Renal Disease Flashcards
physiology, DIKD, CrCl, CKD, dosing, CKD complications, dialysis
proximal tubule function
Na Ca and Cl are filtered into the nephron
pH regulated with H and bicarb exchange
SGLT2 transporter is here
where do SGLT2-i work
proximal tubule
descending LOH function
water reabsorption into the blood
ascending LOH function
water reabsorption via ADH (vasopressin)
~25% Na and Cl reabsorption into blood
Ca resorption
where do loops work and on what receptor
work on the ascending LOH where they block Na K pump to prevent sodium reabsorption
also block Ca reabsorption and can cause dec MBD with time
distal convoluted tubule function
K, Na, Ca, pH regulation
~5% of Na a reabsorbed into the blood here
thiazides work here and increase Ca reabsorption and are therefore bone-protective
collecting duct function
connect kidney to ureter
H2O and electrolyte final balancing via ADH and aldosterone
MRAs work here to dec Na and H2O reabsorption without affecting K
aldosterone function
increases K excretion in collecting duct
risk factors for DIKD
dec renal BF (HF, CKD, HLD, dec BP)
inc age
nephrotoxins
what are the major nephrotoxins
AGs
Amph B
loops
vanco
cisplatin
cyclosporine
NSAIDs
polymixins
radiographic contrast dye
tacrolimus
what is the BUN
amount of nitrogen in the blood that comes from urea, a waste product of protein metabolism
as renal disease progresses, kidneys are unable to filter urea out of the blood as it should
normal <20
what is Scr
waste product of muscle metabolism
norm 0.6-1.3
what GFR is stage 3a
45-59
what GFR is stage 3b
30-44
what GFR is stage 1
> /= 90
what GFR is stage 2
60-89
what GFR is stage 5
</= 15
what GFR is stage 4
15-29
how do we delay CKD progression
treat comorbidities DM and HTN
finerenone
first line for CKD + HTN +/- hyperalbuminuria
ACE or ARB