CKD Flashcards
Hypertension
- physiology
- aim
- Physiology
-Glomerulus - podocytes and foot processes. Filtration–>protein free
-Causes proteinuria, reduction in filtration, raised Cr and Urea
RAAS –>Hypertension
–ABPM: loss of nocturnal dip. - Aim
<140/90 (w/o albuminuria), <130 (with albuminuria)
Anaemia
- physiology
- aim
- treatment
- Hypoxia-inducible-factor (HIF) is a main driver for EPO synthesis.
- Less EPO produced in kidney
-Aim Hb 100-115
Treat
-Iron tf then EPO
A/E EPO
HTN
flu like sx
Acidosis
patho
treatment
kidneys unable to synthesise ammonia to bind to H+
a/w increased mortality
treatment: sodium bicarb
HyperK
patio
treatment
RAAS inhibition + tubulo-interstitial dysfunction
Resonium
Dialysis
CVD
- patho
- prognostic markers
HTN, DM, CKDMB–> Vasc calcifications, inflammation, anaemia, proteinuria
Prognostic markers - elevated PO4, FGF-23 levels
Renal bone disease
Physiology
Inadequate PO4 clearance –> stimulates FGF-23
- FGF-23 –> reduce Vit D and PO4 gut absorption
- PTH stimulation from low Vit D and High PO4 - increases Ca and promotes EPO resistance
Renal bone disease
Treatment
-diet
-PO4 binders - Sevelamer, Lanthanum (Ca based)
OP - bisphosphonates
FGF-23
secretion
function
secreted by osteocytes
Function
- Increase PO4 excretion
- Suppress formation of calcitriol in gut –> decrease PO4 absorption from gut
- Stimulation of PTH –>increases renal PO4 excretion
Calciphylaxis
RF
Mortality
- also known as calcific uremia arteriolopathy
- painful skin lesion due to cutaneous arteriolar calcification –>tissue ischemia and infarction
- mortality in 1 year 50% due to sepsis
RF - female, ESRF, Caucasian, comorbidities, medications - Warfarin, Steroids, Ca-based binders, Vit D
Calciphylaxis
- Mx
- Avoid hyperCa
- Keep PO4 low
- Stop Ca supplements + Ca-based PO4 binders
- Avoid high Ca dialysate baths
- Use Cinacalcet for hyperPTH
- Avoid triggering meds - ie Warfarin
- Sodium Thiosulfate (Side effects ofsodium thiosulfateinclude metabolic acidosis and fluid overload)
