4 Acute kidney injury Flashcards
Define acute kidney injury. What are some common characteristics/causes?
- aka “acute renal failure”
- reduction in glomerular filtration rate resulting in azotemia (accumulation of waste) developing over days
- kidney size usually preserved (no symptoms of chronic uremia), and usually reversible
- commonly due to renal ischemia or toxins
What are the diagnostic criteria for acute kidney injury (AKI)?
- abrupt reduction in kidney function (within 48 hrs)
- increase in serum creatinine
- reduction in urine output
Define oliguria
Urine output < 400-500 ml/day
Define azotemia
Elevation of nitrogen waste products (increased BUN) related to insufficient filtering of blood by the kidneys
Define uremia
Illness accompanying kidney failure which results from the toxic effects of abnormally high concentrations of nitrogenous substances in the blood
**aka Azotemia + symptoms
How can you estimate the GFR using serum creatinine levels?
GFR ~ 100/Cr
What is BUN and how is it clinically helpful?
- blood urea nitrogen (nitrogenous waste product of protein metabolism), useful in conjunction with creatinine
- less accurate indicator of GFR than creatinine due to variation in…
- protein intake
- catabolic rate
- tubular reabsorption
Define casts
Microscopic structures in the urine caused by trapping of cellular elements in a matrix of protein secreted by renal tubule cells
What is the differential for granular casts?
- “muddy brown urine”
- seen in cases of acute tubular necrosis (ATN)
How does the body autoregulate GFR under decreased perfusion pressure?
- Increased vasodilatory prostaglandins
- results in afferent dilation
- this response is decreased with age and CKD
- blocked by NSAIDs
- Increased angiotensin II
- results in efferent constriction
- blocked by ACEi/ARBs
What are the 3 categories of AKI?
- pre-renal
*Impaired effective renal perfusion - renal
*Intrinsic renal disease (glomerular, tubular, interstitial, vascular) - post-renal
*Obstruction of urinary flow
What can cause pre-renal AKI?
- volume depletion
- heart failure
- liver failure
**decreased GFR without ischemic or nephrotoxic injury to tubules (NO CAST in urine or histology changes!)
What can cause renal AKI?
-
acute tubular necrosis (ATN; ischemic, toxic, both)
**ATN= most common - inflammation (interstitial nephritis, glomerulonephritis, vasculitis)
- embolism, thrombosis, thrombotic microangiopathy
- neoplasms (infiltrating tumors)
What can cause post-renal AKI?
- Obstruction:
- prostate
- bladder
- stones
- tumor
What are 3 common characteristics of pre-renal AKI?
- oliguria/concentrated urine (increased ang II/ADH due to decreased renal perfusion)
- increased reabsorption of urea -> elevation of BUN out of proportion to creatinine (>20:1)
- usually reversible within 3-4 days if underlying cause is treated
What is the major pathophysiology behind ATN?
- tubular cell injury/necrosis leads to cells sloughing off, binding proteins, and ultimately forming an obstruction which leads to…
- tubular urine “back-leak” -> azotemia
- decreased tubular flow -> oliguria
- casts in urine
What are the morphologic features of ATN?
- tubular dilatation
- attenuation of tubular epithelium
- loss of epithelial cell brush border (of proximal tubule)
- granular cast material
- mitotic figures (regenerative change)
Describe tubule regeneration
- the process of healing after ATN (why treatment can be simply supportive, the kidney will heal itself)
- sublethally injured tubular epithelial cells (NOT stem cells) repopulate by…
- de-differentiating
- proliferating
- migrating
- re-establishing cell polarity
What are the symptoms of post-renal AKI?
- oliguria
- hydronephrosis (distension and dilation of the renal pelvis calyces)
- usually reversible (just remove the obstruction)
What are the etiologies of ATN?
- ischemia (50%)
- sepsis (30%)
- multifactorial (20%)
How do you differentiate pre-renal versus renal AKI?
- assessment of urine sodium excretion (FENa; fractional excretion of sodium)
- sodium excreted/sodium filtered @ glomeruli
- normally ~1%
- volume depletion increases Na reabsorption, so FENa<1%
- if the proximal tubules are injured (as in ATN), Na reabsorption is impaired and FENa>2%
How do you calculate FENa? What is its purpose?
- fractional excretion of sodium (%)
- 100 x U(Na) x P(Cr) / P(Na) x U(Cr)
-
helps differentiate between prerenal azotemia and ATN
- >2% in ATN (+ muddy brown casts)
- <1% in prerenal azotemia (+ bland urine sediment)
What is a rule of thumb to indicate a pre-renal cause of AKI?
If the urine sodium is less than 20 meq/L
**This trick means you can estimate the FENa (less than 20 meq/L sodium means FENa is <1%)
What is the best course of action in a patient with pre-renal AKI?
- give fluids (try to improve renal function)
- infuse NE (to increase BP)
- dialysis to treat uremia if needed
