* Increased fibroblast GF23 * Increased alkaline phosphatase and PTH * Increased phosphate * Decreased serum calcium * Decreased 1,25 Vitamin D
41
What is tertiary hyperparathyroidism?
PTH is released despite raised Ca2+ levels (independently) As a result of PT gland nodular hyperplasia Consequence of advanced CKD
42
Management of CKD mineral bone disease
* Reduce occurance and or severity of bone disease * Reduce CV morbidity and mortality caused by elevated PTH and high phosphate and calcium overload
43
Signs of CKD
* 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
Tests to confirm cause of CKD
* 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?
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