Acute Renal Failure (acute kidney injury) Flashcards
Renal function
o Filtration, Reabsorption, Secretion, Excretion
o 21% cardiac output - 0.4% body weight
o Require adequate perfusion
o Functional unit = nephron
o Glomeruli -> ultrafiltrate -> tubules
o Tubules resorb/secrete solute, H2O
“ End product passed to collecting system
o 750ml-2L/day: homeostatically perfect urine
acute renal failure of acute kidney injury
o Defined - precipitous decline in renal filtration function
o Characteristics:
“ Rise in serum creatinine from baseline
“ Decreased GFR
“ Alteration in urine output, concentration
“ Active urine sediment - casts
“ Changes in urine sodium concentration
who gets acute renal failure and whos at risk
o Renal perfusion alterations
“ Hypotension (shock), hypovolemia (volume loss)
o Diabetics, HTN: early end-organ damage
o Kidney injury: drugs, contrast, trauma
o Rheumatologic/Collagen Vascular Dz: progression
o Intrinsic Kidney Disease
o Blood pressure will alter perfusion rates through the kidney
kidney problems - markers
o UA micro and Chem Panel
“ First clues to presence of Dz
o Volume: definitions
“ Polyuria: >2500ml/24hrs
“ Oliguria: <500ml/24hrs
“ Anuria: <100ml/24hrs
o Concentration (specific gravity)
“ On dipstick/UA: 1.005-1.020
“ Sick kidneys don’t concentrate normally
o Urine sediment on micro
“ Active or bland? Casts or no casts?
o Serum Creatinine
“ Chem panel: 0.6-1.2mg/dl
“ Skeletal muscle, diet
“ Filtered and secreted, balanced amount in serum - normally
“ Increase = glomerular/tubular injury/Dz
“ Indicates Dz presence - not etiology of problem
“ Rises late: GFR already reduced by ~50%
“ Normal creatinine does not equal normal GFR
o Cbc contributes NOTHING to kidney function
o These are the first clues that kidney problems are present
o Dialysis patients are usually the people with anuria
o Small increases in creatinine are a big deal
o If you have a rise in creatinine on chem panel, you already have a GFR reduction of 50% because creatinine rises later on in the liver disfunction situation
kidney function - markers
o BUN: Blood Urea Nitrogen " Chem panel: 5-20mg/dl " Nitrogenous waste from cellular protein breakdown " Elevated in: dehydration renal dz, GI bleeding, etc o BUN to Creatinine Ratio " Helpful in determining etiology of AKI o Urine Microalbumin " Albumin to creatinine ratio o Glomerular Filtration Rate " GFR is estimated (120mL/min) " Calculations - not exact " Reduction implies renal Dz " Progression is marker in CKI " Increase = improvement o Cystatin C w/ creatinine " May be useful in early Dz o BUN to creatinine ratio is usually about 10:1 í that's normal o CKI í chronic kidney injury
Azotemia and uremia
o Terms that describe degree of failure
o Azotemia
“ Retention of nitrogenous wastes
“ Inadequate renal filtration, decreased GFR
“ Increased creatinine, renal “insufficiency”
o Uremia
“ Severe azotemia, renal “failure”
“ Creatinine high, GFR very low
“ Clinical symptoms/consequences of renal failure
Disease duration - key to ddx
o Acute - hours to days
o Rapidly progressing - weeks to months
o Chronic - progressive, months/years
“ May have acute insult on chronic failure
o Compare UA, creatinine from previous
“ No previous? Sx duration
o Hospitalized pt’s close monitoring - daily
“ Monitor events - hypotension, drugs, contrast
o You can have an acute hit to your renal function while having chronic kidney
Causes of ARF/AKI
o Think - where in the system?
o Prerenal
o Intrarenal (Intrinsic)
o Postrenal
o How do you think about acute kidney injury í how do you characterize it
“ Is it prerenal, intrarental, or postrenal
Prerenal causes of ARF/AKI
o Think - hypoperfusion o Hypotension - low vascular resistance " Shock - all forms " Medication induced o Volume depletion - intravascular " Dehydration, blood loss (trauma, GI) " "third spacing": burns, hypoalbuminemia o Decreased cardiac output " MI, CHF, arrhythmias, PE, etc.. o Low blood pressure
prerenal AKI
o Most common form - 50-80%
o Acute time course - creatinine elevated
o BUN to Creatinine Ratio =/>20/1
o Glomeruli, tubules are intact
o “Bland” sediment (no casts)
o Most prerenal AKI is reversible if treated promptly
“ GFR will return to near normal if reversed
o Acute prerenal on chronic renal failure
Intrarenal/intrinsic causes
" Structural injury/insult to kidney itself o Prerenal, postrenal causes excluded " Glomerular " Tubular " Vascular
Intrarenal cause - clomerular
o AGN: Acute glomerulonephritis
“ Hx, UA, urine sediment key to DDx
“ Postinfectious, rheum, IgA nephropathy, hereditary Dz, DM, etc
“ BUN to Creatinine ratio also =>20/1
“ Focal or diffuse glomerular damage
“ Focal: mild AKI - dysmorphic RBC’s, red cell casts (nephritic), mild proteinuria
“ Diffuse: signif AKI - nephritic w/ heavy proteinuria (nephrotic), HTN, edema
Intrarenal causes - tubular
o ATN - Acute tubular necrosis
“ Most common cause intrinsic AKI - 80%
“ Common in hospitalized pt’s
“ **Prerenal AKI not resolving with volume
“ BUN to Creatinine ratio <20/1 (10/1 common)
“ Increase in urine Na - >2%
“ Active sediment
“ “Muddy brown” granular & epithelial cell casts
“ Nephrotoxins: Abx, IV contrast, etc…
“ Ischemia: sepsis, rhabdomyolysis, burns, heat stroke, venomous bites
“ Most common kidney infection í prerenal
“ Most common intrarenal = acute tubular necrosis
o AIN - Acute interstitial nephritis
“ Drugs (NSAID’s, Abx), long list
“ Infections, autoimmune disorders
“ Fever, rash, eosinophilia
“ Active sediment - white cell casts
“ White, red cells, variable proteinuria
“ BUN to Creatinine ratio <20/1
“ Dx - renal biopsy but…consider temporal relation to drugs, stop the offender, monitor
“ Rash = vasculitis
Intrarenal causes: vascular
o Large Vessel Dz:
“ Malignant HTN, renal artery occlusion, emboli
o Small Vessel Dz, Vasculitis common
“ Thrombocytopenia (HUS/TTP)
“ Hemolytic uremic syndrome (HUS)
“ Thrombotic thrombocytopenic purpura (TTP)
“ Scleroderma
o Malignant HTN í blood pressure that increases so rapidly that it causes acute end organ damage
Postrenal causes
o Think: obstruction of urine flow out o Anywhere, eminently reversible o Must obstruct both kidneys to cause ARF " Unless the pt has only one… o Prostatic Dz, malignancy - common o Stones, blood clots, crystals
estimating GFR @ bedside
o Cockcroft-Gault: Creatinine Clearance (CrCl)
“ Best for CKD, may overestimate GFR (uses old creatinine assays)
“ ((140-Age) X (weight in kg)) / (serum creat X 72)
“ Normal: 90-140ml/min males; 80-125 females (X 0.85)
o MDRD equation: Modification of Diet in Renal Disease
“ More accurate than CrCl; best for CKD, not acute; commonly used
“ 175 x serum creat x age Add calc: (x .742(F)); (x 1.210(AA))
“ GFR >90 normal, GFR <60 abnormal
estimating GFR
o CKD-EPI: Chronic Kidney Dz Epidemiology Collaboration
“ Better in mild Dz; better for risk prediction
“ Recently: better than CrCl or MDRD
“ GFR = 141 * min(SerumCreat/kappa, 1)alpha * max(SerumCreat/kappa, 1) -1.209 * 0.993Age * Sex * Race
“ Use a calculation app…
o Other methods:
o Serum Cystatin C
“ Alternative to creatinine-based calculations
“ Studies: best in conjunction with creatinine - not superior to others
o Pediatric GFR
“ Schwartz formula
o 24hr urine Creatinine Clearance
Assessing tubular function
o Tubular function assessed by solute concentration in urine over 24hrs. Especially Na " Sodium retention = prerenal " Sodium dumping = sick tubules o Urine osmolarity o Urine Na concentration o Fractional Excretion of Na - FENa
Calculating FENa
” FENa = fractional excretion of sodium
“ Distinguishes ATN from Prerenal AKI
o Best in advanced AKI only
“ Urine Na X Plasma Creatinine/Plasma Na X Urine Creatinine X 100 (as %)
“ Prerenal, AGN <1%
“ ATN: usually high, =/>3%, AIN variable: 1-3%
“ Postrenal =/>1%
