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Renal 3 > Alex: Chronic Kidney Disease (Progression and Complications) > Flashcards

Alex: Chronic Kidney Disease (Progression and Complications) Flashcards

1
Q

What is true of individual rates of decline in terms of GFR in CKD ?

A

Each person with CKD has their own individual rate of decline of GFR that is unique to them and stays the SAME throughout the course of their disease

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2
Q

At what GFR do you usually give dialysis or transplant ?

A

GFR < 15, ( she usually shows it under 10)

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3
Q

List the two non-modifiable risks for progression of CKD

A

Race and Gender

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4
Q

What are 3 Modifiable risk factors for the progression of CKD ?

A

HTN
Diabetes
Compensetory Hyperfiltration (Intraglomeruar HTN and Nephron Hypertrophy)

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5
Q

At what BP should you consider ACEi or diuretic to help prevent CKD complication in patients with Diabetes Mellitus Type II?

A

Trick question ! BP should have nothing to do with it. BP lowering meds can be given to any DM2 patient for prevention of CKD and its complications

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6
Q

What is the BP goal for patients with Stage I-IV CKD who also have Proteinuria or Diabetes ?

How about for Stage I-IV w/o proteinuria ?

A

125/75 or less

135/85

Compare this to BP goals for the ten pop ( 140/90)

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7
Q

what percentage of people with CKD have controlled HTN ?

A

Less than 40%

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8
Q

How many drugs is the average patient with CKD and HTN on to control BP ?

A

At least 2

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9
Q

Most therapies to control BP do so by altering what regulatory system ?

A

RAAS

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10
Q

What molecule in the RAAS pathway is the most important target for reducing Intraglomerular pressure in Compensatory Hyperfiltration ?

A

Angiotensin II (It causes vasoconstriction of the efferent arteriole)

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11
Q

What adverse effects does AT II cause ?

A

Glomerular capillary hypertension
Abnormal glomerular permselectivity
Mesangial cell proliferation
Induction of TGF-b with increase in extracellular matrix
Stimulation of adrenal production of aldosterone

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12
Q

What do the adverse effects of AT II ultimately cause ?

A

Interstitial fibrosis

Glomerulosclerosis

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13
Q

List the 4 classes of drugs that will shift the RAAS axis

A

ACEi
ARB
Aldosterone Inhibitors
Renin Inhibitors

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14
Q

Administration of ACE or ARBs will lead to which effects within the glomerulus ?

A

Decreased efferent arteriole vasoconstriction

Decreased glomerular filtration pressure

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15
Q

By limiting RAAS activation of Intraglomerular HTN and Glomerular HTN, what process is being limited by the use of Anti-RAAS drugs ?

A

Glomerular scarring and fibrosis

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16
Q

ACE and ARBs have been shown to slow the progression of CKD in patients who are Diabetic , Non-Diabetic or both ?

A

BOTH !

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17
Q

ACEi and ARBs decrease glomerular fibrosis and scarring by decreasing of inhibiting which 4 processes ?

A

Mesangial deposition
Proteinuria
Release of TGF-b
Inhibition of pro-collagen formation.

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18
Q

Aggressive treatment with ACE/ARB’s is needed at which BP’s for patients with CKD ?

A

SBP< 130 & DBP< 80 mmHg with presence of 1-2 gm/d proteinuria

Even more aggressive BP goals with diabetic nephropathy or greater degrees of proteinuria

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19
Q

What is the goal for decreasing baseline proteinuria in patients with CKD ?

A

Try to decrease it by 50%

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20
Q

What is more important : Increasing GFR by glomerular hyper filtration or preventing scarring by keeping GFR low ?

A

PREVENTING SCARRING …Increasing GFR is good in the short run but it is a map-adaptive consequence of CKD.

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21
Q

What electrolyte is important to check with anyone who is on RAAS inhibitors ?

A

K+

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22
Q

What class of drugs should you avoid when dealing with patients with CKD ?

A

NSAID’s

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23
Q

Why might you see anemia in CKD ?

A

The kidney produces erythropoietin. In CKD this is diminished due to fibrosis of specialized tubular cells that produce this.

Leads to Normochromic, normocytic anemia (Look normal, have normal B12 and iron levels. Just not enough RBC’s.

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24
Q

What is the treatment for anemia due to CKD ?

A

Human recombinant Erythropoietin (EPO) (IV or sub-cue)

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25
Q

At what hemoglobin levels should you treat anemia in CKD ?

A

when hemoglobin 10

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26
Q

What are patients who receive Human recombinant Erythropoietin (EPO) therapy at risk for ?

A

Thrombosis (cardiovascular events, stroke, vascular events are also seen.)

27
Q

What is the first step in activating Vit D ?

A

hydroxylation at the 25 position by the liver

28
Q

What is the second step in activating Vit D ?

A

Hydroxylation at the 1 position by the kidney

29
Q

What is the name of the active form of Vit D ?

A

Active form of vitamin D is called 1,25 Vitamin D

30
Q

What would you expect the 1,25 Vitamin D levels in the body to be in a patient with CKD ?

A

They will be decreased (25 Vitamin D is normal however)

31
Q

Normally, phosphorous levels in the body are maintained by dietary intake and cellular turnover/lysis of bone matrix while being filtered by the kidney. What would you expect the plasma levels of phosphorous to be in a patients with CKD ?

A

HIGH

Low GFR reduces the amount of phosphate lost in the urine

32
Q

What is the serum level of Ca++ in patients with CKD ?

A

Typically, low

33
Q

low Ca++ levels will signal the release of which endocrine molecule ?

A

PTH

34
Q

High Phosphorous levels (as seen in CKD) will lead to the release of which endocrine molecule ?

A

PTH (So , low Ca++ and High phis. –> PTH release.)

35
Q

PTH will lead to increased production of this molecule that Increases intestinal Ca (mostly) and Phos absorption ?

A

1,25 (OH)2 Vitamin D

36
Q

What effect does PTH have on renal action towards phos and 1,25 (OH)2 Vitamin D ?

A

Increases renal calcium reabsorbtion and phosphate excretion

37
Q

What affect does PTH have on bone osteoclasts ?

A

Increases osteoclast bone resorbtion to increase Serum Ca++

38
Q

High serum levels of PTH will have what effect on FGF-23 release in the bone ?

A

It will increase the release of FGF-23

39
Q

What is the effect of FGF-23 on 1,25 Vit D levels

A

Inhibits 1-alpha hydroxylase thus 1,25 Vit D levels

40
Q

What effect dos FGF-23 have on phosphate ?

A

Increases renal phosphate excretion

41
Q

What effect does FGF-23 have on PTH ?

A

Decreases PTH secretion

42
Q

What is the overall pattern for those with CKD in regards to levels of Ca++, Vit D, PTH and FGF-3

A

Decreased:
Ca++,
Vit D

Increasd :
PTH (probably an adaptation to low Ca++ and
FGF-3 (has the effect of decreasing VitD and thus Ca)

43
Q

What is the trade off hypothesis ?

A

The physiologic response to an alteration in body homeostasis may fully or partially correct the imbalance in the short term yet have detrimental effects over time

44
Q

Define Primary Parathyroidism

A

Autonomous development of a solitary parathyroid adenoma

Characterized by hypercalcemia and hypophosphatemia (Increased Ca++ release from bone, increased Phos secretion)

45
Q

Define Secondary Parathyroidism

A

Compensatory increase in PTH levels as an appropriate response to a stimulus of:
Hypocalcemia ( leads to increased PTH release)
Hyperphosphatemia (PTH increases excretion of Phos)

FOUND PRIMARILY IN PATIENTS WITH CKD !

Produces a nodular hyperplasia

46
Q

What is an example of a high bone turnover disease due to excess PTH , seen in CKD?

A

Osteitis fibrosa cystica

47
Q

What is an example of a low bone turnover disease see in in CKD ?

A

Osteomalacia

48
Q

What is recommended regarding Phos levels when trying to prevent bone disease ?

A

Maintain serum phosphorous <5.5 mg/dl:

49
Q

What should dietary intake of Phos be to help prevent bone disease ?

A

Dietary phosphorous restriction (800-1000 mg/d)

50
Q

What are two calcium based ‘binders’ of dietary phosphorous ?

A

Calcium carbonate

Calcium citrate

51
Q

What are two Non-calcium based binders of phosphorous ?

A

Sevalamer- (Renagel and Renvela)

Lanthanum – (Fosrenol

52
Q

Aluminum based antacids can also be used to bind phosphorous but what must be avoided when using these?

A

avoid prolonged rx due to possible aluminum accumulation in the brain causing encephalopathy

53
Q

How often must you monitor PTH , Ca++ and Phos once patient reaches Stage III CKD ? (GFR of 30-59)

A

Every 3-6 months

54
Q

What can you give to counteract VIt D depletion in a manner that raises the active Vit D levels leading to decreased bone loss ?

A

Calcitriol (1,25 (OH)2D3)

55
Q

What Vit D receptor Agonist can be given to help stop bone loss by stopping PTH release ?

A

Calcimimetics (cinacalcet-SensiparR)

binds to the calcium receptor and mimics high calcium levels in an attempt to make the parathyroid cells stop producing PTH

High PTH levels will lead to bone loss

56
Q

What is the leading cause of death to those with CKD ?

A

Cardiovascular disease

Contributing factors include:
Hypertension
Diabetes mellitus
Hyperlipidemia
Vascular calcification
Smoking
Others- Vitamin D deficiency, FGF-23
57
Q

What occurs to the media of blood vessels in patients with CKD ?

A

Calcification
Linear deposits along elastic lamellae. At most severe, a dense circumferential sheet of calcium crystals (Arteriosclerosis)

58
Q

Where else in the vasculature might you see calcification in patients with CKD ?

A

The Intima (Atherosclerosis)

Diffuse punctate morphology. Aggregates of calcium crystals

59
Q

What is the physiologic response in the body to counteract the metabolic acidosis seen in CKD ?

A

Dissolution of bone to increase bicarbonate in the blood.–> Increased bone loss

60
Q

To treat metabolic acidosis seen in CKD, you can give bicarb tablets or Sodium citrate solution. What is a side effect of this treatment ?

A

All HCO3 preparations must be given as a sodium salt therefore patient run the risk of accumulating excess sodium
May require more diuretic therapy

61
Q

As CKD progresses, sodium retention occurs and the patients go into positive daily sodium balance. What will this lead to ?

A 
FLuid retention (Increased extracellular volume leading to edema and possibly pulmonary edema
)
62
Q

What is the treatment of choice for fluid retention in CKD ?

A 
Thiazide diuretics (up to stage 4 . Dependent on GFR for effectiveness)
Loop diuretics (stage 4 and higher. Not dependent on GFR)
63
Q

Is there a direct correlation between BUN or Creatinine serum concentrations and the development of Uremic Syndrome ?

A

There is no direct correlation between the absolute level of BUN and creatinine in the plasma and the development of uremic symptoms

64
Q

What are common manifestations of uremic syndrome ?

A 
Anorexia/weight loss
Nausea
Vomiting
Pericarditis
Peripheral neuropathy
CNS abnormalities

Renal 3 (17 decks)

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