Clinical I: Acute Kidney Injury Flashcards
Define acute kidney injury (AKI)
- Dramatic decrease in renal function
- Increases in BUN + plasma creatinine + oliguria
- *its purpose is to compensate for other pathology in the body by decreasing the kidneys functionality
Which pt populations are commonly affected by AKI?
- chronically ill
- sepsis pts
Name the three types of AKI
pre-renal: azotemia
intrinsic: ATN
post-renal: prostatic or solitary kidney disease
Which ratio can we use to help determine what type of AKI we have?
BUN: creatinine ratio
>10.1 : prerenal
10.1: intrinsic
<10.1: postrenal
Which drugs are associated with pre-renal azotemia?
NSAIDs and ARBs/ACEinhib
they cause an abolition of autoregulation and can lead to more kidney damage in pts with decrease ECF
What are the causes of pre-renal azotemia?
Think of systemic stuff that would lead to decrease renal blood (RBF):
- CHF
- hemorrhage
- stenosis or occlusion
- NSAIDs/ARBs + ECV
Consequences of pre-renal azotemia?
- may progress to acute tubular necrosis
- decrease in GFR and FENa*
- increase BUN & BUN:creatinine ratio
*(body holds on to BUN and Na to perserve volume)
What are the general causes of acute post-renal failure?
blockage of outflow from the kidney
commonly caused by:
- stones
- solitary kidney diseaese
- intraabdominal: pelvic cancer
Ways to diagnose post-renal failure?
phys: fullness in abdomen and urge to urinate upon palpation
imaging: ultrasound and volume scanner
What is post obstruction diuresis and with which type of AKI is associated?
- after clearing a post-renal obstruction, pts may become volume depleted as the body attempts to normalize the volume overload
- may lead to altered electrolyte status: hyperK and tubular acidosis
- pts must be monitored closely and catheters clamped if loosing too much fluid
Name the types of intrinsic AKI
Acute tubular necrosis
Acute interstitial necrosis
Acute glomerular disease
Vascular
Which type of intrinsic AKI has phasic nature? Name the phases.
ATN: injury phase > repair phase
oligouric/injury phase = HTN + volume overload + brown urine
polyuric/repair phase: after necrosis and casts clear tublue = urine flows
What are the most common causes of ATN?
- sepsis
- IV contrast
- nephrotoxic exposure
- high risk: elderly, diabetics, and HTN pts
How does BUN:creatinine and GFR change in intrinsic AKI?
GFR: decreases
BUN:creatinine ratio: increases
What are the vascular conditions that can lead to intrinsic AKI?
- malignant HTN: found in critically ill pts
- scleroderma
- may also be caused by: encephalopathy, hemorrhage, ACS, eclampsia
Which kidney disease rarely leads to AKI?
acute glomerular disease: nephrotic and nephritic syndrome
What are the common causes of acute interstitial nephritis?
- *Meds: antimicrobials, NSAIDs
- autoimmune
- infection
*most common cause
What are the classic symptoms associated with interstitial nephritis?
- fever
- rash
- peripheral + URINE eosinophilia
What findings may you see on phys exam of people with AKI?
dry status: skin tinting, dry mucosal membranes, neck veins flat when @ zero degrees
wet status:
- abdominal jugular reflux: press on stomach and examine jugular impulse; if yes = + finding
- S3 gallop
- peripheral edema/ascities
What diagnostic tools are helpful to diagnose AKI?
- careful patient hx
- labs: URINALYSIS, renal indices (BUN&creatinine) , urine indices (electrolytes)
- renal ultrasound
- BUN:creatinine ratio
- intrinsic vs pre-renal chart
Treatment for AKI
- find cause and fix it: increase ECV!
- discontinue nephrotoxic drugs
- supportive therapy: nutritional support, manage infections
Differences between prerenal and intrinsic/ATN AKI?
prerenal:
- hyaline casts
- >500 urine osm
- <20 urine Na
- < 1% Na excretion
- <35% urea excretion
- more concentrated urine: 1.020
intrinsic:
- abnormal
- >300 urine osm
- >40 urine NA
- >2% Na excretion
- >35% urea excretion
- less concentrated urine: 1.010
What are the indications for hemodialysis?
AEIOU:
Acidosis
Electrolytes
Intoxication: Meds
Overload: pulm edema?
Uremia
Prevention of AKI?
- Avoid nephrotoxic drugs in volume depleted patients: ACEinhb and ARBs*
- prophylax tumor lysis patient** and IV contrast*** patients
*remember they prevent autoregulation!
**tumor lysis = leads to uric acid build up
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