Adaptations to reductions in kidney function Flashcards
why could the kidneys fail to adapt?
too few nephrons
maladaptive adaptations can result in
- progression of kidney disease
2. complications of CKD in other organs
mechanisms of adaptation in glomerular and tubular
- glomerular : hypertrophy and increased kidney blood flow
2. tubular: alt. in reabsorption and/or secretion of solute
true or false in CKD total body sodium remains near normal until late stages
yep
what occurs in pt. even when sodium excretion per neprhon rises and DT sodium reabsorption is suppressed
HTN
potassium adaptation
increased excretion matched by the increase in potassium secretion
failure of adapatation for potassium in CKD
aldosterone deficiency such as during hyporenine (hypoaldosteronism states)
treatment for hyperkalemia in CKD
- low potassium diet
2. resins
in early stages of CKD we see the the balance between H+ and HC)3 is normal due to increased in
- NH3 generations
2. H+ secretion due to an increase in Na/H+ aantiporter and basolateral Na/HCO3 and change from type A to type B
in late stages of CKD metabolic acidosis develops due to decreased
- NH3 generation
- H+ secretion
- HC)3 reabsorption
tradeoffs to adaptation in the kidney
- increase NH3 lead to inflammation
2. increase risk of kisney stone
tradeoffs to adaptation in the Bone
1.loss of bone calcium due to the mobilization during acidosis leading to osteopenia
tradeoffs to adaptation in the muscle
- increased NH3 requires glutamine which is acquired through the breakdown of muscle “wasting”
CKD-MBD
systemic disorder of mineral and bone metabolism due to CKD
CKD MBD
- laboratory
- Bone
- Vasculature
- laboratory: abn. of Ca and Phosphorous, TH or vit. D metabolism
- Bone: abn. in bone turnover, mineralization, volume and linear growth or strength
- Vasculature: vascular or other soft tissue calcification
abn of mineral metabolism
- decrease in phosphate excretion
- decrease in free ionized calcium concentration
- decrease in alpha-hydroxylation of Vit. D
- increase in PTH
- increase in fibroblast growht factor
FGF-23 is released from
osteoclasts and osteoblasts in response to hyperphophatemia
FGF-23 reduces expression of ________ transporters in the PCT leading to a decreased in reabsorption
phosphate
FGF- 23 decreases 1-25 hydroxy vit. D synthesis by inhibiting ______ in tubular cells
1-alpha-hydroxylase activity
The ___________ represents the protean manifestations of waste retention
uremic syndrome
why do we see anmeia in CKD?
- iron deficiency
- reduction in red cell survival
- EPO resistance due to uremic toxins
adaptation to anemia might lead to
- increased C.O
- left ventricular hypertrophy and cardiac symptoms
- decrease in vascular resistance