C - Renal Function Flashcards
what is the best measure of kidney function
GFR
what is a normal GFR
120ml/min / 7.2L/hr
3 functions of kidney
waste excretion
metabolic balance including acid:base
water / urine excretion
what is the function of the glomerulus
water and low molecular weight molecules component filtrate, retains high molecular weight molecules
what is the function of the tubules
resorption of glomerular filtrate
by how much does GFR change with each year of life
1ml/min/yr
what can be used to estimate GFR
clearance
what is clearance
volume of plasma that is cleared of a substance per unit time
features of a suitable clearance molecule
not charged
not metabolised
not bound to serum proteins
freely filtered at glomerulus
what is the equation for clearance
C = U x P
what is the gold standard molecule to measure GFR
inulin
why is blood urea not used as a measure of GFR
increased by high protein intake or bleeding
decreased by liver disease and low protein intake
variable resorption by tubular cells
where is creatinine made
muscle cells
what does creatinine clearance depend on
muscle mass, age, sex, ethnicity
can decrease in surgery, starvation, steroid use
how is creatinine related to GFR
plasma creatinine ratio is inversely related to GFR
does a normal plasma creatinine ratio mean GFR is normal
NO - there is a lag between GFR dropping and plasma creatinine increasing
what is the cockcroft gault equation
eCCR = (1.23 x (140-age) x weight) / serum creatinine
when can cockcroft gault not be used
CKD
what is the MDRD equation
eGFR = (186 x (creatinine x 0.0113) ^-1.154) x age ^-0.203
when can MDRD not be used
healthy people - it’s only for CKD
pregnant people
doesn’t take into count weight so not for young / heavy
what does the CKD-EPI equation take into account
age, sex, race, serum creatinine
give an alternative molecule to creatinine
cystatin C
why is cystatin C a good alternative to creatinine for eGFR
independent from weight / muscle mass
reflects eGFR more accurately
good for xs muscle bulk patients
name types of urine exams
urine dip
MC&S
24hr urine collection
when is 24hr urine collection used
creatinine clearance estimate
stone forming electrolytes
if the dipstick is -‘ve for blood, is haematuria excluded?
YES
what does urine dip test for
pH, specific gravity, protein, blood, leucocyte esterase, nitrites, ketones, flucose
what proteins are detected / not detected on urine dip
albumin IS
bene jones proteins are NOT
if leucocyte esterase is negative, is this significant?
YES
what does nitrities on urine dip indicate
bacteria - esp gram neg
does glucose on urine dip = DM ?
NO - can be other things
urine with RBCs in indicates what
glomerular disease or stones
urine with casts in indicates what
glomerular disease
calcium oxolate stones. what has happened?
anti freeze poisoning
Ix for ?stones
<24hr PC = CT KUB
plain XR KUB
USS KUB - if preg / kid
IV urogram
when do you get staghorn calculi
chronic infection
contrast GFR decline in AKI and CKD
AKI = abrupt
CKD = slow
Is AKI or CKD reversible?
AKI is, CKD isn;t
What is the general Mx principles of AKI vs CKD in terms of aim of Tx
AKI = diagnose and reverse disease
CKD = limit progression and symptomatic
define AKI
rapid reduction in kidney function (acid base control, electrolytes, fluid)
what 2 measures are used to differentiate severity of AKI
serum creatinine
urine output
define the serum creatinine levels of the 3 levels of AKI
S1 = sCr raised by >26umol/L OR 1.5 to 1.9 x reference
S2 = sCr raised by 2 to 2.9 x reference
S3 = sCr raised by >3x ref or by >354umol/L
define the urine outputs of the 3 levels of AKI
S1 <0.5ml/kg/hr for 6-12 hours
S2 <0.5ml/kg/hr for >12 hours
S3 <0.3ml/kg/hr for >24 hours
name the 3 classifications of AKI
pre renal
renal
post renal
what causes pre renal AKI in general
poor renal perfusion (ischaemia) due to dysfunctional renin-aldosterone system
causes of pre renal AKI
dehydration (true volume depletion)
low BP
oedematous - HF / liver failure
renal artery sclerosis
drugs that alter glomerular blood flow
name drugs that can cause pre renal AKI
NSAIDs
calcineurin inhibitors
ACEi / ARB
diuretics
what is ATN & is it bad
acute tubular necrosis
- YES - irreversible ischaemic damage to tubules
4 causes of intrinsic renal AKI
vascular - vasculitis
glomerular - nephritis
tubular - ATN
interstitial
3 causes of intrinsic renal injury
amyloidosis
lymphoma
myeloma
what causes post renal AKI in general terms
physical obstruction to urine flow
causes of post renal AKI
ureteric obstruction - stones etc
prostate / urethra obstruction - BPH, cancer
blocked catheter
when is post renal AKI irreversible / reversible
irreversible = slow relief of blockage –> ischaemia, interstitial scaring, tubular damage
reversible = quick relief of obstruction
prognosis of AKI (% recovery etc)
40% full recovery
20% die
40% have some damage in between
how does AKI heal (4 processes)
haemostasis
inflammation
proliferation
remodelling
describe the spectrum of CKD
increased risk factors –> early damage –> lowered GFR –> renal failure –> death
describe the 5 stages of CKD
1 = kidney damage with normal GFR
2 = mild drop in GFR
3 = moderate drop in GFR
4 = severe drop in GFR
5 = end stage kidney failure
what is GFR of stage 1 CKD
> 90
what is GFR of stage 2 CKD
60-89
what is GFR of stage 3 CKD
30-59
what is GFR of stage 4 CKD
15-29
what is GFR of stage 5 CKD
<15 or dialysis
causes of CKD
DM ***** top cause
atherosclerotic renal disease
HTN
chronic glomerulonephritis
infective / obstructive uropathy
PCKD
name 4 consequences of CKD
progressive failure of homeostatic function
hormal function failure
CVD
uraemia and death
describe features of failure of homeostatic function seen in CKD
acidosis as can’t excrete H+ ions
muscle / protein degredation
osteopenia
heart dysfunction
Tx of failure of homeostatic function in CKD
oral sodium bicarb
features of hormonal function failure seen in CKD
anaemia - reduced epo producing cells
renal bone disease - fractures, pain, osteoporosis, osteomalacia, osteitis fibrosa
what is ostitis fibrosa
osteoclastic resorption of calcifed bone and replaced by fibrous tissues –> browns tumours
why can’t you just give epo to anaemic CKD patient
they increase BP
they won’t work if low iron, low folate, TB, Ca, hyperparathyroidism
how can CKD affect CVS
vascular calcification of arteries
ureamic cardiomyopathy *** mortality
3 phases of uraemic cardiomyopathy
LV hypertrophy
LV dilatation
LV dysfunction
