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Renal Medicine > Chronic Kidney Disease > Flashcards

Chronic Kidney Disease Flashcards

1
Q

CKD

A

Subtle decrease in function

Greater than 3 months

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2
Q

Kidneys function

A

Regulate what’s in the blood - remove waste, steady electrolytes, regulate water
Make hormones

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3
Q

Kidney - blood flow

A

Renal artery - blood enters through this
Goes to glomeruli - filtered - filtrate moves to renal tubule (GFR)
Normal = 100-120 ml/min/1.73m^2 (slightly less in women, decrease in age too)

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4
Q

Hypertension + kidney -> CKD

How?

A

Kidney - wall thickens - narrow lumen - less blood and oxygen - ischaemic injury - immune cells slip in - growth factors - extra cellular matrix - golmerulo-sclerosis - scarring - chronic kidney disease

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5
Q

Most common cause of CKD?

A

Diabetes
Excess glucose sticks to proteins (Non-enzymatic glycation)
Efferent arteriolar - stiff and narrow
Obstruction - blood can’t leave glomerulus as easy
Increased pressure - hyperfiltration
Supportive cell - more matrix - expands glomerulus
Glomerulus-sclerosis = CKD

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6
Q

Other causes of CKD (not DM or HTN)

A

Lupus and RA
Infection (HIV)
Long term use of medications e.g NSAIDS
Toxins e.g. tobacco

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7
Q

High urea in kidney - can cause…

A

General symptoms e.g. Nausea and loss of appetite Can cause encephalopathy -> asterixis -> coma and death
Pericarditis
Bleeding- less clot formation
Uraemia frost - crystals in skin

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8
Q

Potassium level - kidney

A

CKD - less potassium excreted, more in blood - hyperkalaemia

Cardiac arrhyhtmias

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9
Q

Calcium levels and the kidney

A

Kidney activates Vitamin D
Calcium absorption from diet

But in CKD, less activation of Vit D, less calcium in blood = HYPOcalcemia
PTH release - bones lose calcium - resorption - weak and brittle (renal osteodystrophy)

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10
Q

Hormones + the kidney

A

Low fluid filter - release renin - increase BP
Fall in GFR = more renin = high BP (HTN)
CKD Can cause HTN and can be caused by HTN

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11
Q

Kidney - erythropoietin

A

Production of RBC from bone marrow stimulation

In CKD, less, so less RBC = anaemia

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12
Q

Diagnosis of CKD

A

Changes in GFR over time
CKD - GFR under 90
Irreversible kidney damage under 60
Biopsy to confirm (glomerulosclerosis)

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13
Q

Treating CKD

A

Manage underlying cause
Dialysis
Transplant

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14
Q

Staging of CKD based on GFR

A 
G1: GFR >90mL/minute/1.73m^2
G2: GFR 60 to 89 mL/minute/1.73m^2
G3a: GFR 45 to 59 mL/minute/1.73m^2
G3b: GFR 30 to 44 mL/minute/1.73m^2
G4: GFR 15 to 29 mL/minute/1.73m^2
G5: GFR <15 mL/minute/1.73m^2
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15
Q

Albuminuria - predictor of …

A

Severe chronic kidney disease

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16
Q

Mild, moderate, severe albuminuria

Albumin to creatinine ratio

A

Mild - <30mg/g
Moderate - 30 to 300 mg/g (microalbuminuria)
Severe - >300mg/g (macroalbuminuria)

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17
Q

Renal US in CKD

A

ADPKD - may explain CKD in some people

Smaller kidney + atrophic - CKD

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18
Q

Renal biopsy+serology - look for cause of glomerulonephritis

A

Tissue under microscope
Different studies can be done
Check ANA + RF, ANKA, HIV, hepatitis

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19
Q

Additional LABS in CKD

A

High potassium
High phosphate
Low calcium (due to less vit D)
High or Low sodium
Less RBC - normocytic anaemia
High acid, low bicarbonate - ABG - metabolic acidosis likely
Lipid panel to check triglycerides and LDL (go up)
PTH - severe CKD - goes up
In severe CKD - hypercalcaemia may happen if PTH gets high enough!

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20
Q

Treatment for CKD - Reduce progression of the disease

How?

A

Reduced GFR - activation of renin - increase BP! So, need to decrease BP
ACE inhibitors OR ARBs OR K+ sparring diuretics e.g. Spironolactone

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21
Q

Aim of BP in CKD

A

130/80 or less than!

HTN - fluid overload prevention, reduction in water loss so fluid retention! - diuretics like loop diuretics

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22
Q

Reduce fluid overload in CKD - how

A

Water and sodium restriction - reduce fluid retention and overall BP
Diuretics also volume overload

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23
Q

Diabetes - high glucose - causing arteriosclerosis
How to prevent these glucose levels?
Aim of HbA1C ?

A

Insulin if needed
If type 2, anti diabetic drugs e.g. metformin
Also weight loss, diet changes

Aim of HbA1C <6.5% (48mmol)

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24
Q

Glomerulonephritis - what is this

How to treat?

A

Damage to the tiny filters inside the kidneys (glomeruli)
Autoimmune diseases may cause this
Treat with steroids/ DMARDs

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25
Q

ADPKD - treat …

A

Secondary HTN to reduce CKD progression to renal transplant

But ultimately it may lead to this

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26
Q

Renal transplant is often needed in who?

A

Adults with PCKD

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27
Q

Discontinue … in CKD to halt progression

A

Nephrotoxic drugs

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28
Q

Treatment of CKD - Renal Replacement Therapies

A

Dialysis

Kidney transplant

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29
Q

High potassium in CKD - what to give?

A

Give insulin - potassium in
SABA - beta 2 receptor activation
Bicarbonate in presence of acidosis
Wee out potassium - high dose of diuretic (loop diuretic) +/- thiazide diuretic
Also give fluid if depleted (pull out potassium through bottom, sodium poly stream)

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30
Q

Hyperphosphataemia in CKD

Treat

A

Phosphate binder - pull phosphate through gut to remove in faeces (prevents absorption)

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31
Q

Low calcium in CKD?
Low vitamin D?
What do we give?

A

Give calcium!!!

Give vitamin D supplementation

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32
Q

High PTH in CKD? How to treat

A

More PTH due to low calcium
Increase blood calcium levels sometimes - severe CKD due to hypercalcaemia
But in general, high PTH leading to high calcium levels, address high PTH and high Ca

Secondary hyperparathyroidism (can be tertiary in severe CKD)
To treat - block PTH by giving cinacalcet
If this fails - may have to give a parathyroidectomy!

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33
Q

Cinacalcet - what is this?

A

Drug which reduces PTH which leads to a decrease in serum calcium conc
Is used in CKD which has high PTH and high Ca levels as a result, helps to bring these down
If it fails - may need to do a parathyroidectomy

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34
Q

Reduce complications of CKD - EPO decreased if kidneys are damaged - RBC low…
How to treat?

A

We give when Hb is low - if 80-100 or under(roughly) start to treat with EPO

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35
Q

Reduce complications of CKD - inhibit RAAS to prevent HTN worsening (due to elevated renin levels, so secondary HTN)
How?

A

ACEi
ARBs
Potassium sparring diuretics e.g. eplerenone AND Spironolactone
Aim for 130/80 or lower

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36
Q

Decrease water balance complications in CKD

A

Reduced GFR
Water retention - fluid overload
Pulmonary oedema, HTN, peripheral oedema
Give diuretics!
Loop diuretic, can add thiazide later to pull off more water
Pull off more - potassium sparing diuretics
Sodium and water restriction is also another way to do this - salt intake reduce, water intake limited, daily weights

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37
Q

Modifications to prevent fluid overload in CKD

A

Due to reduced GFR, water retention can occur
Leading to fluid overload
Can give diuretics (usually loop, then thiazide, then k+ sparring)
BUT can also do
Daily weights
Reduced salt intake
Fluid restriction!

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38
Q

Acidosis related to CKD - how to reduce the complications of severe acidosis

A

Retain protons, reduce bicarbonate reabsorption (peed out)
Resulting in acidosis (less than 7.2 = affects cardiac system, electrolyte abnormalities, resistance to vasopressors) warrants treatment with sodium bicarbonate infusion

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39
Q

Albuminuria in CKD - how do we manage this?

A

Reduce the complications associated with this
Leaky capillaries - albumin in urine - low albumin in blood, leading to third spacing of fluid and increase in lipid synthesis

Decrease in albumin - protect against the protein in urine - ACEi and ARBs can help in proteinuria
Check albumin creatinine ratio - lots of protein in urine, and associated high BP
Put on ACEi or ARB

Complications of these drugs - can increase potassium and bump in creatinine

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40
Q

Reduce complications in CKD associated with high triglycerides and LDLs

A 
Reduce albumin - liver makes TG and LDLs 
Give STATINS (good therapeutic regimen)
Platelet dysfunction - DDAVP (desmopressin) activate platelets and increase activity and induce clots when needed
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41
Q

Worsening CKD:
worsening acidosis / electrolyte abnormalities/ intoxication/ volume overload/ uraemia that is refractory to medical therapy
OR
GFR reducing to stage 4/5, may have to progress to….

A

Dialysis - may bridge to kidney transplant

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42
Q

GFR reaching … is when transplant+dialysis is planned

A

When it is about 20 this is when this is planned

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43
Q

When do most people start dialysis?

A

Around GFR of 12

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44
Q

Conservative care in CKD when GFR is very low?

A

Dialysis too much, not suitable for transplant, have lots of other conditions

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45
Q

Donated kidney - options and candidate requirements?

A

Living donor or deceased donor
Living donor - family member/friend - last longer, transplant can happen earlier
Deceased donor often takes years

46
Q

Dialysis types - haemodialysis

A

Haemodialysis - outside the body
Blood through artificial kidney - dialyser - 4hours 3 times a week - IV through fistula (artery + vein in arm) or neck access
Can be done at home while sleeping, but most often in hospital

47
Q

Peritoneal dialysis

A

Tube into peritoneum - dialysate solution in for a few hours - diffuses waste products out of blood
Takes 20-30 mins

48
Q

Peritoneal dialysis - 2 options

A

Continuous ambulatory peritoneal dialysis (CAPD) 4 exchanges every day, can move as normal in between
Automated peritoneal dialysis (APD) does exchanges at night while you sleep

49
Q

Which treatment in dialysis?

Hospital or home?

A

DIALYSIS at home - hard to self manage and problem solve at home
Alcohol/drug addiction/ cognitive impairment/ other conditions - no reliable helpers = hard to do at home some people can’t use peritoneal dialysis either if they have had lots of abdominal surgeries

Challenges to overcome to do it at home:
Limited vision/hearing
Learning problems
Extra training required 
But nurses may be able to help 
If you can manage an ATM, can manage home dialysis !
50
Q

Home dialysis - pros

A

Fear of needles
Not happy following fluid restriction or diet required for haemodialysis - so peritoneal dialysis better for these people
Personal reasons - flexibility and control
Far away from hospital
Don’t want to travel to hospital 3x a week
Possible to travel but need a clinic if you use haemodialysis

51
Q

Dialysis - outcomes of PD vs HD

A

Patients that are candidate for both usually do the same on both dialysis
Patients should get the info ahead of time and pick the dialysis best for them!
Comprehensive education is necessary to encourage people to pick the right one for them

52
Q

Haemodialysis, peritoneal dialysis and renal transplant are all forms of RRT that are indicated for …

A

Haemodialysis, peritoneal dialysis and renal transplant are all forms of RRT that are indicated for end stage renal disease.

53
Q

Chronic kidney disease (CKD) can be defined by the presence of kidney damage or reduced kidney function for …

A

Chronic kidney disease (CKD) can be defined by the presence of kidney damage or reduced kidney function for three or more months.

54
Q

Reduced kidney function is suggested by a reduction in the glomerular filtration rate (GFR) or by evidence of kidney damage which can be characterised by the presence of one or more of the following pathological markers:

A

Albuminuria (e.g. albumin:creatinine ratio > 3 mg/mmol or > 30 mg/g)
Urinary sediment abnormalities (e.g. white cell or red cell casts)
Radiological abnormalities (e.g. polycystic kidneys)
Pathological abnormalities (e.g. seen on renal biopsy)
History of kidney transplantation

55
Q

Albuminuria (e.g. albumin:creatinine ratio > .. mg/mmol or > … mg/g)

A

Albuminuria (e.g. albumin:creatinine ratio > 3 mg/mmol or > 30 mg/g)

56
Q

The classification of CKD is now based on two factors: what are they?

A

chronicity and the precence of a reduced GFR or evidence of kidney damage.

57
Q

The definition of CKD is the presence of either of the following for 3 months (i.e. chronicity) or more:

A

1) Marker of kidney damage:
Albuminuria (> 3 mg/mmol, i.e. A2/3)
Abnormalities (including electrolyte derangement) secondary to tubular disorders
Structural abnormalities
Abnormalities on histology
History of kidney transplant
2) Reduced GFR: GFR < 60 ml/min/1.73 m2 (i.e. G3a-G5)
The GFR and ACR are two of the key measures in defining someone with CKD. The change towards using ACR in the classification of CKD reflects the increased risk of acute on chronic injury, end stage disease and all-cause mortality in patients with a high ACR. KDIGO define a number of classes of GFR and ACR based on their measurements.

58
Q

CKD is increasingly common with advancing age and stages 3-5 affect up to …% of the adult population. The higher the stage of CKD, the more frequent monitoring patients require. This helps to identify and manage complications and plan for RRT.

A

CKD is increasingly common with advancing age and stages 3-5 affect up to 8.5% of the adult population. The higher the stage of CKD, the more frequent monitoring patients require. This helps to identify and manage complications and plan for RRT.

59
Q

There are numerous causes of CKD, but the majority of cases are secondary to … (3)

A

There are numerous causes of CKD, but the majority of cases are secondary to diabetes mellitus, hypertension and glomerulopathies.

60
Q

Major causes of CKD

A 
Hypertensive nephropathy
Diabetic nephropathy
Glomerulopathies
Inherited kidney disorders (e.g. PCKD)
Ischaemic nephropathy (e.g. vascular disease)
Obstructive uropathy
Tubulointerstitial diseases
Medications
61
Q

Aetiology + Pathophysiology of CKD - overview

A

Approximately 1 million nephrons are present in each kidney from birth. These nephrons contribute to the kidneys ability to maintain adequate glomerular filtration and allows the kidney to perform its normal functions (e.g. volume regulation, acid-base balance).

As we age there is a progressive loss in renal mass and a number of structural changes occur (e.g. glomerulosclerosis) leading to a decline in renal function. Following a peak in the third decade of life, there is an estimated annual decline of 1 mL/min/year in eGFR.

Regardless of the underlying cause, renal disease leads to progressive loss of nephrons and a subsequent reduction in the GFR. As the disease progresses, structural abnormalities may occur leading to kidney damage (e.g. albuminuria), and eventually, the kidneys start to lose their ability to carry out normal functions.

62
Q

Patients are generally asymptomatic with CKD, but start to develop non-specific symptoms at more advanced stages (e.g. eGFR < …/min).

A

Patients are generally asymptomatic with CKD, but start to develop non-specific symptoms at more advanced stages (e.g. eGFR < 45ml/min).

63
Q

Symptoms of CKD

A 
Frequently asymptomatic in early stages
Anorexia & nausea
Fatigue & weakness
Muscle cramps
Pruritus
Dyspnoea
Oedema
64
Q

Signs of CKD

A 
Pallor (secondary to anaemia)
Hypertension
Fluid overload (e.g. raised JVP, peripheral & pulmonary oedema)
Skin pigmentation
Excoriation marks
Peripheral neuropathy​
65
Q

Diagnosis of CKD

A

The diagnosis and subsequent monitoring of CKD is based on evidence of kidney damage and the measurement of the serum creatinine and urinary ACR.

66
Q

Indicaations for CKD testing?

A 
Diabetes
Hypertension
Acute kidney injury
Obesity with metabolic syndrome
Cardiovascular disease
Structural renal tract disease
Proteinuria or persistent haematuria
Family history

NICE recommend the use the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation for calculating the eGFR.

67
Q

Depending on the results of the … and …, patients can be classified into a particular stage of CKD. In patients with stable CKD it is important to repeat these tests within 3 months. Those with pronounced albuminuria (> 70mg/mmol) or significantly reduced eGFR (G4 or G5) require referral to a nephrologist.

A

Depending on the results of the eGFR and ACR, patients can be classified into a particular stage of CKD. In patients with stable CKD (e.g. eGFR < 60ml/min without acute deterioration or ACR between 3 and 70 mg/mmol), it is important to repeat these tests within 3 months. Those with pronounced albuminuria (> 70mg/mmol) or significantly reduced eGFR (G4 or G5) require referral to a nephrologist.

68
Q

In CKD - Those with evidence of persistent … in the absence of infection should be investigated for malignancy.

A

In CKD - Those with evidence of persistent haematuria in the absence of infection should be investigated for malignancy.

69
Q

Urine investigations in CKD diagnosis, monitoring and assessing for complications (5)

A 
Urine dipstick
Urine microscopy
ACR (spot test)
ACR (24-hour collection)
Electrophoresis (e.g. myeloma)
70
Q

Bloods - diagnose, monitor and assess for complications of CKD.

A 
FBC
U&Es (inc. eGFR)
Bone profile
PTH
Bicarbonate
LFTs
Lipid profile
Autoimmune screen (e.g. ANCA, ANA)
Myeloma screen
71
Q

Imaging -to help diagnose, monitor and assess for complications of CKD.

A

Renal ultrasound
Magnetic resonance angiography
Echocardiogram
ECG (high risk of CVS disease)

72
Q

Renal biopsy (useful in the identification of … causes of CKD)

A

Renal biopsy (useful in the identification of intrinsic causes of CKD)

73
Q

The principles of CKD management are to…

A

The principles of CKD management are to treat the underlying cause, prevent or slow progression (e.g. renoprotective therapy), treat associated complications and plan for RRT.

74
Q

… therapy is aimed at slowing the progression of CKD, independent of the aetiology.

A

Renoprotective therapy is aimed at slowing the progression of CKD, independent of the aetiology.

Renoprotective therapy is centered around blood pressure control and reducing proteinuria. Specific blood pressure targets have changed with the release of the new NICE chronic kidney disease guidelines.

75
Q

Renoprotective therapy is centered around blood pressure control and reducing proteinuria. Specific blood pressure targets have changed with the release of the new NICE chronic kidney disease guidelines.

A

Renoprotective therapy is centered around blood pressure control and reducing proteinuria. Specific blood pressure targets have changed with the release of the new NICE chronic kidney disease guidelines.

A standard BP target of < 140/90 mmHg should be aimed for in patients with CKD. This is broadly in line with the NICE guidelines on hypertension. However, if the ACR is > 70 mg/mmol then a tigher blood pressure control may be targeted.

In adults with CKD, hypertension and an ACR ≤ 30 mg/mmol, the advice on choice of anti-hypertensive should be line with the NICE guidelines on hypertension. In patients with more significant proteinuria, the ideal blood pressure agent in an ACE inhibitor or angiotensin receptor antagonists (both renin-angiotensin system antagonists). These drugs are both antihypertensive and antiproteinuric.

76
Q

A standard BP target of < 140/90 mmHg should be aimed for in patients with CKD. This is broadly in line with the NICE guidelines on hypertension. However, if the ACR is > … mg/mmol then a tigher blood pressure control may be targeted.

In adults with CKD, hypertension and an ACR ≤ … mg/mmol, the advice on choice of anti-hypertensive should be line with the NICE guidelines on hypertension. In patients with more significant proteinuria, the ideal blood pressure agent in an ACE inhibitor or angiotensin receptor antagonists (both renin-angiotensin system antagonists). These drugs are both antihypertensive and antiproteinuric.

A

A standard BP target of < 140/90 mmHg should be aimed for in patients with CKD. This is broadly in line with the NICE guidelines on hypertension. However, if the ACR is > 70 mg/mmol then a tigher blood pressure control may be targeted.

In adults with CKD, hypertension and an ACR ≤ 30 mg/mmol, the advice on choice of anti-hypertensive should be line with the NICE guidelines on hypertension. In patients with more significant proteinuria, the ideal blood pressure agent in an ACE inhibitor or angiotensin receptor antagonists (both renin-angiotensin system antagonists). These drugs are both antihypertensive and antiproteinuric.

77
Q

Offer a renin-angiotensin system antagonist in patients who are:

A

Offer a renin-angiotensin system antagonist in patients who are:

Diabetic and have an ACR ≥ 3 mg/mmol (even in the absence of hypertension)
Hypertensive and ACR > 30 mg/mmol
ACR > 70mg/mmol (even in the absence of hypertension)

78
Q

Before starting an ACE inhibitor or ARB patients need a …

A

Before starting an ACE inhibitor or ARB patients need a baseline renal function assessed. The blood test should be repeated between 1-2 weeks after starting or any dose increase.

79
Q

NOTE: do not routinely offer a renin–angiotensin system antagonist in CKD if the pretreatment potassium is > … mmol/L.

Why?

A

NOTE: do not routinely offer a renin–angiotensin system antagonist in CKD if the pretreatment potassium is > 5 mmol/L.

Coadministration of RAAS inhibitors is associated with a higher incidence of serum potassium >5.5 mmol/L (≈5%). Rates of hyperkalemia are also increased in patients with risk factors such as HF or CKD

80
Q

RAAS inhibitors - what electrolyte abnormality can occur?

A

Hyperkalaemia - so in those with K+ over 5 do not start these routinely

81
Q

Other therapies for CKD

A

Statin therapy: prescribed in line with NICE recommendations for the use of statins
Smoking cessation
Antiplatelets for secondary prevention of CVS disease

82
Q

A number of important complications develop as a consequence of CKD, which include anaemia, …, mineral and bone disorders, fluid overload and ….

A

A number of important complications develop as a consequence of CKD, which include anaemia, hyperkalaemia, mineral and bone disorders, fluid overload and acidosis.

83
Q

Complications of what?

A

CKD

84
Q

What anaemia is typical of CKD?

A

Anaemia

A normocytic normochromic anaemia is typical of CKD. This anaemia is normally multifactorial. A significant factor in advanced disease is a reduction in the production of erythropoietin (EPO), the hormone that drives erythropoiesis.

85
Q

The main management for anaemia in CKD is the use of …

A

The main management for anaemia in CKD is the use of erythropoietin-stimulating agents (ESA) such as epoetin alfa.

86
Q

Hyperkalaemia in CKD

A

The ability of the kidneys to maintain adequate acid-base homeostasis and electrolyte balance diminishes with worsening renal function. Many medications, including NSAIDs and potassium-sparing diuretics, may worsen hyperkalaemia. Furthermore, uncontrolled metabolic acidosis may also worsen potassium handling.

Acute rises in potassium should be managed as a medical emergency. This involves stabilisation of the myocardium (with calcium gluconate) and driving potassium into the intracellular compartment (with insulin/dextrose). Chronic elevations in serum potassium can be managed with low potassium diets, potassium-binding resins and correction of acidosis.

87
Q

Mineral and bone disorders in CKD

A

In CKD, disorders of mineral and bone metabolism reflect a complex spectrum of pathology that results from abnormal calcium and phosphate handling. In health, the kidneys have an important role in the maintenance of calcium homeostasis. They are able to activate vitamin D (calcitriol), a fat-soluble vitamin important for absorption of calcium from the gastrointestinal tract. They are also involved in the reabsorption of calcium and excretion of phosphate.

88
Q

In disease, reduced kidney function (usually associated with a GFR < 30ml/min) leads to hypocalcaemia, hyperphosphataemia and hyperparathyroidism (secondary hyperparathyroidism). These biochemical abnormalities may then lead to boney pathology (e.g. adynamic bone disease, osteomalacia, osteoporosis and osteitis fibrosa cystica). The term ‘renal …’ is used exclusively for this type of bone pathology seen in CKD.

A

In disease, reduced kidney function (usually associated with a GFR < 30ml/min) leads to hypocalcaemia, hyperphosphataemia and hyperparathyroidism (secondary hyperparathyroidism). These biochemical abnormalities may then lead to boney pathology (e.g. adynamic bone disease, osteomalacia, osteoporosis and osteitis fibrosa cystica). The term ‘renal osteodystrophy’ is used exclusively for this type of bone pathology seen in CKD.

89
Q

In disease, reduced kidney function (usually associated with a GFR < 30ml/min) leads to …calcaemia, …phosphataemia and …parathyroidism

A

In disease, reduced kidney function (usually associated with a GFR < 30ml/min) leads to hypocalcaemia, hyperphosphataemia and hyperparathyroidism (secondary hyperparathyroidism). These biochemical abnormalities may then lead to boney pathology (e.g. adynamic bone disease, osteomalacia, osteoporosis and osteitis fibrosa cystica). The term ‘renal osteodystrophy’ is used exclusively for this type of bone pathology seen in CKD.

90
Q

The management of mineral and bone disorders in CKD requires management of the underlying biochemical abnormalities

Hypocalcaemia: …
Hyperphosphataemia: …
Hyperparathyroidism: …

A

Hypocalcaemia: dietary supplements and calcitriol.
Hyperphosphataemia: dietary restriction and phosphate binders.
Hyperparathyroidism: calcimimetics or surgery.

91
Q

Fluid overload in CKD

A

In the presence of significantly reduced GFR, the kidneys are unable to adequately controlled fluid volume. This leads to hypervolaemia and patients may have evidence of peripheral oedema, ascites, raised JVP, gallop rhythm and bilateral pleural effusions.

Fluid overload can be managed with a combination of fluid restriction, reduced sodium intake and the use of oral diuretics (e.g. furosemide).

92
Q

Acidosis in CKD

A

Patients with CKD have an increased tendency to retain hydrogen ions because of abnormalities in their acid-base homeostasis.

This leads to low bicarbonate levels and management generally involves the use of oral sodium bicarbonate therapy.

93
Q

Haemodialysis overview

A

Haemodialysis involves the removal of waste products and other substances by passing blood through a dialysis machine. Blood comes into contact with a semi-permeable membrane, which contains the dialysate on the other side. Substances may then diffuse between the two fluids (blood and dialysate).

Haemodialysis requires intravenous access in the form of an arteriovenous fistula or an artificial line (e.g. portacath). Patients usually have haemodialysis 3-4 times a week for several hours.

94
Q

Peritoneal dialysis overview

A

Peritoneal dialysis is achieved by using the peritoneal cavity as the primary site of ultrafiltration. A catheter (e.g. Tenckhoff catheter) is inserted into the abdominal cavity, which allows the infusion of the dialysate. The dialysate then dwells within the abdomen using the peritoneum as a semi-permeable membrane for the transfer of waste products. The dialysate can then be removed after a certain amount of time and the procedure repeated.

In general, peritoneal dialysis can be achieved by continuous ambulatory peritoneal dialysis (CAPD) where multiple exchanges are made each day, or by automated peritoneal dialysis (APD) where the exchange is made overnight when the patient sleeps.

95
Q

Renal transplant overview

A

Renal transplant is considered the gold-standard for RRT. Transplantation may be from living donors or non-living donors as long as there is MHC compatibility, which may mediate graft rejection. Non-living donors include donors after cardiac death (DCD) and donors after brain death (DBD).

Renal transplantation requires the use of long-term immunosuppressive therapy to stop the recipient’s immune system from ‘attacking’ the donor tissue.

Despite the overt success of transplantation, it can be associated with a number of complications including graft rejection, complications from immunosuppressive agents (e.g. malignancy, infection) and disease recurrence.

96
Q

What is considered the gold-standard for RRT?

A

Renal transplant

Transplantation may be from living donors or non-living donors as long as there is MHC compatibility, which may mediate graft rejection. Non-living donors include donors after cardiac death (DCD) and donors after brain death (DBD).

97
Q

Renal transplantation requires the use of long-term …

A

Renal transplantation requires the use of long-term immunosuppressive therapy to stop the recipient’s immune system from ‘attacking’ the donor tissue.

98
Q

Renal transplant is considered the gold-standard for RRT.

Despite the overt success, it can be associated with a number of complications - what are these?

A

Despite the overt success of transplantation, it can be associated with a number of complications including graft rejection, complications from immunosuppressive agents (e.g. malignancy, infection) and disease recurrence.

99
Q

Which of the following describes three key endocrine functions of the kidneys?

A Erythropoietin production, renin release and activation of vitamin D
B Thrombopoietin production, angiotensin release and activation of vitamin D
C Erythropoietin production, renin release and parathyroid hormone release
D Thrombopoietin production, angiotensin release and parathyroid hormone release
E Erythropoietin production, renin release and aldosterone release

A

A

The kidneys play a role in a number of endocrine systems. These actions become deranged in chronic kidney disease.
Erythropoietin is produced and released by the kidneys (the primary stimulus for erythropoiesis) from fibroblast-like cells. Renin, released by granular cells of the juxtaglomerular apparatus, is the first part of the renin-angiotensin system (RAS). RAS is responsible for aldosterone release, fluid retention and raised blood pressure/renal blood flow. The kidneys are responsible for the final stage of vitamin D activation. Activated vitamin D increases serum calcium by promoting calcium absorption, reducing its excretion and increasing its release from bone.

100
Q

leads to cardiac arrhythmias.

Which of the following treatment options helps protect the myocardium in acute hyperkalaemia?

A	Insulin & dextrose
B	Salbutamol
C	Calcium resonium
D	Calcium gluconate
E	Oxygen
A

D

The management of acute hyperkalaemia should start with the administration of 10ml 10% calcium gluconate, as this helps to protect the myocardium.
Subsequent management to help drive potassium back into cells includes nebulised salbutamol and insulin given alongside dextrose (e.g. 10 units of ACTRAPID with 100mls of 20% dextrose).

Calcium resonium is considered a polystyrene cation exchange resin. This can be given orally and it acts to remove potassium by exchanging it for calcium ions within the resin. This choice of management reduces serum potassium slowly.

101
Q

What is the most common cause of death in patients with CKD?

A

Cardiovascular disease is the most common cause of death in patients with CKD.
Causes of death include heart failure, myocardial infarction and stroke. Incidence is significantly greater than that seen in the general population.

This is for a number of, often complicated, reasons. CKD itself is associated with conditions that increase the risk of cardiovascular death. Diabetes and hypertension are the leading causes of CKD. Patients are at risk of accelerated cardiovascular disease. Atherosclerosis is worsened by uraemia and hyperparathyroidism as well as changes in calcium and phosphate.

This highlights the importance of optimising both patients cardiovascular risk factors and appropriately managing the consequences of CKD.

102
Q

A 69-year-old gentleman has recently been diagnosed with chronic kidney disease and hypertension. You note he is diabetic and has proteinuria. You decide to start him on antihypertensive therapy.

Which of the following classes of medications would be most suitable?

A	Alpha-blocker
B	Beta-blocker
C	Thiazide diuretic
D	Calcium channel blocker
E	ACE inhibitor
A 
ACE inhibitors (e.g. ramipril) are the drug of choice in the management of hypertension in CKD.
These drugs have both antihypertensive and antiproteinuric properties to help prevent the progression of CKD. They are considered renoprotective therapy and should be used alongside appropriate cholesterol-lowering therapy, smoking cessation and consideration of anti-platelet therapy as secondary prevention for CVS disease.
103
Q

A 69-year-old gentleman has recently been diagnosed with chronic kidney disease and hypertension. You note he is diabetic and has proteinuria. You decide to start him on antihypertensive therapy.

Which of the following is the most appropriate BP target you should aim for?

A	< 160/100 mmHg
B	< 150/90 mmHg
C	< 140/80 mmHg
D	< 130/80 mmHg
E	< 120/80 mmHg
A

Management of hypertension is a key component of renoprotection in patients with CKD.
A standard BP target is < 130/80 mmHg if the patient is diabetic or has albuminuria. Therapy utilises ACE inhibitors and angiotensin receptor antagonists (renin-angiotensin system antagonists). These drugs are both antihypertensive and antiproteinuric.

Renin-angiotensin system antagonists should be offered to patients who are:

Diabetic and have an ACR of 3 mg/mmol or more.

Hypertensive and ACR of 30 mg/mmol or more.

ACR > 70 mg/mmol independent of CVS disease.

Outside of these parameters, hypertension should be treated in accordance with normal NICE guidance and aim for targets < 140/90 mmHg.

104
Q

Management of hypertension is a key component of renoprotection in patients with CKD.
A standard BP target is < …/80 mmHg if the patient is diabetic or has albuminuria. Therapy utilises ACE inhibitors and angiotensin receptor antagonists (renin-angiotensin system antagonists). These drugs are both antihypertensive and antiproteinuric.

A

Management of hypertension is a key component of renoprotection in patients with CKD.
A standard BP target is < 130/80 mmHg if the patient is diabetic or has albuminuria. Therapy utilises ACE inhibitors and angiotensin receptor antagonists (renin-angiotensin system antagonists). These drugs are both antihypertensive and antiproteinuric.

105
Q

Renin-angiotensin system antagonists should be offered to patients who are:

A

Diabetic and have an ACR of 3 mg/mmol or more.

Hypertensive and ACR of 30 mg/mmol or more.

ACR > 70 mg/mmol independent of CVS disease.

106
Q

An 87-year-old gentleman presents to his GP complaining of fatigue. He has stage 4 chronic kidney disease likely secondary to his hypertension. A series of blood tests reveals he is anaemic with a Hb of 87. The blood film demonstrates a normocytic normochromic appearance.

Which hormone deficiency is likely implicated in the aetiology of this patients anaemia?

A	Erythropoietin
B	Renin
C	Activated vitamin D
D	Thrombopoietin
E	Angiotensinogen
A

A

107
Q

Which of the following is the most common cause of chronic kidney disease?

A	Diabetes mellitus
B	Glomerulopathies
C	Autosomal dominant polycystic kidney disease
D	Renal artery stenosis
E	Urinary tract obstruction
A

The two most common causes of chronic kidney disease in the United Kingdom are diabetes mellitus and hypertension.
The glomerulopathies are another common aetiological mechanism for the development of CKD, which include a wide variety of pathology.

108
Q

Which of the following define Stage 3a of chronic kidney disease?

A	eGFR: < 15
B	eGFR: 30-45
C	eGFR: 60-90
D	eGFR: 45-60
E	eGFR: 15-30
A

D

Chronic kidney disease is most commonly categorised by the eGFR +/- evidence of kidney damage (persistent changes present for > 3 months).

109
Q

Chronic kidney disease results in …calcaemia, …phosphataemia and …parathyroidism.

A

Chronic kidney disease results in hypocalcaemia, hyperphosphataemia and hyperparathyroidism.

110
Q

The kidneys play an important role in activation of vitamin D. The kidneys play an important role in activation of vitamin D. The activation of vitamin D is a two-step process.

Cholecalciferol (vitamin D) undergoes two hydroxylation reactions, the first in position 25 by the liver to Calcidiol (25-hydroxy vitamin D) and again in the kidneys to give Calcitriol (1, 25-hydroxy vitamin D). Calcitriol is also termed activated vitamin D.

A

The kidneys play an important role in activation of vitamin D. The activation of vitamin D is a two-step process. Cholecalciferol (vitamin D) undergoes two hydroxylation reactions, the first in position 25 by the liver to Calcidiol (25-hydroxy vitamin D) and again in the kidneys to give Calcitriol (1, 25-hydroxy vitamin D). Calcitriol is also termed activated vitamin D.

Renal Medicine (17 decks)

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