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Renal > Chronic Kidney Disease > Flashcards

Chronic Kidney Disease Flashcards

1
Q

What are people with CKD most likely to die from?

A

Cardiovascular events

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2
Q

CKD is defined as what 2 things?

Which determines the stage of the disease?

A
  1. kidney damage
  2. GFR less than 60 for more than 3 months

The GFR determines the stage and is the best assessment of overall kidney function

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3
Q

What is the gold standard for measuring GFR and why is it not used?

A

Inulin or iothalamate clearance is the gold standard but it is not used frequently because:

  1. it is an exogenous substance so you need to IV the patient to have them reach steady state
  2. It is expensive
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4
Q

What are the drawbacks of using CCr for measuring GFR?

What can it be averaged with to give a more accurate assessment of glomerular function?

A
  1. depends on muscle mass, race, gender, age
  2. tends to overetimate GFR in patients with kidney disease
  3. tends to underestimate in patients on trimethoprim (bactrim) and cinetidine

Average the CCr with the urea because Cr tends to overestimate and urea tends to underestimate.

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5
Q

What are the 2 equations that can estimate GFR bedside? Which is better to use in people with a GFR below 90?

A
  1. Cockcroft-Gault
  2. MDRD

They take into account ethnicity, gender, age, serum Cr

MDRD is better for patients with GFR below 90

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6
Q

What physical exam finding is a usual marker of kidney damage?

A

increased proteinuria

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7
Q

What is characteristic of stage 1 CKD?

A
  1. persistent proteinuria (>3 months)

2. normal or increased GFR (>90)

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8
Q

What is the preferred method for measuring proteinuria?

A

Total Protein to Cr ratio

or

Albumin to Creatinine ratio

These are both better than measuring timed urine collection (many errors)

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9
Q

What are the 5 stages of CKD?

A 
1- persistent proteinuria with increased/normal GFR
2- kidney damage with GFR 60-89
3- GFR 30-59
4 - GFR 15-29
5- GFR <15
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10
Q

What stages of CKD should be treated by

  1. taking care of comorbid conditions
  2. intervening to slow progression
  3. reducing cardiovascular disease

What specific measures are taken?

A

Stages 1 and 2

Evaluate and treat BP by:

  1. block RAAS (ACEI/ARB)
  2. low protein diet
  3. control glucose
  4. treat hypercholesterolemia
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11
Q

What is the GFR cutoff for stage 3 CKD?

What should be evaluated and treated at this stage?

A

GFR 30-59

  1. anemia
  2. malnutrition
  3. bone disease
  4. neuropathy
  5. quality of life
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12
Q

What is the GFR cutoff for stage 4?

What treatment should take place at this stage?

A

15-29

Prepare for renal replacement therapy

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13
Q

What is the GFR for stage 5 CKD?

What should be evaluated and treated?

A

Evaluate uremia levels, look for dialysis options and kidney replacement.

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14
Q

When is it recommended to assess for kidney disease? How is the assessment performed?

A

ALL health encounters.

  1. calculate eGFR
  2. test for presence/absence of proteinuria
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15
Q

What happens to salt and water excretion per glomerulus and overall as the patient progresses in CKD?

A

The renal mass shrinks (less glomeruli) so the remaining glomeruli will increase filtration (hyper) in order to recover the loss of the other glomeruli.

This results in increased excretion per nephron but normal to slightly decreased Na/H20 excretion overall

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16
Q

What is the goal for salt balance in the diet of a patient with CKD?

What tells you if the salt intake is too low? too high?

A

A level of salt that keels the patient normotensive, at a constant weight with only slight edema

6-8 g/day is the starting point

Too low if the patient loses weight and becomes more azotemic

Too high if the patient gains weight and has edema and hypertension

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17
Q

When a patients GFR drops below 20, salt-restricted diets may exceed the capacity of the kidney to excrete. What should be added to the treatment regimen if this is the case?

A

Add a diuretic (specifically furosemide 2x daily)

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18
Q

Are people with CKD more likely to develop hypernatremia or hyponatremia?
What should fluid intake be for a person with CKD?

A

Equally because they lose the ability to concentrate AND dilute the urine as the kidney becomes progressively impaired.

Water intake should equal urine output plus 1000 to 1500 ml/day for insensible loss

19
Q

How is a hyponatremic volume-overloaded patient be treated?

How should a hyponatremic, hypovolemic patient be treated?

A

Volume overloaded- restrict water intake

hypovolemic- water restriction with judicious addition of salt. Withdraw of diuretic

20
Q

K balance is maintained until the GFR falls below what value?
What are the 2 ways it is able to maintain the balance?

A

10

  1. increase extrarenal excretion (colon)
  2. increase excretion via the remaining working nephrons
21
Q

If there is hyperkalemia at a GFR above 10, what is the likely problem?

A
  1. TIN (type IV RTA)

2. RAAS disturbance

22
Q

What is the initial treatment for someone with CKD that has developed hyperkalemia?

If after this and it persists, what would you treat the patient with if they were also:

  1. edematous/hypertensive
  2. acidotic

If STILL persisting, what do you add?

A
  1. K restricted diet (50-70mEq)
  2. If it persists:
    Furosemide -esp if edematous or hypertensive bc increases distal delivery
    NaHCO3 if acidotic (acid brings K out of cells, base pushes it back in) also, increases distal delivery (NRA)
  3. If STILL persisting add K-binding resin (Na polystyrene) given with sorbitol to prevent constipation
23
Q

As CKD progresses, patients develop metabolic acidosis. At first it is _______________ but as the insufficiency advances, it becomes ______________________________.

If left untreated, what can acidosis lead to?

A

NG ——-> acid gap

It can lead to:

  1. bone resorption
  2. protein catabolism
  3. dyspnea and malaise
24
Q

What therapy must be provided to prevent the bone pathology associated with CKD?

What are complications?

A

Keep bicarb above 22 because the acidotic conditions are what really contribute to the bone resorption and protein catabolism.

NaHCO3 tablets – complications are:

  1. increased volume
  2. met alk
  3. aluminum with citrate absorption –>toxicity
25
Q

What is the effect of CKD on phostphate and calcium?

Early and Late

A

Early : As the GFR declines, serum phosphate rises which causes a reciprocal decrease in serum Ca.

The decrease in Ca causes a release of PTH which is able to increase phosphate excretion by the remaining nephrons. This returns Ca and P levels to normal range (but at the expense of increasing PTH).

Late:
Stage 3 have elevated PTH and evidence of osteitis fibrosa cystica of bones. Eventually even the extreme PTH can’t overcome P retention and the person becomes hyperphosphatemic

26
Q

What are the 2 things that lead to hypocalcemia in a patient with CKD?

A
  1. decreased GFR increases serum phosphate which lowers serum Ca
  2. decreased renal mass leads to a decline in circulating 1,25 vit D leading to hypocalcemia (because less is absorbed from the intestine AND vit D is not inhibiting PTH causing secondary hyperparathyroidism)
27
Q

What is primary treatment for patients with CKD and hyperphosphatemia?

A
  1. phosphate restricted diet (cut out eggs, meat, cream, cheese)
  2. phosphate binder to increase fecal excretion
28
Q

When oral phosphate binders are necessary, how does one determine whether to use calcium or non-calcium binders?
Why is it crucial to make this distinction?

A

Look at the calcium x phosphate product

Normal Ca = 9
Normal P = 4
Normal product = 36

If P is higher than 7 or product is higher than 63, use a non-calcium binder.
If a ca binder is used above 7 or 63, the patient will have metastatic calcifications

29
Q

In patients with stage 3 CKD and increased PTH,
what should be measured and replenished if low?

What should you use to replenish if the patient is in stage 3, 4 with normal 25 vit D levels?

A
  1. Increased PTH means high P, low Ca.
    You want to check 25 vit D levels and replenish if they are low (*there is enough kidney function to convert to 1,25)
  2. Active 1,25 vit D
30
Q

Should the target PTH for patients with CKD be higher, the same or lower that for people without?

A

Higher because it is required for normal bone remodelling

31
Q

What are the four manifestations of renal osteodystrophy with CKD?

A
  1. osteitis fibrosa cystica- increased PTH
  2. osteomalacia- decreased vit D
  3. adynamic bone disease
  4. mixed uremic
32
Q 
What is osteitis fibrosa cystica?
What is the clinical presentation?
What do radiographs show?
What lab value will be elevated?
What are the 2 general choices for management?
A

A persistent secondary hyperparathyroidism resulting in high bone turnover (due to increased PTH)

Clinical: bone pain and increased fracture risk
Radiograph: reabsorption in phalanges/clavicle

Alkaline phosphatase will be elevated

Manage with:

  1. vit D analog or cinacalcet
  2. reduce phosphate
33
Q

What is adynamic bone disease?
Is it high or low turnover?
What stage of CKD does it present in?

A

It is a low turnover condition in Stage 5 CKD due to overuse of Vit D or calcium loading which results in a hypoparathyroidism

34
Q

In what stages of CKD does anemia become apparent? What causes it?
What is the most deleterious complication of anemia?
What should be used to treat? What level of Hb should treatment be started?

A

4 or 5- there is a reduced production of epo

It can lead to LV hypertrophy and cardio complications

Erythropoeiten Stimulating agens (ESAs) should be initiated in patients with CKD and a Hb below 9.

35
Q

Patients with CKD and anemia who are not responding to ESAs should be assessed for what concurrent malaties?

A
  1. Fe deficiency
  2. blood loss
  3. infection
  4. secondary hyperparathyroidism etc etc
36
Q

What is the BP target for patients with minimal proteinuria?
What is the BP target for patients with significant proteinuria?

What is the preferred anti-hypertensive in patients with CKD?

A

Minimal (less than 1g) = 130/80

Significant = 125/75

ACEI or ARB

37
Q

What is the guidelines for using ACEI and ARB for CKD?

What are 2 negative effects?

A

It is drug of first choice.
Since it blocks AII, it will reduce efferent arteriolar resistance and lower intraglomerular pressure decreasing the GFR.

Neg effects:

  1. You will see a slight increase in serum Cr but this is acceptable up to a 30% increase in serum Cr after initiation of ARB/ACEI
  2. hyperkalemia
38
Q

What are the 2 effective therapies for patients with ESRD?

How do you decide which to use?

A
  1. Peritoneal dialysis
  2. Hemodialysis

Patient decides which to do, but consider motivation, underlying conditions, social support

39
Q

What are the symptoms associated with uremia?

A

Elevated BUN and Cr cause:

  1. nausea, vomiting
  2. altered food taste
  3. anorexia
  4. sleep wake cycle disturbances
40
Q

When does the typical patient receive dialysis?

A

3 times a week for 4 hours a session

41
Q

How does hemodialysis work?

A

You use a semipermeable membrane to separate the blood from a dialysate compartment.

  1. Solutes flux across the membrane as determined by concentration gradient. (urea out of blood, bicarb into blood)
  2. fluid is removed via ultrafiltration which uses a transmembrane pressure gradient (a small amount of solute is also removed via solute drag)
42
Q

What are the 2 types of peritoneal dialysis?

A

CAPD- chronic ambulatory peritoneal dialysis where 2 L of diasylate is infused into peritoneal space where the fluid remains for 6 hours. Repeat 4 exchanges a day

CCPD - continuous cycling peritoneal dialysis where an external device allows 10-12 L of diasylate to cycle through peritoneal space during sleep

43
Q

How does peritoneal dialysis differ from hemodialysis chemically? clinically?

A

Chemically- it uses osmotic pressure (enhanced by glucose) instead of hydrostalic pressure for ultrafiltration. Lactate is used instead of bicarb in peritoneal because bicarb would precipitate with Ca and Mg.

Clinically- patient can perform peritoneal themselves so there is less hospital visits

Renal (11 decks)

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