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renal > C. CKD > Flashcards

C. CKD Flashcards

1
Q

what is CKD

A
  • an abnormality of kidney function or structure/loss of nephrons
  • present for more than 3 months (long term)
  • CKD is not reversible (unlike AKI) – results in a need for artificial replacement or transplantation (not medicines)
  • as kidney dysfunction progresses, some co-existing conditions become more common and increase in severity
  • the body might accumulate harmful quantities of fluid, electrolytes, and wastes
  • there may be few signs until severe deterioration has occurred
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2
Q

what conditions increase your risk of CKD

A
  • diabetes
  • hypertension
  • AKI (multiple)
  • CV disease
  • structural renal tract disease, recurrent renal calculus or prostatic hypertrophy
  • multi system diseases with potential kidney involvement (eg - systemic lupus: affects lots of smooth membrane)
  • family history of ESKD (GFR category G5) or hereditary kidney disease
  • opportunistic detection of haematuria from a dipstick test
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3
Q

how does diabetes increase risk of CKD

A
  • hyperglycaemia damages blood vessels, albumin gets through pores created
  • nerve fibres can be damaged causing problems with emptying the bladder as you don’t feel sensations and hence get strain on bladder, and get damage due to toxins in urine
  • if urine remains in bladder for a long time, an infection can develop from the rapid growth bacteria in urine that has a high sugar level
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4
Q

how does hypertension increase risk of CKD

A
  • high intraglomerular pressure, which impairs glomerular filtration
  • damage to the glomeruli increases protein filtration leading to microalbuminuria or proteinuria
  • increasing proteinuria is associated with a poor prognosis for CKD and CVD
  • relationship between the two is cyclic as CKD can contribute to or cause hypertension
  • increased BP damages blood vessels in the kidney
  • impairs the kidneys ability to filter fluid and water from the blood, leading to an increase of fluid volume in the blood, therefore causing an increase in blood pressure
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5
Q

risk factors for CKD progression

A
  • CV disease
  • proteinuria
  • AKI
  • hypertension (control through ACEi/ARB)
  • diabetes (control through good glycaemic control)
  • smoking
  • African, African-Caribbean or Asian family origin
  • chronic use of NSAIDs
  • untreated urinary outflow tract obstruction (kidney stones)
  • high BMI (weight loss)
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6
Q

ACEi/ARB in AKI and CKD

A
  • nephrotoxic in AKI
  • renoprotective in CKD
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7
Q

what are the therapeutic aims in CKD

A
  • identify patients with CKD early
  • reduce further damage to the kidneys
  • Identify and address causes of CKD
  • Prevent or delay progression to end-stage renal disease (ESRD) and for renal replacement therapy
  • prevent and manage complications of CKD
  • reduce risk of CV disease
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8
Q

what is the pharmacist’s role

A
  • ensure all medicines are clinically appropriate
  • ensure prescribed medicine doses are appropriate for the stage of CKD
  • ensure optimal management of symptoms is achieved
  • support risk reduction of modifiable risk factors for CKD progression
  • provide lifestyle advice to reduce modifiable risk factors for CKD progression (Stop smoking service, regular exercise, maintain healthy weight)
  • those prescribed drugs known to be nephrotoxic should have annual eGFR check:
  • Calcineurin inhibitors
  • Lithium
  • NSAIDs
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9
Q

how can you delay or prevent progression

A
  • lifestyle advice
  • Regular exercise
  • Maintain healthy weight
  • Stop smoking
  • BP control
  • Target <140/90mmHg
  • Diabetic / proteinuria <130/80mmHg
  • Prescribe statins (prevent cholesterol build up in blood vessels so get a more sustainable blood circulation)
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10
Q

complications of CKD

A
  • Na+ and water balance disrupted so get hypertension, oedema leading to heart failure
  • K+ disrupted so get hyperkalaemia
  • reduced elimination of nitrogenous wastes causing uremia causing coagulopathies and bleeding and pericarditis (impaired immune system, skin disorders, GI manifestations, neurologic manifestations, sexual dysfunction)
  • EPO production decreased so get anaemia
  • acid base balance disrupted so get metabolic acidosis and skeletal buffering leading to osteodystrophies
  • activation of vitamin D reduced so get hypocalcemia, hyperparathyroidism and osteodystrophies
  • decreased phosphate elimination so get hypocalcemia, hyperparathyroidism and osteodystrophies
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11
Q

treatment for sodium retention and volume overload

A
  • sodium restriction
  • diuretics
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12
Q

treatment for hyperkalemia

A
  • dietary restriction
  • avoid NSAIDs
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13
Q

treatment for metabolic acidosis

A

sodium bicarbonate (basic) neutralises sodium

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14
Q

treatment for hyperphosphatemia

A

phosphate binders gather phosphate in gut before its absorbed and you poo it out

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15
Q

treatment for anaemia

A
  • EPO stimulating agents
  • iron replacement
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16
Q

what is the BP target in CKD

A

<140/90mmHg

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17
Q

what is the BP target if you have diabetics/proteinuria (ACR > 70mg/mmol)

A

<130/80mmHg

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18
Q

what guidelines do you follow if ACR <30mg/mmol

A

NICE hypertension guidelines

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19
Q

how do ACEIs and ARBs decrease BP

A
  • reduce RAAs
  • slow CKD progression
  • keep glomeruli healthy by reducing the pressure and lower ACR ratio
  • can also lower the risk of CV disease
19
Q

what antihypertensive if ACR>30mg/mmol

A

ARB or ACEi (titrated to the highest licensed dose that the person can tolerate)

19
Q

when should you stop ACEIs/ARBs

A
  • if serum creatinine rises >30% from baseline or
  • eGFR drops >25% with no other cause, or if serum potassium increases to 6.0 mmol/L
  • this will prevent AKI
20
Q

how are ACEIs renoprotective in CKD

A
  • decrease BP, renal blood flow
  • decrease K+ secretion
  • get hyperkalaemia
21
Q

what is albuminuria/proteinuria

A
  • albumin in urine >30mg/mmol
  • there should be very little or no albumin in your urine
  • normally long term (chronic)
  • albuminuria is not a separate disease
  • it is a symptom of many different types of kidney disease and a significant risk factor for complications
  • having albumin in your urine can be a sign of kidney disease, even if your estimated glomerular filtration rate (eGFR) is above 60 or “normal”
22
Q

ACEIs/ARBs for proteinuria

A
  • for adults with CKD and diabetes (type 1 or type 2) offer an ARB / ACEi (titrated to the highest licensed dose that the person can tolerate) if ACR is 3 mg/mmol or more
  • for adults with CKD but without diabetes refer for nephrology assessment and offer an ARB or an ACEI (titrated to the highest licensed dose that they can
    tolerate), if ACR is 70 mg/mmol or more
  • people with kidney disease or heart failure can still
    benefit from an ACEI or ARB even if they do not have high blood pressure
23
Q

why are statins used in CKD (HARMFUL IN AKI)

A
  • adults with CKD are at a higher risk of heart attacks (MI) and strokes
  • CKD causes a systemic, chronic pro-inflammatory state contributing to vascular and myocardial remodelling
  • statins to reduce cholesterol levels in blood
  • atorvastatin 20mg OD for the primary prevention or secondary prevention of CVD
  • increase dose if we do not achieve a >40% reduction in non-HDL cholesterol and eGFR is >30ml/min/1.73m
  • discuss with renal specialist if higher doses are required and eGFR<30ml/min/1.73m2
  • fibrates, nicotinic acid, bile acid sequestrants, omega3 acid components should not routinely be offered for CVD to CKD patients
24
Q

process of homeostasis in anaemia

A
  • stimulus: low blood oxygen carrying ability due to decreased RBC count, Hb, availability of oxygen
  • kidney (and liver to a smaller extent) releases EPO
  • EPO stimulates red bone marrow
  • enhanced erythropoiesis increases RBC count
  • oxygen-carrying ability of blood increases
25
Q

how does anaemia occur in CKD

A
  • damaged kidney
  • impaired production of EPO
  • reduced number of RBCs

*take FBC, see Hb

26
Q

diagnosis of renal anaemia

A

consider if:
- eGFR <45mL/min
- Hb <110g/L
- develop symptoms attributable to anaemia
- exclude other causes of anaemia

27
Q

how can you determine iron status

A

TSAT (transferrin saturation level test)
- iron deficiency is present if the TSAT is less than 20%, and iron overload if it exceeds 40%

Ferritin levels
- a protein inside your cells that stores iron. It allows your body to use the iron when it needs it. A ferritin test indirectly measures the amount of iron in your blood

they measure the amount of iron stores in body (not blood - Hb)

28
Q

how can you correct iron stores

A

IV ferinject and dose is based off iron study results and weight

29
Q

EPO stimulating agents (ESA)

A
  • epoetin alfa, darbepoetin
  • aim to achieve Hb of 100 – 120g/L
  • usually supplied on homecare/admin on dialysis days
  • withhold and refer if BP >170/100 mmHg
30
Q

how can mineral and bone disease present (CKD-MBD)

A
  • abnormalities of calcium, phosphorus, parathyroid hormone and vitamin D metabolism
  • abnormalities of bone turnover, mineralisation, volume and strength
  • vascular or soft tissue calcification (lined with calcium-like compounds and can’t stretch)
31
Q

why does MBD occur

A
  • due to impact on kidneys usual function of excreting phosphate, waste products and activating vitamin D
32
Q

how to manage CKD-MBD

A
  • manage hyperphosphatemia (dietary restrictions and phosphate binders)
  • administer activated vitamin D (alfacalcidol), vitamin D analogues (cholecalciferol - needs activated) or calcimimetics
  • surgical removal of all of part of parathyroid glands
33
Q

dietary management of hyperphosphataemia

A
  • referral to renal dietician
  • aim for a reduced dietary intake but maintain nutritional requirements
  • main dietary sources are high protein foods or phosphate additives
  • advice to check labels for additives
34
Q

phosphate binders for hyperphosphataemia

A
  • individualised for each patient
  • bind to dietary phosphate in small intestine to form an insoluble compound that cannot be absorbed so need to take with food
  • many interactions (often prevent adsorption of other drugs): Levothyroxine (avoid lanthanum within two hours) with monitoring of thyroid function tests with all binders,
    Doxycycline (avoid lanthanum within two hours, avoid calcium acetate within three hours),
    Ciprofloxacin bioavailability is reduced by 50% when administered with binders (avoid lanthanum within two hours, avoid calcium acetate within three hours, avoid concomitant use of sevelamer)
35
Q

rules on phosphate binders

A
  • Calcium carbonate and lanthanum tablets must be chewed
  • Lanthanum tablets may not be suitable for patients with dentures
  • Sachets of lanthanum are available to sprinkle on food
  • Calcium acetate and sevelamer must be swallowed whole
  • Sevelamer sachets must be dispersed in 60ml of water. If this is being taken three times daily, this may have an impact on the amount of fluid the patient can take in, if on a strict fluid restriction
  • Check adherence as palatability can be problematic
  • Patients may split their binders up based on phosphate in food: for example, six binders per day is not a rigid two binders three times daily but can be four binders with a large phosphate meal, and one with each of the other meals
36
Q

most common phosphate binder

A

calcium acetate (Renacet)
- 1g 3x daily
- usual 1st line

37
Q

how to treat hyperparathyroidism

A

Vitamin D supplements
- Colecalciferol or ergocalciferol to treat vitamin D deficiency in people with CKD and vitamin D deficiency (<30ng/mL)
- If vitamin D deficiency has been corrected and symptoms of CKD-MBD persist, offer activated vitamin D, alfacalcidol or calcitriol, to people with a
GFR <30ml/min/1.73m2
(Alfacalcidol starting dose 250mg)

Calcium mimetics (cinacalcet)
- Refractory secondary hyperparathyroidism with high or normal calcium and a high PTH

Parathyroidectomy

38
Q

what is metabolic acidosis

A
  • Due to reduced reuptake of bicarbonate
  • Increase in the hydrogen ion concentration in the systemic circulation
  • Treat if eGFR <30mL/min/1.73m2 and serum bicarbonate is <20mmol/L
  • Oral Sodium Bicarbonate
  • May slow progression
  • Review if renal replacement initiated
39
Q

oedema

A
  • fluid and sodium retention
  • fluid restriction and LDs needed
40
Q

itching

A
  • uraemia (uric acid and urine)
  • antihistamines and emollients
41
Q

restless leg syndrome

A
  • uraemia, anaemia, hyperphosphatemia
  • clonazepam
42
Q

nausea

A
  • uraemia
  • antiemetics (cyclozine)
43
Q

stress ulceration

A
  • physiological responses, more acid released
  • histamine receptor antagonist or PPI
44
Q

gout

A
  • decreased uric acid excretion
  • allopurinol, colchicine

renal (13 decks)

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