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Year 3 Medicine Block > RENAL: CKD > Flashcards

RENAL: CKD Flashcards

1
Q

What are indications for renal replacement therapy?

A

Hyperkalaemia even after medical therapy
Metabolic acidosis even after medical therapy
Fluid overload which is not helped by diuretics
Uraemic pericarditis
Uraemic encephalopathy
Intoxications

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2
Q

What is uraemia?

A

High urea.

Waste products that should be removed via urination accumulate in the blood. This is due to reduced kidney function

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3
Q

What are symptoms of uraemic encephalopathy?

A
  • Vomiting,
  • confusion,
  • drowsiness,
  • reduced consciousness
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4
Q

Define CKD

A

Chronic kidney damage which is permanent and progressive.
Have:
- abnormal albumin excretion / decreased kidney function
- present for more than 3 months

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5
Q

What can cause CKD?

A
  • DM,
  • HTN,
  • age (decline as age +),
  • glomerulonephritis,
  • polycystic kidney disease,
  • medications - NSAIDs, PPIs, lithium.
  • Obstructive nephropathy.
  • Recurrent pyelonephritis
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6
Q

What are RF for CKD?

A
  • Older age,
  • HTN,
  • DM,
  • smoking,
  • medications which affect kidney
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7
Q

How does CKD present?

A

Asymptomatic
Pruritis (itching)
Loss of appetite
Nausea
Oedema
Muscle cramps
Peripheral neuropathy
Pallor
HTN

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8
Q

What investigations would you do for suspected CKD?

A

1) U&Es - to check eGFR. Need to be 2 tests 3 months apart to confirm ddx of CKD
2) Urinanalysis - urine albumin:creatinine ratio. >3mg/mmol is significant
3) Urine dipstick - haematuria
4) Renal USS

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9
Q

Write out/speak aloud stages of CKD (the G score):
G1 = eGFR ?
G2 = eGFR ?
G3a = eGFR ?
G3b = eGFR ?
G4 = eGFR ?
G5 = eGFR ?

A

G1 = eGFR >90
G2 = eGFR 60-89
G3a = eGFR 45-59
G3b = = eGFR 30-44
G4 = eGFR 15-29
G5 = eGFR <15

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10
Q

In CKD, what is the A score based on?

A

The ALBUMIN: creatinine ratio

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11
Q

What are the stages involved in the A score in proteinuria?
A1 = ?
A2 = ?
A3 = ?

A

A1 = <3mg/mmol so normal to mildly increased
A2 = 3-30mg/mmol so moderately increased
A3 = 30+ mg/mmol so severely increased

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12
Q

What eGFR is needed for a diagnosis of CKD?

A

less than 60

OR proteinuria has to be present

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13
Q

What are complications of CKD?

A

Anaemia of chronic disease
Renal bone disease
CVD = number 1 cause of mortality!!!
Hyperparathyroidism (secondary or tertiary)
HTN
Malnutrition
Dialysis related problems

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14
Q

Who is needed in MDT meeting to manage patients with CKD?

A

Renal physicians
GPs
Renal specialist nurses/home care teams
Dieticians
Pharmacists
Vascular/Transplant surgeons

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15
Q

What are main aims of management in CKD?

A

Slow progression of disease
Reduce CVD risk
Reduce risk of complications
Treat complications

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16
Q

What can be implemented to slow down progression of CKD?

A

Optimising diabetic control
Optimising HTN control
Treat infections promptly
Immunosuppression for GN

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17
Q

How to reduce the risks of CKD complications?

A

Main complication is CVD, so advice on this is appropriate:

  • Exercise, weight loss/maintain healthy weight,
  • Stop smoking
  • control BP - so dietary advice regarding sodium and water intake (+potassium and phosphate)
    -Advise on starting statin
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18
Q

What dose of atorvastatin is offered for primary prevention of CVD?

A

20mg

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19
Q

Why do potassium levels need to be monitored in patient with CKD?

A

CKD can cause hyperkalaemia
ACEi used to treat HTN in CKD also cause hyperkalaemia

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20
Q

Describe how CKD causes anaemia

(the main reasoning taught in Urinary module)

A

Kidney cells produce erythropoietin (EPO)
EPO is a hormone that stimulates production of RBC

In CKD, kidney cells are damaged = can not produce as much EPO = can not produce as many RBC = anaemia

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21
Q

How can anaemia in CKD be managed?

A

Measure haematincis - Vit B12, folate, ferritin, iron, transferrin saturation, reticulocyte Hb. If deficient in any of these, replace these first.

  • Note: IV iron may be better tolerated than PO

If this does not treat anaemia, discuss with renal team to offer EPO stimulating agents - e.g. exogenous EPO

Aim for Hb of 100-120

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22
Q

What features may be present in CKD MBD (mineral bone disease)?

A

Osteomalacia
Osteoporosis
Osteosclerosis `

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23
Q

CKD MBD is a complication of CKD. How would you manage this?

A

Vit D

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24
Q

ESRD is a complication of CKD. How would you manage this?

A

Dialysis
Renal transplant

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25
Q

What is the most important antigen to match in renal transplant?

A

HLA-DR

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26
Q

How does an acute graft rejection present?

A

Presents like infection: fever, rigors Usually picked up by rising creatinine, pyuria and proteinuria

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27
Q

What major complications result in patients needing dialysis?

A

Hyperkalaemia- give calcium gluconate and dextrose
Pulmonary oedema

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28
Q

What are the aims of renal replacement therapy?

A

Remove toxic metabolites
Normalise electrolyte disturbances
Correct volume deficit

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29
Q

What is Renal Replacement Therapy?

A

Dialysis- Peritoneal or Haemodialysis
Renal transplant

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30
Q

How does haemodialysis work?

A

Movement of solute across semi-permeable membrane- molecules that shouldn’t be there ie. ‘dirty’ molecules move across into water, thus cleaning blood Driven by osmotic pressure
3x weekly 4 hr treatment

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31
Q

Why do you need a AvF in haemodialysis?

A

To get blood out of the patient, most veins will collapse so need to arterialise the vein

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32
Q

What are the types of AvF

A

Radial artery joined to cephalic vein
Brachial artery joined to cephalic vein

33
Q

How do you know if the AvF is working?

A

You can feel a thrill or hear a bruit

34
Q

When do you use a central line in dialysis?

A

When you can’t get a AvF

35
Q

Where does the end of the central line sit?

A

Superior vena cava

36
Q

What is the risks with central line for dialysis?

A

Endocarditis
SVC obstruction

37
Q

How often do you need to do PD?

peritoneal dialysis

A

4 x a day, every day, as less efficient

38
Q

What is the biggest complication of PD

A

Peritonitis due to infection

39
Q

What is encapsulating sclerosing peritonitis?

A

In PD- Peritoneal membrane becomes thickened due to constant exposure due to sugar water, becomes a fibrosis capsule so bowel cannot move- sx of small bowel obstruction

40
Q

What is renal bone disease?

A

Renal failure- cannot hydroxylate Vit d–> means they cannot reabsorb calcium from gut–> serum calcium falls–> parathyroid hormone activated–>uses osteoclastic activity to increase serum calcium

Parathyroid goes out of control–> tertiary hyperparathryoidism–>Parathyroid increases calcium even when it doesn’t need to–> hypercalcaemia

41
Q

How do you try to avoid hyperparathryoidism?

A

vit D

Or parathyroidectomy–> give calcium in the long time

42
Q

What is renal anaemia?

A

Reduction in EPO
Normocytic anaemia

43
Q

How do you treat renal anaemia?

A

Oral iron tablets, if that doesn’t work give
Give EPO injection
IV Iron

44
Q

What is the complication to giving EPO?

A

May increase BP
Too much Hb can lead to viscous blood leading to hypercoaguable state

45
Q

Why are pts on dialysis at risk of not surviving transplantation?

A

Due to cardio complications- pts likely to have diabetes or HTN which leads to increase CVS risk

46
Q

What do you need to suppress during transplantation?

A

CD4 + T helper cell–> can’t produce NKC or B cells

47
Q

What are the complications of immunosuppression for kidney transplant?

A

Opportunistic infection e.g. miliary TB
Cancer: melanoma, lymphoma
Karposi sarcoma

48
Q

What drugs do you give to immunosuppress a patient prior to transplant?

A

Mycophenolate
Azathioprine
Calcineurin inhibitors- tacrolimus and cyclosporin
Steroids

49
Q

What are some long term side effects of ciclosporin?

A

Nephrotoxicity- tubular atrophy and fibrosis
Gum hypertrophy
Hypertension
Atherosclerosis

50
Q

Important differentials of CKD?

A

Diabetic kidney disease
Glomerulonephritis
Obstructive uropathy

51
Q

Indication for dialysis in CKD patient?

A

CKD stage 5 - end stage renal disease

52
Q

Features of osteomalacia?

A

bone pain, proximal myopathy, and waddling gait

53
Q

Link between CKD and osteomalacia?

A

phosphate is renally excreted, if there is impaired renal function - phosphate will build up, ‘dragging’ the calcium out of the bones resulting in osteomalacia

54
Q

First line management of CKD induced osteomalacia?

A

Limit dietary phosphate

55
Q

Aside from diet, how else can you manage CKD induced osteomalacia?

A

phosphate binder e.g Sevelamer- non-calcium-based phosphate binder, it binds to dietary phosphate and prevents its absorption.

56
Q

What is Dialysis disequilibrium syndrome?

A

Rare
Usually caused by cerebral oedema- treat by reducing ICP
Neurological symptoms due to rapid removal of urea
Headache, nausea, vomiting, disturbed consciousness, convulsions, coma

57
Q

Most common complication of haemo-dialysis?

A

Diaslysis induced hypotension

58
Q

Hb target for CKD patients being treated for anaemia?

A

Hb 100-120

59
Q

What factors contribute to anaemia in CKD?

A

Decreased production of EPO from kidney
Absolute iron deficiency - poor absorption/malnutrition
Functional iron deficiency - inflammation/infection
Blood loss
Shortened RBC survival
Bone marrow suppression from uraemia
Medication induced anaemia
Deficiency of B12 or folate

60
Q

What needs to be present for CKD-MBD to be diagnosed in a pt with CKD?

A

Evidence of one or more of:
- Abnormal metabolism of vitamin D or levels of PTH, calcium, phosphate, alkaline phosphatase
- Vascular and/or soft tissue calcification
- Abnormal bone turnover, metabolism, volume, linear growth or strength

61
Q

A pt with CKD has a low bone turnover. What could this mean they have?

A

Adynamic bone disease
Osteomalacia

62
Q

What is Osteitis Fibrosa?
1. give the features
2. Give symptoms

A

Features:
* loss of bone mass
* weakening of bones and calcified structures - this is replaced with fibrous tissue (peritrabecular fibrosis)
* formation of small cyst-like brown tumours

Symptoms:
* Bone pain
* tenderness
* fractures
* skeletal deformities

63
Q

A patient has CKD which has progressed. Describe the levels of the following as either increased or decreased:
1. Fibroblast growth factor-23
2. ALP
3. Phosphate
4. PTH
5. Serum calcium
6. Vit D

A
  1. Fibroblast growth factor-23 = Increased
  2. ALP = Increased
  3. Phosphate = Increased
  4. PTH = Increased
  5. Serum calcium = Decreased
  6. Vit D = Decreased
64
Q

Define tertiary hyperparathyroidism

A

Occurs when PTH release continues despite raised serum Calcium levels

65
Q

How is CKD-MBD managed?

A

Reduce the severity/occurrence of renal bone disease
Reduce CVS morbidity and mortality caused by elevated serum levels of PTH and high phosphate levels and calcium overload.

AIM: control serum phosphate, calcium and vit D levels.
* Dietary phosphate reduction
* Phosphate binder
* Vit D supplemenation (if low) / vit D analaogue
* Ca - treat if hypo/hyper (can be either) either by supplementing or binder
* Persistently elevated PTH - parathyroidectomy or calcimimetic therapy is indicated.

66
Q

When do you use Ramipril in kidney disease?

A

In patients with proteinuria, an ACE inhibitor such as ramipril is used first-line in patients with coexistent hypertension and CKD, if the ACR is > 30 mg/mmol.

They are also used regardless of a patient’s blood pressure if the ACR is > 70 mg/mmol.

67
Q

What causes Osteotits fibrosa cystica?

A

Cause: Unchecked hyperparathyroidism
* overproduction of PTH
* PTH causes Ca release from bones - blood - reabsorption of calcium in kidney
* this results in hypercalcaemia

68
Q

What conditions might lead a pt to develop hyperparathyroidism and therefore develop a complication such as Osteitis fibrosa cystica ?

A
  • Parathyroid adenoma (majority)
  • Genetics -( i.e. familiar hyperarathyroidsim, MEN type 1)
  • Parathyroid carcinoma
  • Renal - End stage renal disease
69
Q

Why does End stage renal disease lead to hyperparathyroidism?

A
  • In ESRD the kidneys fail to produce calcitriol (a form of vitamin D)
  • Vit D facilitates the absorption of calcium into bones.
  • When calcitriol levels decrease, parathyroid hormone levels increase
  • This causes calcium to be removed from the bones and released into the blood
70
Q

What is Secondary hyperparathyroidism?

A
  • elevation of parathyroid hormone (PTH) secondary to hypocalcaemia.
71
Q

What causes secondary hyperparathyroidism ?

A
  • Any disorder that results in hypocalcaemia will elevate parathyroid hormone.
  • CKD - MOST COMMON
  • malabsorption syndromes
  • chronic inadequate sunlight exposure, acting via alterations in vitamin D, phosphorus, and calcium.
72
Q

Secondary hyperparathyroidism (SHPT) is a complication of CKD. This is important in the pathogenesis of CKD-mineral bone disorder (MBD).

Define CKD-MBD

A
  • a systemic disorder of mineral and bone metabolism due to CKD.

This is due to either one or a combination of the following:
* abnormalities of calcium, phosphorus, PTH, or vitamin D metabolism
* abnormalities in bone turnover, mineralisation, volume, linear growth, or strength
* vascular or other soft tissue calcification

73
Q

Potential clinical findings in pt with AKI?

A

Signs: Reduced urine output (oliguria), dehydrated (NO moist mucous membranes, reduced skin turgor, sunken eyes). Confusion, drowsiness,

Who: over 65, RF present (see BS on this), Hx off AKI.

74
Q

Differentials of AKI?

A

CKD (i.e. a progression of CKD staging/acute on chronic kidney disease)

BMJ also states 1) increased muscle mass which shows elevated Cr. 2) Drug side effect leading to elevated creatinine (trimethoprim).

75
Q

What are principals of management in AKI?

A

Find and treat causes (e.g. sepsis, drugs, obstruction):

Bloods/Blood Cultures, urine dip, bladder scan, ultrasound renal tract, ECG

Stop renotoxic drugs

Give IV fluid

Treat complications

Consider dialysis if indicated

76
Q

How to test for proteinuria. What values are significant?

A

1) Albumin: creatine ratio
2) >3mg/mol = proteinuria
3-30mg/mol moderately increases
>30mg/mol severely increased

77
Q

When to refer to a nephrologist for a pt with Proteinuria?

A
  • a urinary albumin:creatinine ratio of 70 mg/mmol or more, unless known to be caused by diabetes and already appropriately treated
  • a urinary ACR of 30 mg/mmol or more, together with persistent haematuria (two out of three dipstick tests show 1+ or more of blood) after exclusion of a urinary tract infection
  • consider referral to a nephrologist for people with an ACR between 3-29 mg/mmol who have persistent haematuria and other risk factors such as a declining eGFR, or cardiovascular disease
78
Q

Management of proteinuria?

A
  • ACEi > 30mg/mol if they have HTN, >70mg/mol regardless of BP
  • consider SGLT

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