AKI Flashcards
classic biomarkers of AKI and pluses and minuses
serum creatinine: most often used; but really only measures GFR in a steady state- so it overestimates GFR when GFR is declining and underestimates GFR when it is getting better.
urine output is less widely used and does not correlate as well with prognosis as creatinine, but may be more sensitive to injury later on.
What are some of the risks associated with AKI?
-AKI in a hospitalized patient increases the risk of mortality, regardless of reason for being in the hospital -AKI increases the risk of developing CKD. (hazard ratio of 10; 5X risk of ESRD).
Causes of pre-renal AKI
- hypovolemia, either absolute or relative. absolute is through hemorrhage, GI bleed, vomiting/diarrhea vol. depletion.
relative is stuff like low cardiac output or low oncotic pressure. - hypotension (sepsis, anesthesia, meds)
- pharm: NSAIDs, ACE-Is, ARBs
or - vascular: thrombosis, emobulus, dissection.
How do pharm agents lead to AKI
NSAIDs cause constriction of the afferent arteriole because they inhibit prostaglandin production. Prostaglandins are responsible for dilating the afferent arteriole and preventing kidney ischemia in settings of low renal perfusion.
ACE-Is and ARBs dilate the efferent arterioles, which can be dangerous in the setting of acute volume depletion.
BUN:Cr ratio in pre-renail AKI: explanation
ratio > 20.
this is because proximal urea absorption will be increased in states of vol. depletion to help with Na and water reabsorption- but Cr can’t be reabsorbed, so ratio will rise above normal.
FeNa for pre-renal AKI
theoretically, in pre-renal states, urine sodium should be low (in pre-renal states, proximal sodium reabsorption should increase). the FeNa equation helps us normalize this value. In pre-renal states FeNa is less than 1%
pre-renal AKI urinalysis.
bland- no cells, no casts except maybe some hyaline casts. no blood, WBCs, and minimal protein in pre-renal AKI.
post-renal AKI cuases
ureter, bladder neck or urethra problems.
ureter- consider clots, tumors, lymphadynopathy.
bladder: consider tumors, clots, BPH, neurogenic bladder
and urethra- consider tumors, strictures, obstructed catheters. But, obstruction must be BILATERAL- otherwise the other kidney will help compensate.
physiology of post-renal AKI
again, remember that it must be bilateral if a patient has normal kidneys.
GFR will be maintained even with complete obstruction, in part through prostaglandins that dilate the afferent arteriole. But, tubular dysfunction will be great- you will see problems with Na reabsorption, impaired acid secretion, and impaired K secretion, which may lead to hyperkalemia.
Dx of post-renal AKI
- ultrasound to look for dilation of renal pelvis.
- bland or bloody urinalysis, maybe with crystals. RBCs will NOT be dysmorphic. Crystals would be sodium oxalate crystals?
Urine sodium would be low at firs, but would rise to above 40 (unitless) once tubular injury begins (above 4 on FeNa)
Causes of intrinsic renal AKI
small vessel (atheroembolic, scleroderma, malignant HTN, TMA?), glomerular (RPGN- rapidly progressive glomerulonephritis and vasculitis), tubular (acute tubular necrosis may be toxic or ischemic; obstructive causes also possible), interstitial (acute interstitial nephritis, infection, infiltration)
ATN: causes
ischemic or nephrotoxic. ischemic is fron shock, burns, severe acute volume depletion and shows patchy necrosis throughout the tubule. toxic is either from an endogenous source like myoglobin or hemoglobin, or from an exogenous source like aminoglycoside antibiotics, or iodinated contrast. Toxic ATN shows concentrated necrosis in the PCT and other proximal structures.
Pathophysiology of ATN
ischemia leads to tubule cell injury and vasoconstriction. This can be kind of a vicious cycle- injured tubular cells loose their polarity and thus have difficulty with sodium reabsorption. Increased sodium delivery to the distal portions of the kidney signals the activation of the renin-angiotensin system, which exacerbates kidney ischemia.
Dx of ATN
- increased urine Na and FeNa
- Granular casts and renal tubular cells. Often these are thicker muddy brown casts- they are thicker because the tubular walls are degrading.
Course of ATN
usually starts with some kind of pre-renal insult, followed by further intrinsic damage to the kidney. you can recover at any time. Recovery is often seen in the first 2 wks, but it can take months, esp. in people with rhabdomyosis.
