AKI Flashcards
AKI can be __ or ___
which is worse?
oliguric
non-oliguric
*oliguric is worse
acute kidney injury definition
GFR decreases by >/ 25% within hours to days
three categories acute kidney injury
hemodynamic or pre-renal-imbalance of blood supply an ddemand
intrinsic or renal-okay blood supply with direct injury
obstructive or post-renal
what phase persists as long as insult is present?
apoptosis and sloughing phase
what do sympethetics do in renal injury
vasocon–>decrease renal BF–>increase NA reabs
pre-renal azotemia
littel, concentrated low Na urine; pre-renal
muddy brown casts
acute tubular necrosis
what is the main shift between AKI and ATN
urine osmolarity becomes isothenuric to the plasma
clinical causes of hemodynamic acute kidney injury
decrease in ECFV
- -hypobvolemia (hemorrhage, diarrhea)
- -hypervolemia (edematous state)
- -euvolemia (sepsis, SIRS, cap leak)
three types of intrinsic (renal) AKI
glomerular
tubulo-interstital
vascular
three ways tubular injury causes a decrease in GF
sloughing off cells decreases GFR
back-leak- holes in tubule let filtered blood go back
macula densa senses increased Na and Cl flow–>increases afferent tone–> decreases GFR
when does allergic interstital nephritis start
7ish days after causative agent
what will you see with AIN
WBC in urine
hallmark of rhabdo
pink urine + for heme but no blood on microscopy
treat of rhabdo
hydration and alkalinization of urine
Ig light chain
usually a marker of MM and non-oliguric
why do you get hyperuricemia
tumor lysis or inherent errors of purine metabolism
how does uric acid fuck up the kidney
crystallyzes in tubules and reabsorbed by PCT into tubulointerstium–>produces inflammatory rxn with giant cell
treatment of uric acid issues
volume expansion/alkalosis
xanthien oxidatse inhibitors (allopuritinol)
labs for uric acid issue
oliguric or non-oliguric
urine sediment bland or with crystals
serum UA >10
increase circulating phoshphatase and LDH
exogenous toxins that mess up kidneys
NSAIDs
iodinated contrast-moa
calcineurin inhib (cyclosporine, tacrolimus)–vasocon
aminoglycoside antibiotics-moa –>tubulue specific (RTA)
amphotericin B–>distal RTA, nephrogenic DI
Cisplatinum:distal tubular tox
crystals taht mess up kidneys
acyclovir idinavir methotrexate sodium phosphate quinolone
what else do aminoglycoside antibiotics cause
ototoxicity
renal vein occlusion
non-oliguric
loin pain
occurs in hypercoag states (cancer, nephrotic syndrome, sepsis)
thrombotic microangiopathies
occlusion of vessels with proliferating endothelial and platelet/fibrin thrombi
what do you see with thrombotic microangiopathies
oliguric aki
no cells or casts
post-renal AKI
obstruvtive
how does obstructive aki present
NOT oliguric back pressure is lower than GFR but highte than medullary capillary pressure nonanion gap acidosis (type IV) dilute urine hyperkalemia!
obstruction quick word
type IV RTA
polyuria with medication
induced nephrogenic diabetes insipidus
proximal RTA
myeloma
aminoglycosides
platinum
suggestive of bence jones protein
elevated urine protein with negative dipstick
indications for dialysis
volume overload
hyperkalemia
acidosis
uremia
multiple organ failure patients
cant do dialysis so solution is continuous venous-venous filtration which replaces plasma with electrolyte soln
definition of oliguria
<30 ml/hr