Lecture 56 - Physiological Adaptations to CKD Flashcards
what markers are used for tracking CKD?
why?
Cr and BUN
Cr - production rate is constant and relative to muscle mass
Production = filtration = elimination
A patient with CKD has been eating a high salt diet, what happens and why?
what is the FeNa of a CKD patient?
Patient will become edematous
FeNa > 1%
With decreased GFR; slow to eliminate extra Na; positive Na Balance = EDEMA
why is Urine Output a poor maker for kidney function
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
Where does the bulk of K excretion come from? how might this be affected in CKD patients
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
H+ excretion with CKD:
what three factors alter H+ excretion
Decreased H+ excretion:
1) decreased NH4 generation
2) decreased HCO3 reclamation
3) Decreased ability to generate pH gradient
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 _______
• 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
Describe the pathogenesis of renal osteodystrophy
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
FGF 23 - what is it ? is it elevatd or decreased in Renal osteodystrophy?
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
how do you treat Renal Osteodystrophy?
Decrease PO4 intake Use of PO4 gut binding resins Vit D replacment therapy Ca2+ receptor antagonists Parathyroidectomy
iatrogenic disease resulting from therapies of RO
Adynamic Bone disease – too much PTH suppression
Osteomalacia: too much ALOH3 use (a chelator of PO4)
how does CKD cause anemia
decreased EPO
approach to treatment in CKD patients?
what is the go to long term drug therapy?
Treat the underlying disease (HTN, DM)
Long term drug therapy: ACE I, ARBs (prolongs progression to ERSD and need for dialysis)