10 - Acute Kidney Injury Flashcards
What is acute kidney injury? What is it commonly caused by?
Aka acute renal failure.
Reduction in glomerular filtration rate resulting in azotemia over days. Absence of symptoms of chronic uremia and kidney size is usually preserved.
Commonly due to renal ischemia or toxins.
What are diagnostic criteria for acute kidney injury?
An aburpt (within 48 hrs) reduction in kidney function:
- increase in serum creatinine level
- reduction in urine output
Define: oliguria, azotemia, and uremia?
Oliguria: urine output <400-500 ml/day
Azotemia: elevation of nitrogen waste products related to insufficient filtering of blood by the kidneys
Uremia: illness accompanying kidney failure which results from the toxic efects of abnormally high concentrations of nitrogenous substances in the blood (azotemia + symptoms)
What is serum creatinine and how it is handled by the kidneys? What are limitations to estimations made using serum creatinine?
Breakdown product of skeletal muscles, production remains constant over time.
- Filtered at the glomerulus and clearance can be used to estimate GFR.
- Serum levels are inversely proportionate to GFR (GFR ~100/Cr)
- Unlike inulin, creatinine is also secreted in the nephrone and creatinine clearance overestimates GFR.
What is blood urea nitrogen (BUN) and how is it used clinically?
Nitrogenous waste product of protein metabolism.
Less accurate indicator of GFR than creatinine due to variation in protein intake, catabolic rate, and tubular reabsorption.
Useful in conjunction with creatinine in the differential dx of renal disease.
What are urinarlysis casts? What are granular casts?
Casued by trapping of cellular elements in a matrix of protein secreted by renal tubule cells.
Granular casts (muddy brown urine) are seen in cases of acute tubular necrosis.
Describe the autoregulation that allows us to maintain a relatively constant GFR when we have decreased perfusion pressure?
Increased vasoidltory prostaglandins act to vasodilate hte afferent arteriole.
Increased angiotensin II constricts the efferent arteriole.
These both work to preserve GFR.
What things can interfere with autoregulation and cause a low GFR when there’s decreased perfusion pressure?
Age, NSAIDs, and chronic kidney disease present the afferent arteriole from dilating.
ACE-I and ARBs present the efferent arteriole from constricting (they reduce glomerular pressure in chronic kidney disease but can cause acute kidney disease through this mechanism).
What are the three categories of acute renal injury?
Pre-renal: impaired effective renal perfusion
Renal: intrinsic renal disease (glomerular, tubular, interstitial, vascular)
Post-renal: obstruction of urinary flow
What is the physiologic basis for prerenal AKI?
Due to decreased effective renal perfusion which results in increased AngII and ADH causing increased renal reabsorption of sodium in the PT and water. Ultimately causing a concentrated urine and oliguira (not enough urine).
Decreased GFR without ischemic or nephrotoxic injury to tubules.
What happens to BUN in prerenal AKI?
Increase reabsorption of urea causes elevation of BUN out of proportion to creatinine (>20:1)
Usually reversible within 3-4 days if underlying cause is treated.
What do you see in the tubular epithelium in prerenal AKI?
Normal tubular epithelium.
What is “renal” AKI? What are some causes and what is the most common cause?
Acute injury involving the tubules, glomeruli, interstitium, or vasculature.
- acute tubular necrosis (ATN): ischemic, toxic, both
- inflammation: glomerulonephritis, tubulointerstitial nephritis, vasculitis
- embolism, thrombosis, thrombotic microangiopathy
- neoplasms
ATN in the most common cause of renal AKI
What is the mechanism and morphologic features of acute tubular necrosis?
Tubular dilitation
Attentuation of tubular epithelium (breaks into epithelium)
Loss of epithelial cell brush border (falls apart)
Granular cast material
Mitotic figures (regenerative change)
What is seen on histology in acute tubular necrosis?
Early ATN: see a cast, tubular epithelial cells broken off into the lumen
Later: fully necrotic tubules, no polarity. Hard to tell where the lumen is. Urine made is basically leaks back and causes azotemia and obstruction causes oliguria (less urine)
Fibrosis can also be seen.
How does tubule regeneration occur in acute tubular necrosis (ATN)?
Sublethally injured tubular epithelial cells repopulate by:
- de-differentiation > proliferation > migration > re-establishing cell polarity
- this process takes weeks to months
No convincing evidence ob tubule by intrarenal or extrarenal stem cells
What is post-renal AKI?
Obstruction of the urinary tract at any level that affects both kidneys: bladder outlet obstruction, ureteral obstruction
- Should be ruled out in all pts with oliguria
- Usually reversible with relief of obstruction
- Results in hydronephrosis - distension and ilation of the renal pelvix calyces.
How would you distinguish re-renal AKI from acute tubular necrosis?
Based on changes in renal tubular sodium reabsorption.
If you give fluid to someone with acute tubular necrosis, they may become volume overloaded because the necrosis is causing a blockage that prevents excretion whereas fluid would help someone with pre-renal AKI.
What is are the two most common causes of acute renal failure?
Acute tublar necrosis first then pre-renal AKI.
How do you diagnose AKI?
Pre-renal and Acute tubular necrosis: differentiate by assessment of urine sodium excretion
Post-renal: exclude with renal imaging (ultrasound or CT scan)
What does fractional excretion of sodium (FENa) tell you about the nature of AKI?
Normally FENa is ~1% because 99% of Na is reabsorbed.
In the setting of volume depletion (pre-renal azotemia): urine Na reabsorption should be increased in the proximal tubules so FENa <1%
If the proximal tubules are injured (acute tubular necrosis-renal AKI): sodium reabsorption will be impaired so FENa is >2%
What type of AKI would you expect if your FENa is >2%? What would be seen on urine microscopy?
Acute tubular necrosis (renal AKI) with muddy brown casts.
What type of AKI would you expect if your FENa is <1%? What would be seen on urine microscopy?
Pre-renal azotemia with bland urine sediment.
What is ATN characterized by?
Injury and loss of tubular epithelial cells.
How would you treat pre-renal AKI?
Administer saline to increase blood volume.
