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Cards (202)
Acute Kidney Injury (AKI)
Characterized by
abrupt decline
in kidney function =>
elevated serum
creatinine and/or reduction in urine output
AKI leads to an ↑ in Cr to
1.5
times (or more) baseline and
low
urine output
AKI onset is
sudden
(hours to days), varies from mild to severe and is often reversible, but
mortality
is high
Dialysis
may be required for
AKI
Who is at risk for development of an AKI
Patients with
infections
Patients with
low blood pressure
Patients exposed to
nephrotoxins
Sepsis
is the most common cause of
AKI
Pre-Renal AKI
Decrease in
glomerular filtration
and
perfusion
Decrease in renal
blood flow
Intra-Renal AKI
Direct damage to renal tissue/tubules
ATN
- most common in
renal
causes of AKI
Post-Renal
AKI
Mechanical obstruction
of urinary outflow
Pre-Renal AKI
Hypovolemia
Altered
peripheral vascular resistance
Cardiac disorders
Sudden drop in
BP
leads to a
higher
AKI risk
Usual cause of Intra-Renal AKI is direct damage to
tubules
Causes of Intra-Renal AKI
Prolonged
renal
ischemia
Nephrotoxic
drugs
Organic
solvents
Acute
hemolysis
Acute
glomerulonephritis
Post-Renal
AKI
Obstruction of urine flow due to
stones
tumors
enlarged
prostates
urethral
scarring or
infection
Process of pre-renal AKI
1. Decreased
blood flow
2. Lower
GFR
3.
Compensation
by the RAAS
4. Still not enough to maintain
normal
GFR
5.
Less urine
formed
6.
Less waste product
excreted
Process of intra-renal AKI
1. Injury of the epithelial lining of the tubules
2.
Inflammation
/swelling/loss of
function
3. Cells
die
4. Collect at
renal tubules
5. Obstruct mvt of
filtrate
6. UP
intratubular
pressure
7. DOWN
GFR
8. DOWN
UO
9.
Azotemia
Azotemia
Waste
products levels too
high
in the blood
Post-Renal AKI Process
1. Obstruction of
outflow
from
kidney
2. Intratubular pressure
UP
to push against
obstruction
3. DOWN
GFR
Initiation of AKI
1.
UP CR
2.
UP BUN
3.
DOWN UO
Maintenance of AKI
1. Lasts
days
to
weeks
2. Usually
nonoliguric
then oliguric then
anuric
3.
Fluid
retention and
edema
4. HTN
apparent
5. Metabolic
acidosis
6. Fluid and electrolyte
imbalance
7.
Anemia
8.
Waste
product accumulation
Anuria
Lack of
urine
(pee) production
Oliguria
Low
urine output
Recovery of AKI
1. Return of
BUN
, creatinine, eGFR toward
normal
ranges
2. May have
diuretic
phase
3. Recovered ability to
excrete
waste
4. Risk for
hypovolemia
and
hypotension
5. Risk for hyponatremia,
hypokalemia
,
dehydration
6. May take
12
months to stabilize
Diuresis
indicates leaving the maintenance stage of an ATN and entering the
recovery phase
Confusion in recovery phase may be due to
hypovolemia
and hypotension leading to ↓
PO4
reaching the brain
Glomerulonephritis
Immune-mediated inflammation of the urinary tract (primarily the
glomerulus
)
Both kidneys are equally affected in
Glomerulonephritis
Causes of
Glomerulonephritis
Drugs
Infection
Immune
disorders
Glomerulonephritis
Characterized by
proteinuria
Hematuria
Decreased
urine production
Oliguria
Acute Glomerulonephritis
AKI
Acute
Oliguria
LOW
GFR
Rapidly Progressive
Glomerulonephritis
Acute Glom
that didn’t resolve leading to
CKD
Chronic
Glomerulonephritis
Acute
injury resolved but
inflammation
persistent
Nephrotic
Glomerulonephritis
Atypical
Acute
Poststreptococcal Glomerulonephritis
The immune attack on the strep infection causes
antigen-antibody
complexes to form
Acute Poststreptococcal
Glomerulonephritis
most often affects children aged
3-7
Symptoms of Acute Poststreptococcal Glomerulonephritis
Oliguria
Edema
Hypertension
Urinalysis:
WBC
, RBC,
protein
, erythrocyte casts
Blood work:
UP
Urea,
UP
Creatinine
Most UTIs ascend and occur from
bacteria
entering the
urethra
E.coli
is the most common
pathogen
leading to UTI
Major defense against
ascending
bacteria
The
flushing
effect of
urine
flow
Most at risk for UTI
Females
Any
obstruction
in urinary tract
See all 202 cards