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Nephrology > Chronic renal Failure and Dialysis > Flashcards

Chronic renal Failure and Dialysis Flashcards

1
Q

Definition of CKD?

A

Main definition:
eGFR <60 for at least 3 months
- ie need at least 2 reading to define CKD (otherwise could just be an AKI)

Other definitions (irespective of GFR):
- persistent albuminuria
- Glomerular haematuria
- Structural abnormality (on imaging)
- Pathological abnormality (on Bx)

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2
Q

What groups of normal (ie nil disease) adult pts is eGFR not appropriate for?
What is the main group of unwell adults in which eGFR is not used?

A
  • Pregnant pts - this is a hyperfiltration state and eFGR may be false high
  • Body builders (lots of muscle means lots of Cr production)
  • Malnourished/cachectic pts
  • Pt taking extra Cr supplements (ie body builders)

Pts with AKI
- should use Creatine

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3
Q

Very elderly pt without known CKD has eGFR of 60. Is this CDK?

A

Not necicarily, eGFR falls as we age but not ususally less than 60

Therefore if see pt with eGFR <50 then this is not just aging

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4
Q

GOld standard for eGFR measurement?

A

Inulin test

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5
Q

Stages of CKD G1-5? Explain the stages of albuminuria A1-3?

A

G1 >90
G2 60-90
G3a 45-60
G3b 30-45
G4 15-30
G5 <15 (end stage)

Measurements in mg/mmol (the usual ACR measurement)
- A1 normal - 3mg/mmol
- A2 3-30mg/mmol
- A3 >30mg/mmol

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6
Q

Why is ACR preferred to PCR in looking at CKD?

A

ACR is more specific to glomerular disease
PCR also includes tubular secreted proteins
- therefore if see high PCR and low ACR then this is probably ATN (tubular damage but not glomerular)

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7
Q

What are some examples of “tubular proteins”?

A

Immunoglobulin, light chains etc

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8
Q

What is nephrotic range protinuria?

A

ACR >300mg/mmol OR >3g/day on 24hr urine collect

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9
Q

Why is albuminuria important to quantify?

A

Significant albuminuria increases risk of CKD or progression of CKD, and increases risk of AKI

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10
Q

What is the main cause of morbidity and mortality in pts with CKD?

A

Cardiovascular disease
- much more likely to die of CVD than end up on dialysis
- If you do end up on dialysis, the main cause of death is withdrawal of treatment, followed by cardiovascular disease

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11
Q

What are some features of CKD on USS?

A

Small kidneys - indicates disease has been present for quite some time
- May see asymmetrical kidenys (ie one is small other looks normal)

Cortical thinning - loss of glomeruli

May see cortical scarring indicating long term consequence of reflux or recurrent infections

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12
Q

Situations in which to Bx kidney?

A
  • AKI not resolving
  • Transplant AKI of unclear cause / not imprroving
  • CKD with progressive / rapid loss of function (ie 10-15 eGFR per year)
  • Nephrotic range protinuria
  • Acute nephritis / glomerularnephritis

Can also be used for assessment of treatment response or prognosis

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13
Q

Managment principles in CKD?

A
  • Management of underlying disease (ie DM, HTN, GN)
  • Lifestyle change (same as would recomend in CVD/DM pts)
  • Remove/avoid nephrotoxics
  • Management BP
  • reduce albuminuria
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14
Q

Why is weight loss good for renal function in pts with CKD?

A

Wight loss reduced albuminuria irrespective of cause of CKD
- obesity causes increase glomerular filtratrion pressure that causing increased albuminuria

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15
Q

What medications can be used to reduce albuminuria independantly?

A

ACEI/ARB (these can reduce indep of blood pressure)
SGLT2
Spironolactone (Finerenone in T2DM pts)
Non dihydropyridine CaC blockers (verapamil and diltiazem)

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16
Q

Pts renal funciton drops a bit post starting ACEI. Should you continue ACEI?

Pt who has been on ACEI for many years. CKD now progressed to end stage. Should you stop the ACEI?

A

Yes, this is expected. Does not represent an AKI, glom filtration pressure decreases slightly with AACEI/ARB which results in decreased eGFR

No, continue it
- if they are on nephroprotective agents, keep them on it unless very good reason to stop

17
Q

Common complications of CKD (especially CKD with eGFR <30)?

A

Hypertension
Fluid overoad
Anaemia
Metabolic acidosis
Vitamin D deficiency/Renal bone disease/Electrolyte distirbances

18
Q

What is the recommended maximum daily salt intake for CKD pts?

A

1500mg per day (1.5g)

19
Q

Where and how does acetazolamide work?

A

Acetazolamide works in the proximal tubule
- Blocks the carbonic anhydrase, causes increased Sodium bicarb excretion

Not used in clinical practice as causes acidosis
- Used in ICU for ICU conditions

20
Q

Where and how does Manitol work?

A

This is an osmotic diuretic, it is filtered by glom then pulls water into proximal tubule by osmotic pressure. Nil pharmocodynamic action

21
Q

Where and how do Loop diuretics work?

A

Block the Na/K ATPase co-transporter in the ascending loop of henle, thereby reducing the meduillary tonicity and causing water to be retained in the tubules
- Causes increased sodium, potassium and chloride secretion

Therefore electrolyte complications include Hyponatraemia and hypokalaemia

22
Q

Where and how do thiazides work?

A

Blocks the sodium chloride co-transporter in the DCT
- causes hyponatraemia as a complication

23
Q

What is the corner stone of managing fluid overload in CKD pts? What drugs can be used?

A

Need to manage the salt
- CKD pts dont have a water excretion problem, they have a salt excretion problem

Non pharm:
- Need to reduce the salt with Na restriction +/- fluid restriction

Pharm:
- thiazides are first line for fluid overload (unless acute fluid overload). Pts are usually already on thiazide for BP control
-> thiazides are usually not very good tho because effect depends on the amount of Na that reaches the DCT. In CKD there isn’t much Na, therefore the diuretic effect is minimal-
- Loop diuretic: effect will depend on the degree of renal failure

24
Q

What aetiology of CKD generally speaking will require higher loop diuretics to achieve the same effect?

A

GLomerular disease (ie GN, HTN, DM related CKD)
- this is because need to get the drug through the diseased glom so need much more

25
Q

What is sequential blockade in CKD? what is it used for?

A

sequential blockade of the nephron with mutliple different class diuretics (loop, then thiazide, then MRA)
- used in fluid overload control

26
Q

What needs to be investigated/ corrected prior to starting an ESA?

A

Iron
- BM needs iron to make cells. ESA wont help if the iron is low
- aiming for ferretin 200-500 and Tsat 20-30% (higher targets than in non CKD pts

27
Q

What is the main principle behind ESA use in pts with CKD?

A

Symptoms managment
Reduce transusions and associated risks

28
Q

Target Hb for treating with ESA?

A

Hb 110

29
Q

Most common cause of EPO resistance?

A

Iron def

Then others:
- inflammation/infection
- High PTH
- B12/folate def (also required for haematapoesis)
- hypothyroid

30
Q

Protein amount per day for CKD pts?
Protein for pts on HDx?

A

0.6g/kg/day
1.2g/kg/day

31
Q

Why do CKD pts get acidosis? How is it managed?

A

H+ retention and inability to generate new bicarbonate

Managed with bicarb replacement aiming for bicarb >21
- this does incur a salt load but usually by this stage pts are on furosemide so it doesnt matter as much

32
Q

What happens to phospahte, Ca, and PTH in CKD?

A

As CKD gets worse, phosphate retention increases
- PTH level increased which promotes phosphate retention and mobiles calcium from the bone
- Phosphate in the blood binds calcium, resulting in hypocalcaemia which the body responds to by increasing PTH to mobilise Ca from the bone and to increase phosphate excretion

  • For a period of time, the phosphate level remains normal despite the progressive drop in phosphate excretion. This is due to the compensation of increased calcium mobilizations by increased PTH. However after a period of time, this system decompensates and serum phosphate begins to rise
  • Phosphate rises, PTH rises, FGF23 rises and calcium drops

Kidney is also responsible for conversion of 25OH vit D into 1,25OH vit D (active form). In advanced CKD this is impaired.
therefore active vitamin D levels drop, and calcium absorption from teh gut is imparied

33
Q

Basic treatment for CKD bone mineral disorder?

A
  • Calcium replacement orally (dont take with food)
  • Phosphate binds (take with food to bind dietary phosphate)
    -> sevelemer
  • Acitve vitamin D replacment (calcitriol)
  • CInacalcet if suspect tirtiary hyperparathyroidism
34
Q

Are flozins indicated for CKD without T2DM? What is teh specific criteria?

A

Yes
Have to have reduced GFR and albuminuria

35
Q

Pt with CKD, put on flozin then eGFR drops by 10. stop the drug or not?

A

No
FLozin are expected to acutley drop the eGFR similar to starting an ACEI. Long term beneficial

36
Q

Pt has severe itch on HDx, how to manage?

A

Moisturizer
Evening primrose oil
Carefully use of pregab and gabapentin (dose reduced)

37
Q

Main difference between CRRT and HDx?

A

CRRT is slower and can be used for haemodynamically unstable pts, therefore most appropriate for ICU pts with AKIs

Nephrology (3 decks)

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