1/32
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced |
---|
No study sessions yet.
How is acute kidney injury defined?
an abrupt decline in kidney function over 7 days or less that may represent injury, risk for damage, or actual damage to the kidney itself
KDIGO serum creatinine for stage 1 AKI
1.5-1.9 times baseline in 7 days OR >= 0.3 mg/dL increase in 48 hours
KDIGO urine output for stage 1 AKI
< 0.5 mL/kg/hr for 6-12 hours
KDIGO serum creatinine for stage 2 AKI
2.0-2.9 times baseline in 7 days
KDIGO urine output for stage 2 AKI
< 0.5 mL/kg/hour for >= 12 hours
KDIGO serum creatinine for stage 3 AKI
3.0 times baseline in 7 days OR increase in SCr to >= 4 mg/dL OR initiation of renal replacement therapy OR in patients < 18 years with a decrease in eGFR to < 35 mL/min per 1.72 m2
KDIGO urine output for stage 3 AKI
< 0.3 mL/kg/hour for >= 24 hours OR anuria for >= 12 hours
what are the three AKI classifications?
Pre-renal AKI, Intrinsic AKI, Post-renal AKI
examples of Pre-renal AKI
decreased kidney perfusion (severe dehydration) and decreased effective circulating volume (heart failure)
what occurs when there is decreased kidney perfusion and decreased effective circulating volume?
decreased renal blood flow which leads to hypoperfusion of kidneys (leads to decrease in GFR and increased Na/H2O reabsorption at the proximal tubule) - these lead to increased aldosterone and ADH secretion, increased Na/H2O reabsorption at the distal tubule, and AKI/oliguria
what causes intrinsic AKI?
glomerulonephritis, tubulointerstitial nephritis, acute tubular necrosis, vasculitis, and is often drug induced
if intrinsic AKI is left untreated most forms of kidney injury will result in ______________________
ATN (acute tubular necrosis)
what is the pathophysiology of ischemic ATN?
autoregulation of afferent arteriole constriction decreases oxygen demand in the medullary nephrons to prevent damage via macula densa cells and tubuloglomerular feedback
what happens to GFR when the kidneys work to protect medullary nephrons in ischemic ATN?
GFR decreases
T/F: if there is severe hypoxia or presence of multiple risk factors in ischemic ATN, they will overwhelm protective mechanisms and lead to AKI
true
what effects decrease the risk of ischemic ATN?
decreased tubular transport, decreased GFR, prostaglandin E2, adenosine, bradykinin, nitric oxide
what are some exacerbating effects of ischemic ATN?
nephrotoxic medications (aminoglycosides, amphotericin, IV iodinated contrast), NSAIDs, angiotensin II, calcium, myoglobin
exmaples of post-kidney AKI
nephrolithiasis, benign prostatic hyperplasia (BPH), and malignancy
How can kidney stones, BPH, and malignancies cause AKI?
there is an obstruction to urine outflow which leads to increased intraluminal pressures, release of inflammatory mediators, cellular and interstitial edema, renal vasoconstriction, medullary hypoxia, renal tubular injury - ultimately leading to decreased GFR
where can kidney stones obstruct?
in the renal pelvis or ureter
what can kidney stone obstruction cause?
hydronephrosis
functional changes that indicate AKI
increase in traditional biomarkers of kidney injury (SCr, BUN), change in glomerular and/or tubular function, and absence of true damage to the kidney
kidney damage that indicates AKI:
presence of glomerular and/or tubular injury, or is identified by novel biomarkers (NGAL-Marker, TIMP2 and IGFBP7 markers, and KIM1 markers)
what does the NGAL-marker indicate?
proximal tubule injury
what do the markers TIMP2 and IGFBP7 indicate?
cell cycle arrest
what does KIM1 indicate?
proximal tubule injury
what is the timeline definition for Acute kidney disease (AKD)
AKI for > 7 days but not yet CKD (occurs after 90 days)
what are the complications of AKI?
edema/flid overload, electrolyte imbalance, acid/base imbalance, uremia, risk of CKD, and risk of CVD
what is uremia?
Azotemia with symptoms
what is azotemia?
an elevation of BUN > 20 mg/dL
how is uremia diagnosed?
a constellation of clinical findings and laboratory abnormalities
symptoms of uremia?
decreased appetite, change in taste, anorexia, nausea/vomiting, pruritis, altered mental status/encephalopathy
what condition is an indication for emergent dialysis therapy (extracorporeal kidney replacement therapy)?
uremia