Lecture 56 - Physiological Adaptations to CKD Flashcards

1
Q

what markers are used for tracking CKD?

why?

A

Cr and BUN

Cr - production rate is constant and relative to muscle mass
Production = filtration = elimination

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2
Q

A patient with CKD has been eating a high salt diet, what happens and why?

what is the FeNa of a CKD patient?

A

Patient will become edematous

FeNa > 1%

With decreased GFR; slow to eliminate extra Na; positive Na Balance = EDEMA

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3
Q

why is Urine Output a poor maker for kidney function

A

CKD: Cannot concentrate urine as well; but the body needs to excrete a minimum amount of solute per day

in order to do so – CKD patients might produce mcuh more urine

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4
Q

Where does the bulk of K excretion come from? how might this be affected in CKD patients

A

K - excreted in the distal nephron (principle cells) by ROM K Channles –

Drugs that interefere with K secretion; CKD patients at risk for hyperkalemia

  • eg: Spironolactone, ACE I
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5
Q

H+ excretion with CKD:

what three factors alter H+ excretion

A

Decreased H+ excretion:

1) decreased NH4 generation
2) decreased HCO3 reclamation
3) Decreased ability to generate pH gradient

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6
Q

Early CKD there is a ______Metabolic acidosis, due to _______

Later CKD there is a _______ metabolic acidosis, due to ______

Acidosis in part can lead to the development of _______
which can be partially treated by _______

A

• Early CKD: Non AG acidosis — decreased NH3 genesis

Late CKD: High AG Acidosis – decreased excretion of Titratable Acids

Renal Osteodystrophy (H+ balance bufffered by bones)

Can treat with HCO3 replacement

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7
Q

Describe the pathogenesis of renal osteodystrophy

A

Kidney contains enzyme necessary for hydroxylation of Vit D to its active form (1,25 (OH)2 Vit D)

Decreased Vit: less gut absorption of Ca2+

Decreased PO4 excretion (chealator of Ca2+) = More PO4 in the serum; decreased Ca2+

Overall Less Ca2+ = Increased PTH activity (parathyroid hyperplasia)
Bone Re-absorption

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8
Q

FGF 23 - what is it ? is it elevatd or decreased in Renal osteodystrophy?

A

New biomarker for RO

Normal role: acts on the kidney to increase PO4 excretion and decrease PTH activity

Kidney disease, receptors are destroyed, therefore FGF23 concentration elevated in RO

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9
Q

how do you treat Renal Osteodystrophy?

A
Decrease PO4 intake
Use of PO4 gut binding resins 
Vit D replacment therapy 
Ca2+ receptor antagonists 
Parathyroidectomy
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10
Q

iatrogenic disease resulting from therapies of RO

A

Adynamic Bone disease – too much PTH suppression

Osteomalacia: too much ALOH3 use (a chelator of PO4)

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11
Q

how does CKD cause anemia

A

decreased EPO

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12
Q

approach to treatment in CKD patients?

what is the go to long term drug therapy?

A

Treat the underlying disease (HTN, DM)

Long term drug therapy: ACE I, ARBs (prolongs progression to ERSD and need for dialysis)

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