acute kidney injury Flashcards
aki definition
aka acute renal failure Reduction in glomerular filtration rate resulting in azotemia developing days later Commonly due to renal ischemia or toxins Usually reversible Absence of symptoms of chronic uremia Kidney size is usually preserved
Diagnostic criteria
an abrupt (within 48 hrs) reduction in kidney function defined as An absolute increase in serum creatinine level of .3 mg/dL or a percentage increase in serum creatinine level of > 50% or a reduction in urine output < 500 ml in 24 hrs
Oliguria, azotemia, uremia
Oliguria- urine output < 500 ml/day
Azotemia- elevation of nitrogen waste products related to insufficient filtering of blood by the kidneys
Uremia: the illness accompanying kidney failure which results from the toxic effects of abnormally high concentration of nitrogenous substances in the blood
Serum creatinine
breakdown product of skeletal muscle, production remains constant over time, filtered at the glomerulus like inulin and creatinine clearance can be used to estimate GFR
Serum levels are inversely proportionate to GFR (should be about 100)
Limitations: creatinine is also slightly secreted in the nephron (overestimates GFR)
Blood Urea Nitrogen
nitrogenous waste product of protein metabolism
less accurate accureate indicator of GFR than creatinine (due to variations in protein intake, catabolic rate, tubular REAB)
Useful in conjuction with creatinine in differential diagnosis of renal disease)`
Urinalysis
Casts: caused by trapping of cellular element in a matrix of protein secreted by renal tubule cells
Granular casts (muddy borwn urine) are seen in cases of acute tubular necrosis
Renal autoregulation
Range is only from 80 10 160
Age, NSAIDS, CKD inhibit vasodilation of prostaglandins of afferent arteriole
ACEis and ARBs dilate efferent
Both end in low GFR
AKI categories
Prerenal: impaired effective renal perfusion, due to volume depletion, heart or liver failure
Renal: Intrinsic renal disease (glomerular, tubular, interstitial, vascular), Acute tubular necrosis, interstitial nephritis, glomerulonephritis, vascular disease
Post renal: Obstruction of urinary flow, could be prostate, bladder, stones, tumors
pre renal acute kidney disease
Due to decreased effective renal perfusion, decreased GFR without ischemic or nephrotoxic injury to tubules
decreased effective renal perfusion–> increased ANG2 and vasopressin –> increased REAB of sodium and water–> concentrated urine –> oliguria
Increased REAB UREA–> elevated BUn out of proportion to creatinine (>20:1)
Usually reversible within 3-4 days if underlying cause is treated
Renal AKI
Acute injury involving the tubules, glomeruli, interstitium, or vasculature
Acute tubular necrosis (ATN): ischemic, toxic, both
Inflammation: glomerulonephritis, tubulointerstitial nephritis, vasculitis
Embolis, thrombosis, thrombotic microangiopathy
Neoplasms: infiltrating tumors
ATN is the most common cause of renal AKI
Acute tubular necrosis morphology
Tubular dilatation, attentuation of tubular epithelium, loss of epithelial cell brush border, granular cast material
mitotic figures
Following ATN tubular regeneration occurs in a coordinated fashion, sublethally injured tubular epithelial cell repopulate the tubules by Dedeferentiation–> proliferation–> migration–> reestablishing cell polarity
No convincing evidence for direct repopulation of tubules by intrarenal or extrarenal stem cells
post renal aki obstructive uropathy
obstruction of the urinary tract at any level that affects both kidneys, should be ruled out in all pts with oliguria, usually reversible with relief of the obstruction, results in hydronephrosis- distention and dilation of the renal pelvis calyces
Fractional excretion of sodium FENA
expressed as amount of sodium excreted over amount sodium filtered by glomeruli
Normally 1% 99% Na REAB
In the setting of volume depletionm urine Na REAB should increase in the proximal tubule FENA<1%
If the proximal tubules are injured (ATN) sodium REAB will be impaired–> FENa >2%
FENa (%) = ( UNa x PCr)/ (PNa xUCr) x 100
