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PM4B > Chronic Kidney Disease (CKD) > Flashcards

Chronic Kidney Disease (CKD) Flashcards

1
Q

Define chronic kidney disease (CKD)

A

Abnormalities in the kidney structure or function, present for > 3 months with implications for health

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2
Q

Give markers for chronic kidney disease (one or more) and has to be present for 3 months?

A
  1. Albuminuria
  2. Urine sediment abnormalities
  3. Electrolyte and other abnormalities due to tubular disorders
  4. Abnormalities detected by histology
  5. Structural abnormalities detected by imaging
  6. History of kidney transplantation
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3
Q

Describe stage 1 CKD (GFR, description) and how to treat it

A

GFR: 90+

Normal kidney function
Urine or other abnormalities point to kidney disease

Treatment:
observation and controlling blood pressure

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4
Q

Describe stage 2 CKD (GFR, description) and how to treat it

A

GFR: 60-89

Mildly reduced kidney function, urine and other abnormalities that point to kidney disease

Treatment:
Blood pressure control
Monitoring 
Estimating progression
Do not need to degrade most drug
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5
Q

Describe stage 3 CKD (GFR, description) and how to treat it

A

GFR: 30-59

Moderately reduced kidney function

Treatment:
Evaluating and treating complications

Happens as a result of age

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6
Q

Describe stage 4 CKD (GFR, description) and how to treat it

A

GFR: 15-29

Severely reduced kidney function

Treatment:
Preparation for renal replacement therapy (RRT)
A lot of drug doses need to be reviewed and the preparation stage requires dialysis- do not want to cause AKI alongside CKD

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7
Q

Describe stage 5 CKD (GFR, description) and how to treat it

A

GFR: <15

Very severe, or end stage kidney failure sometimes called established renal failure

Treatment:
Replacement (if uraemia) is present

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8
Q

Why is it important to report eGFR in these cases

A

Tells you severity of kidney disease stage

Facilitates early diagnosis and treatment of kidney disease to:
Improve prognosis
Reduce mortality
Save money

Powerful predictor:
CVD risk
Progressive CKD

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9
Q

Describe CKD epidemiology

A

Increased prevalence of CKD in UK

Ageing Population: AKI leads to CKD

Increasing rates of:
Diabetes, hypertension, obesity

Higher prevalence in some ethnicities
South asian- higher prevalence in type 2 diabetes
African Caribbean- higher prevalence hypertension

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10
Q

What are the risk factors of CKD

A

Diabetes

Hypertension

AKI

Cardiovascular disease

Structural renal tract disease, renal calculi, prostatic hypertrophy

Autoimmune diseases with potential kidney involvement (SLE vasculitis)

Hereditary kidney disease e.g. polycystic kidney disease

Nephrotoxic drugs- calcineurin inhibitors, lithium, NSAIDs

Kidney stones

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11
Q

Describe the progression of CKD and how to monitor and control it?

A
  1. Doesn’t progress in many people
2. Interventions that slow CKD progression: 
Glycemic control (diabetes)
Blood pressure control:
Target <140/90mmHg in CKD
Target <130/80mmHg in CKD with diabetes
  1. Reducing proteinuria- albumin in urine
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12
Q

Describe hyperkalaemia in relation to CKD (usual levels and treatment)

A

Usual serum potassium 3.5-5.0mmol/L

Patient with CKD (or AKI) less able to excrete potassium and can develop hyperkalaemia

Serum potassium >6.5mmol/L is severe and requires urgent treatment:
- Calcium gluconate 10% bolus over 5 mins- doesn’t remove potassium but stabilises heart and prevents K effect on muscles

  • Actrapid insulin 10 units in 50mL 50% glucose over 5 minutes- promotes cellular uptake of potassium in extracellular area
  • Calcium resonium 15g 3 x day (with laxatives)- ion exchange resin
  • Dialysis if K+ doesn’t respond
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13
Q

Describe the anti-hypertensive treatment with ACEi and ARB

A

Preferred options in CKD as it reduces intra-glomerular pressure and lowers proteinuria

Serum creatinine levels can rise with initial treatment- check these levels 1-2 weeks after starting and stop if the rise is >30% baseline

Risk of hyperkalaemia
Caution if pre-treatment serum potassium >5.0 mmol/l
Check serum potassium 1-2 weeks after starting
Stop if serum potassium increases to 6mmol/litre or more

Titrate to maximum tolerated therapeutic dose

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14
Q

Describe the fluid overload complication of CKD and how to manage it

A
  1. Na+ and fluid balance usually maintained until GFR <10-15ml/min it kicks off
  2. Caution: prescribing fluids sodium and water retention
  3. Management:
    - Dietary sodium restriction
    - Fluid restriction (500-1500ml/24 hour)
    - Diuretic therapy
    Thiazides- less effective if GFR <20ml/min
    Loop diuretics- higher doses required if CKD progresses like Furosemide 240mg BD
    - Limit high volume medication like imodium, loperamide, movicol
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15
Q

Describe the acidosis complication of CKD and how to manage it

A

Regards to pH balance:
1. Reabsorb and eliminate filtered HCO3-

  1. Excrete (or retain) H+
    - Free H+= limited by the minimum attainable urinary pH = 4.5 = excreted as free hydrogen ions in the urine
    - Ammonia (NH3) or ammonium ion (NH4+)
    - Urinary buffers (phosphate)as tirtateable phosphoric acid
    - Retaining hydrogen ions can lead to chronic metabolic acidosis with increased risk of death and CKD progression
  2. Proximal tubule: reabsorbs most HCO3-, H+ and NH4+ secreted then excreted
  3. Distal tubule- secretion of titratable acid
  4. Treatment:
    - Chronic metabolic acidosis: sodium bicarbonate 1g TDS
    IV 1.26% 500ml 2-6 hourly
    Reduces serum potassium concentration- drives H+ ions into the cell so they can be released
    Raises systemic pH (reason why we do it)
    Drives H+ ion release from cells
    Moves K+ into cells
    Caution in fluid retention and raised BP due to sodium
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16
Q

Describe the Dyslipidaemia complication of CKD and how to manage it

A
  1. Abnormal lipid metabolism in CKD
    - Hypertriglyceridaemia
  2. High rates of CVD (and stroke) in CKD
  3. Atorvastatin 20mg daily- all patients offered this (primary or secondary prevention)
    - Higher doses used with caution if GFR <30ml/min as it can cause muscle pain
    - used as secondary prevention if Q risk assessment is greater than 10% in 10 years
  4. Aim to reduce non-HDLs by 40%- increase statin dose if cannot do so
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17
Q

Describe the uraemia complication of CKD and how to manage it

A
  1. Malnutrition secondary to anorexia- appetite affected
  2. Platelet dysfunction with increased risk of bleeding
  3. Nausea and vomiting
    - Anti-emetic treatment with metoclopramide or cyclizine
  4. Pruritus- itching due to build up of ammonia
    - Antihistamine, phosphate binder treatment
    - Menthol cream
  5. Pericarditis- inflammation of fibre sack around heart that means severe chest pain
    - dialysis required immediately
  6. Fatigue
  7. Sexual dysfunction
  8. Neuropathy
    - Restless legs
    - Encephalopathy- affects CNS
    - Imparied mental status
    - Seizures
    - Coma
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18
Q

Describe the CKD mineral and bone disorder (CKD-MBD) complication of CKD and how to manage it

A
  1. Phosphate is excreted by renal tubules
    Kidneys excrete the phosphate
    Vitamin D is activated by the kidneys (changed to 1.25)
    Calcitriol increases absorption of calcium
  2. Vitamin D is activated by kidney and liver
    - Colecalciferol -> 1.25
    dihydroxycolecalciferol (calcitriol)
    - Calcitriol promotes GI absorption of calcium
  3. As GFR reduces:
    - Phosphate excretion reduces: hyperphosphataemia
    - Calcitriol levels fall -> reduce calcium absorption- hypocalcaemia
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19
Q

Describe the mechanism of CKD-MBD

A
  1. Parathyroid hormone (PTH) is secreted from PTH gland
  2. Regulation of bone turnover by releasing calcium from bone
  3. Rises in response to
    Hypocalcaemia
    Hyperphosphataemia
    Low calcitriol levels
  4. Excessive production of PTH is termed hyperparathyroidism
  5. Excessive PTH due to another condition is termed secondary hyperparathyroidism
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20
Q

What is a normal calcium level

A

2.2 to 2.6mmol/L

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21
Q

What are normal phosphate levels

A
  1. 0.8 to 1.5mmol/L is normal
  2. Target phosphate level in CKD
    CKD stage 3-5 0.9 to 1.5mmol/L
  3. CKD stage 5
  4. 1 to 1.7 mmol/L
22
Q

What are the normal PTH levels and how to manage them in various stages of CKD

A
  1. Normal serum: 1.6 to 7.2 pmol/L
  2. Target PTH in CKD
  3. CKD stage 3-5 (not on dialysis)
    - nil specific- suggest only treat when PTH persistently is above normal range
  4. CKD stage 5 (on dialysis)
    - Maintain PTH within 2 to 9 upper limit of normal range
23
Q

Describe the use of activated vitamin D

A

Increases GI absorption of calcium (increase)
Suppresses PTH release (decrease)

Options:
Alfacalcidol
Calcitriol

Starting dose:
Alfacalcidiol 0.25mcg daily= drops

Dose adjustment:

  • Small and infrequent (every 1 to 3 months)
  • Increase to 0.5mcg daily if PTH too raised
  • Reduce to alternate days if hypercalcaemic
  • Low level of vitamin D= PTH
24
Q

Give examples of phosphate binders and describe them

A
  1. Calcium carbonate 500-1500mg
    Calcichew- firstline- increased risk of hypercalcaemia
  2. Calcium Acetate 1g-2g
  3. Lanthanum
    Non calcium based binders can be used to limit positive calcium balance
25
Q

What are the problems with phosphate binders

A

Phosphate binding a difficult concept to explain to patients

Patient may not feel benefits of phosphate lowering and poor adherence
Efficacy relies on dose timing before or with meals
High tablet burden
GI intolerance

Dose increases or binder changed because patients don’t declare poor adherence

26
Q

Describe Tertiary Hyperparathyroidism and its treatment levels

A
  1. Ongoing stimulation of parathyroid glands causing them to become enlarged and being to function autonomously- continue to secrete PTH even if hypocalaemia is corrected
  2. PTH levels extremely elevated
  3. Increased bone turnover (demineralisation)- calcium and phosphate released from bone
  4. Hyperphosphataemia exacerbated (worsens)
  5. Hypercalcaemia can occur
  6. Treatment: cinacalcet or parathyroidectomy
27
Q

Describe the use of cinacalcet, mechanism, dose and indication

A
  1. Calcimimetic agent
  2. Increases sensitivity of calcium sensing receptors to extracellular calcium
  3. Inhibits release of PTH
  4. Recommend:
    PTH > 85pmol/l with hypercalcaemia
    In whom surgical parathyroidectomy removal is contraindicated
  5. Dose- 30 to 180mg per day orally
  6. Nausea can be a problem and important to monitor calcium
28
Q

What are the complications of CKD-MBD

A

Increased fracture risk

Bone and joint abnormalities

Bone and muscular pain

Vascular and soft tissue calcification (increased CVD)

29
Q

Describe the anaemia complication of CKD and how to manage it

A
  1. Occurs when quality of quantity of RBC are below normal
  2. Haemoglobin concentration:
    Men <13.0g/dl
    Non-pregnant women <12.0g/dl
  3. Causes:
    Stress ulceration of chronic disease (minor GI losses)

Chronic HD- loss in circuit

Sampling losses- multiple blood tests

Reduced RBC survival

Dietary inadequacy- dietary restriction to reduce phosphate intake and anorexia due to nausea of uraemia

Poor iron absorption- due to PPI or phosphate binders or uraemia

Reduce erythropoiesis

Impaired erythropoiesis- in presence of adequate erythropoietin and iron

  • infection/inflammatory state
  • ACEi/ immunosuppresants
  • Decreased folate/ vitamin B12 intake
  • Secondary hyperparathyroidism
30
Q

Describe what erythropoietin is

A

Kidneys are the primary source of erythropoietin (EPO) and is a glycoprotein hormone that tells bone marrow to produce RBC

Production of EPO is stimulated by drop in blood oxygenation (hypoxia)

Circulating plasma EPO is low- usually occurs when eGFR falls below 30ml/min

CKD kidneys don’t make enough EPO

31
Q

Describe the use of erythropoietin stimulating agents (ESA)

A

Produce identical response to EPO normally produced by kidneys- tell bone marrow to produce RBC

Examples:
NeoRecormon and Eprex- recombinant Human Erythropoietin

Aranesp- novel erythropoiesis stimulating protein- longer half life than HuEPO

Mircera- longer half life that provides continuous receptor activity

32
Q

What are the benefits of correcting anaemia

A 
Increase in:
Quality of life
Exercise capacity
Endocrine function
Immune function
Muscle metabolism
Sleep patterns
Sexual function
Cognitive function
Nutrition 
Decrease in: 
Cardiac output
Depression
Hospitalisations
Bleeding tendency
Transfusions
angina 
LVH
33
Q

What are the haemoglobin levels of the adult population

A

Adults, young people and children >2years of age

34
Q

Describe the emphasis on iron with erythropoietin stimulating agents (ESA)

A

Iron should be optimised before or coincident with initiation of ESA administration and during maintenance treatments with ESA

35
Q

Describe what reflects total iron stores, cautions, role of transferrin and what transferrin saturation provides?

A
  1. Serum ferritin correlates with tissue ferritin (contains iron) and reflects total available iron stores
  2. Caution in inflammatory states like CKD especially those on dialysis in whom sub clinical inflammation is present (raised CRP)
  3. Transferrin carries iron between stores of reticula-endothelial system to erythropoietic cells in bone marrow
  4. Transferrin saturation (TSAT) provides a good indicator of iron available for erythropoiesis
36
Q

What is absolute iron deficiency and what are the values for it

A

Insufficient iron stores characterised by low Ferritin
CKD < 100ng/mL (<200ng/ml in HD)
Non CKD <30ng/ml
May be corrected by oral iron

37
Q

What is functional iron deficiency and what are the values for it

A

Inability to mobilise iron from liver and other storage sites to bone marrow for erythropoiesis
Characterised by:
Ferritin > 100ng/mL
TSAT < 20%
Common problem in CKD
Requires intravenous iron to respond to administered erythropoietin and correct anaemia

38
Q

What are the advantages and disadvantages of oral iron and what patient groups is it usually for

A

Advantages
Inexpensive
Not associated with severe adverse effects

Disadvantages
GI side effects common
Variable GI absorption

Patient groups:
Pre dialysis CKD- oral iron considered
Peritoneal dialysis- limited efficacy
Haemodialysis- unsuitable

39
Q

What is the main type of intravenous iron available and its side effects

A

Ferinject- single dose of iron, 1g at a time, 1g per week

Side effects:
Hypersensitivity reactions
Anaphylaxis

40
Q

Give examples of erythropoietin stimulating agents

A

Aranesp- initiate at low dose

Eprex/NeoRecormon- shorter half life
4000 units SC once weekly starting dose

Mirecera- monthly dosing

41
Q

What are the side effects of erythropoietin stimulating agents and how to monitor the Hb levels

A

Side effects:
Hypertension
PRCA (pure red cell achalasia)- rare

Increases Hb rate by 1-2g/dL/month

Monitor Hb
2 to 4 weekly in induction phase
1-3 monthly in maintenance phase

Minimum interval adjustments between ESA dose is 2 weeks because of the effect most dose changes will have
Dose adjustments of 25%

42
Q

Describe the renal replacement therapy of Peritoneal Dialysis

A

New solution- glucose solution
Tubing Set
Used Solution

Exchange of peritoneal space in dialysis and can be discarded

43
Q

What is continuous ambulatory peritoneal dialysis (CAPD)

A
  1. Solution left to dwell for 4-6 hours during which time patients can be left to dwell for 4-6 hours which time patients can continue with their daily activities
  2. Exchanges take place 30-40 minutes and are performed 4 times a day
44
Q

What is ambulatory peritoneal dialysis (APD)

A

Performed overnight enabling patients to be dialysis free in a day

45
Q

What are the complications associated with peritoneal dialysis

A

Peritonitis: aseptic technique essential when performing exchanges

Diabetes; secondary to high glucose concentration of dialysate

Sclerosing Peritonitis:
Thickening of peritoneum that encloses small intestine (can cause partial or complete small bowel obstruction)

46
Q

What are the advantages of peritoneal dialysis

A

Independence and freedom for patient

Carried out at home or work

Skilled nursing only required for initial training

Maintain access

Continuous- less fluid and diet restrictions

Do not need to go for dialysis 3 times a week

47
Q

What are the disadvantages of peritoneal dialysis

A

Motivated and competent patient

Not as efficient as haemodialysis

Albumin loss

48
Q

Describe what is involved in haemodialysis

A

Connecting patients circulations to dialysis machine to create a haemodialysis circuit via

  • Arteriovenous fistula (AVF)- removes blood and feed blood into dialysis machine
  • Central venous catheter (CVC)

Blood in haemodialysis circuit is pumped through a dialyser

Dialyser is composed of thousands of hollow synthetic fibres whose walls act as a semi-permeable membranes

Blood flows through fibres and dialysis solution around outside of fibres (opposite direction)- allows toxins to be exchanged and removed in blood

Water and waste products (phosphate and potassium) move between two solutions

49
Q

What is diffusion and ultrafiltration in haemodialysis

A
  1. Diffusion- movement of solutes from fluid with high to low concentration
    - Removes waste products
    - Essential minerals replaced e.g. bicarbonate
  2. Ultrafiltration- movement of fluid under pressure
    - Application of negative pressure to dialyse compartment of dialysed to allow removal of several litres of water and dissolved solutes to remove from blood
50
Q

What are the advantages of haemodilaysis

A

Very efficient

Better for less motivated patients- not motivated at home

51
Q

What are the disadvantages of haemodialysis

A

Fluid and diet restrictions- high protein for higher albumin levels, low salt diet and reduced potassium and phosphate

Rapid changes in fluid and electrolytes

Limiting freedom- 3 times a week in hospital

Expensive (NHS)

Need continuous skilled nursing care

Blood loss- dialysis process loses blood

Access- clotted or infected fistula

52
Q

Describe the role of a renal pharmacist

A 
Advise: 
Medication
Dosing 
Administration- injectables, fluid restriction
Interaction checks
Timing of dosing 
Effect of dialysis on dosing

Patient counselling

Teaching sessions- staff and patients

Developing clinical guidelines

Multi-disciplinary work- outpatient clinic and ward based

Finance reporting

Directorate meetings

Risk management

Error reporting and investigation

Formulary submissions for new drugs

Research

Audit

PM4B (13 decks)

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