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Flashcards in Acute Kidney Injury Deck (21):

Major parameters by which acute kidney injury (AKI) is measured?

GFR (via Cr) and urine output.


3 broad types of cause of AKI?

Pre-renal (reduced blood flow)
Post-renal (obstruction of urine)


Which part of the kidney is best perfused?
Which part most susceptible to ischemic injury?

Best perfused: Cortex.
Most susceptible to ischemic injury: Outer medulla (due to high metabolic activity)

(although... later lectures said acute hypoperfusion can cause a cortical pattern of damage first...)


What does a "pre-renal" cause of AKI really refer to?

Reduced perfusion of the kidney... could be due to hypovolemia, redistribution, low CO, renal vascular disease, etc.


Review: How does autoregulation protect the kidney from drops in BP?

GFR remains pretty constant until blood pressure drops very low (mean arterial pressure < 80mmHg).
This is achieved by dilation/constriction of the afferent and efferent arterioles.


What effect do ACE-inhibitors have on glomerular blood flow and GFR (in the short term)?

A-II causes efferent vascular construction -> increased GFR.
Thus ACE inhibitors / ARBs -> decreased GFR.
(though, of course, you can use them to slow the rate of decline of GFR in CKD)


What affect do NSAIDs have on glomerular blood flow and GFR?

Vasodilatory prostaglandins -> afferent arteriole dilation -> increased GFR.
Thus NSAIDs -> decreased GFR.
(Note that the kidney can't adapt to these changes to maintain GFR like it does to fluctuations in arterial BP... so NSAIDs and ACEi's/ARBs are contraindicated in when BP is low)


What does an elevated BUN/Cr ratio tell you about the cause of a patient's reduced GFR (which will cause elevation of both BUN and Cr)? Why does this happen?

Elevated BUN/Cr suggests that the cause of AKI is pre-renal (low effective volume).
Low effective volume -> ADH release -> avid resorption of urea in the collecting tubule (and there's increased passive resorption).


What will pre-renal (reduced RBF) AKI do to serum Na+ excretion fraction?

EF will be low - Na+ will be avidly reabsorbed in the proximal tubule.
(recall that in hypovolemic states, though aldosterone is upregulated, proximal Na+ reabsorption is increased so much that very little Na+ will even reach the distal nephron)


4 patterns of intrinsic (the problem's in the kidney) AKI?

Acute Tubular Injury (ATN -because this has been called "necrosis"... though there isn't always necrosis)
Acute glomerulonephritis (acute GN).
Acute Tubulointerstitial Nephritis.
Acute Vascular Nephropathy.


2 main types of causes of acute tubular injury (ATN)?



3 medications / substances that can cause ATN?

Aminoglycosides, contrast dye, myoglobin.
(there are certainly many others)


How does the "autoregulation" response to ischemic ATN make the problem worse? How does this happen?

The afferent arteriole paradoxically constricts.
In ATN, things aren't getting reabsorbed -> increased Na+/Cl- delivery to distal nephron -> macula densa stimulation (thinks BP/GFR is too high) -> afferent arteriole constriction.


What happens to the kidney vasculature in ATN?

Endothelial dysfunction -> vascular congestion in outer medulla due to leukocyte accumulation.


What are some bad things that happen to tubules in ATN?

Loss of polarity (eg. Na/K ATPase expressed on wrong side).
Apoptosis/necrosis of tubule cells.
Shedding of tubule epithelial cells into lumen.


What's a characteristic light microscopy finding in urine of patients with ATN?

Muddy brown granular casts (Tam-Horsfall protein).
Epithelial cell casts.


Inflammation is important in ischemic ATN... what's an unexpected inflammation event that happens in ischemic ATN?

Upregulation of inflammatory mediators in distant sites (e.g. in lungs, liver, heart, brain)


What do surviving epithelial cells do to repair after ATN?

Renal tubular cells can de-differentiate and proliferate to regenerate the tubular epithelium.


What will you see in ultrasound of a kidney with post-renal (obstructive) AKI?

Hydronephrosis - dilated renal pelvis / calyces.


Aside from back-pressure, what cause decreased GFR in post-renal AKI?



Acute vs. chronic fluid-electrolyte changes in post-renal AKI? (what other conditions do these changes make it resemble?)

Acute: increased Na+ and H2O retention (looks like pre-renal).
Chronic: Impaired Na+ reabsorption, impaired K+ and H+ secretion (resembles hyperkalemic distal RTA).