Jan18 M1-Acute Kidney Injury Flashcards
3 types of AKI
pre-renal, renal, post-renal
pre-renal AKI def
low BP, blood loss, hemodynamic prob (volume, pressure, fluid)
renal AKI def
disease of parenchyma (glomeruli, mesengium, tubules)
post-renal AKI def
obstruction (problem with urine outflow. stones, BPH, tumor)
causes of pre-renal AKI
relative drop in circulating volume (RAS, NSAIDs, CHF, cirrhosis/ascites, sepsis (vasodilation)) or effective drop in volume (GI loss, bleeding, etc.)
renal causes of AKI (5 main)
- acute GN (nephritic: APIGN, SLE, etc.)
- RPGN/crescentic
- ATN (post-infectious or toxic)
- AIN (drug-induced)
- Intratubular obstruction
post-renal causes of AKI
- prostatic disease
- pelvic or retroperitoneal malignancy
AKI definition
EITHER
1. plasma Cr +50 or + 50% or 50% drop GFR IN A MONTH
OR
2. oliguria (less 30cc/hour or less 200cc/8 hours)
anuria and oliguria def
anuria = less 50cc/day oliguria = less 500cc/day
how to calculate one’s minimal urine output
daily solute load in mosm/1200 mosmkg-1 (which is the max U conc)
ATN as cause vs as consequence of AKI
ATN can cause a renal AKI
ATN can be a consequence of a pre-renal AKI bc of ischemia and damage to the tubules
why ATN occurs
O2 level already low in medulla + high metabolism in the tubules (*PCT and TAL) so vulnerable to low flow
can ATN heal? why?
yes. tubules are epithelial cells, like skin, so they can repair
4 most common causes of AKI in the hospital
ATN, pre-renal, acute on chronic (already vulnerable bc low GFR), obstruction (urinary tract)
how to dx ATN vs pre-renal cause of AKI (clinically with no labs)
pre-renal: Cr and UO improved with fluid
ATN: takes days to months to repair (tubular damage)
labs to differentiate ATN vs pre-renal
ATN: urine sediment has muddy brown casts (dead tubular cells)
pre-renal: no muddy brown casts
can you get pre-renal failure from RAS alone?
no. need to add a clear cut time where the BP drop or gave ACEi
ATN vs pre-renal AKI: how U lytes can help** (must remember!!)**
pre-renal: U Na less 25 mM
ATN: U Na more 40 mM
best test to diff pre-renal vs ATN
FENa (fractional excretion of Na)
FENa value for pre-renal vs ATN AKI
less 1% = pre-renal
1-2% = can be any
more 2% = ATN
FENa formula
(UNa x PCr)/(PNa x UCr) x 100
other tests to check pre-renal vs ATN
serum urea to Cr: above 20 favors ATN (no urea reabso)
U osms: above 500 favors pre-renal (bc holding on to water)
gravity: more 1.020 is pre-renal (bc holding on to wateR)
treatment + what if no improvement in ATN
NS until euvolemia (check ctly volume status
Cr still rising in CHF + worsening = dialysis
how to control BP in unilateral vs bilateral RAS
unilateral: give ACEi (one kidney drops GFR, other increases)
bilateral: can’t give ACEi bc both kidneys drop their GFR
why are the patients hypertensive when they have RAS
RAAS activated. low flow to the kidney
NSAIDs can cause AKI in what specific patients and why
-pt with ongoing CKD
block PGs which dilate the AA
alternative to NSAIDs in CKD patients
ASA or tylenol
8 renal causes of AKI
- myeloma
- rhabdomyolysis
- TTP
- HUS
- AIN
- aminoglycoside toxicity
- contrast nephropathy
- RPGN
pathophgy (1 thing) in multiple myeloma (to the kidneys)
IgG produced by plasma cells can precipitate in the tubule and obstruct it
test to check for multiple myeloma
serum free light chains
rhabdomyolysis pathophgy to the kidneys
myoglobin is toxic to the PCT
pigment cast toxic to the distal tubule
how to check for rhabdo
+ for blood on dipstick but no urine on microscopy
TTP: thrombotic thrombocytopenic purpura. pathophgy to the kidneys
microclots form and go to the kidney, embolize the glomerulus and renal capillaries
why TTP is part of hemolytic anemias
if RBCs go through a microclot’s mesh, they are broken down
how to check for TTP (related to its cause)
ADAMTS13 molecule presence. if absent, is TTP. bc this molecule is supposed to break down endoth-platelet-vWF clots
HUS: hemolytic uremic syndrome pathophgy
damage to renal endothelium causing microembolic in the glomerulus
HUS associated with what
bad e.coli (toxin in it)
AIN def and cause (3 typical)
allergic rx of the kidney typically caused by antibiotics, PPIs and NSAIDs
AIN pathophgy
WBCs aggregate and block the blood flow to the kidney
aminoglycoside toxicity pathophgy
toxicity of certain antibiotics (..mycin) to PCT: tubular toxicity
AIN vs aminoglycoside toxicity and can you take the drug again?
AIN: allergy, can’t take it again
aminoglycoside toxicity: dose was too high, can take it again. not an allergy
contrast nephropathy pathophgy
causes intense renal vasoconstriction
why RPGN and crescents cause a problem
crescent compresses on glomerular capillaries
urine colour in RPGN
red or brown
3 types of RPGN
- anti-GBM
- immune complex (APIGN, lupus, IgA nephropathy)
- pauci-immune
pathophgy of pauci-immune RPGN
microscopic vascular disease where endothelium is damaged and mesengium and podocytes too
why US is the test of choice to verify for an obstruction OF THE URINARY TRACT
check for hydronephrosis
