drugs and the kidney Flashcards
what is best predictor of kidney functions
GFR
what is GFR
sum of filtration across all the nephrons (ml/min)
what is perfect way to measure GFR
give substance that is not secreted or reabsorbed and measure output in urine
what are problems with using Crr
- can have slight variations despite stable GFR
- different assays give slightly different results
- actives SECRETED from proximal tubule
- tied to muscle mass
2 uses of Cr
- use to measure clearance
- 24 hours - used to estimate GFR or clearance
- equations for both
what is equation for clearance and issues
cockroft gault
- overestimate GFR when severely impaired
- imprecise when near normal
4 variables used in estimating GFR
- age
- sex
- serum Cr
- race
what is key to GFR estimation
need to be in steady state
3 general classes of drugs that have a renal effect
- RAAS
- diuretics
- ADH
3 main outcome of RAAS activation
- incr. aldosterone
- vasocontriciton
- increase Na reabsorbtion
4 main drugs that affect the RAAS
- renin inhibitors
- ACEi
- ARB
- blockers of aldo - spironoloactone
what are 4 main classes of diuretics
- carbonic anhydrase inhibs
- loops
- thiazide
- K sparing
main actions of diuretics
- reduce Na content - reduce ECF
- increase Na excretion
- if proximal to CCD - K wasting
action of carbonic anhydrase
- weak
- block in brush border of proximal tubule
- also excrete bicarb
action of loops
- most potent
- can work with thiazides
- block reabsorbtion of Na in thick ascending loop
action of thiazides
block reabsoption at distal collecting duct
4 important SE of thiazides
- dydlipidemia
- hyponatremia
- hyperuricemia
- hypercalcermia
2 main actions of K-sparing
- block aldo from binding
2. bind to the eNaC channel
what is ADH
vasopressin
- inserts aquaporin channels in the medulary collecting duct
- VAPTANS compete for binding with ADH sites
3 drugs associatied with pre-renal AKI
- diuretics
- increase Na loss - RAAS blockade
- block ang2
- results in efferect vasodilation and decreased pressure - NSAIDS
- inhib. prostaglandins
- neeeded to vasodilate afferent arterioles
drugs that can cause tubular necrosis
- aminoglycosides
- amphoceterin
- cisplatin
- IV contrast
** what is clinical picture of drug induced AIN
AKI 7-10 days aftere
- WBC casts
3 options of dose adjustments in renal patients
- none
- increase dosing interval
- reduce dose
what does dose adjustment rely on
- extent it is renally cleared
2. degree of renal impairment
7 step approach to drug dosing in renal disease
- what is GFR (>60 not a prob)
- is the drug effective in low GFR
- is the drug safe in CKD
- is the drug nephrotoxic
- is immediate effect needed to desired
- loading - same
- maintenance - may need to adjust - is the drug extensively elimnationed by kidney
- does the drug have an active/toxic metabolite that is renally excreted
