FeNa = (urine Na x plasma Cr) (plasma Na x urine Cr)
Urine Na < 20. Functioning tubules reabsorb lots of filtered Na
2. ATN (unusual)
Postischemic dz: most of UOP comes from few normal nephrons, which handle Na appropriately
ATN + chronic prerenal dz (cirrhosis, CHF)
3. Glomerular or vascular injury
Despite glomerular or vascular injury, pt may still have well-preserved tubular function and be able to concentrate Na
3. AIN-higher FeNa due to tubular damage
Damaged tubules can't reabsorb Na
Calculating FeNa after pt has gotten Lasix...
Caution with calculating FeNa if pt has gotten Loop Diuretics in past 24-48 h
Loop diuretics cause natriuresis (incr urinary Na excretion) that raises U Na-even if pt is prerenal
So if FeNa>1%, you don’t know if this is because pt is euvolemic or because Lasix increased the U Na
So helpful if FeNa still <1%, but not if FeNa >1%
1. Fractional Excretion of Lithium (endogenous)
2. Fractional Excretion of Uric Acid
3. Fractional Excretion of Urea
A 22yo male with sickle cell anemia and abdominal pain who has been vomiting nonstop for 2 days. BUN=45, Cr=2.2.
D. AIN from NSAIDs
Hyaline casts can be seen in normal pts
NOT an abnormal finding
UA in prerenal ARF is normal
Prerenal: causes 21% of ARF in hosp. pts
Prevent ATN with volume replacement
Fluid boluses or continuous IVF
Intravascular volume depletion
“ Third spacing”
Reduced Cardiac output
Cardiogenic shock, CHF, tamponade, huge PE....
Anaphylaxis, Antihypertensive drugs
You evaluate a 57yo man w/ oliguria and rapidly increasing BUN, Cr.
Acute interstitial nephritis
Muddy brown granular casts (last slide)
Renal tubular epithelial cell casts (below)
Broad casts (form in dilated, damaged tubules)
Relative low BP
May occur immediately after low BP episode or up to 7 days later!
2. Post-op Ischemia
Post-aortic clamping, post-CABG
3. Crystal precipitation
4. Myoglobinuria (Rhabdo)
5. Contrast Dye
ARF usually 1-2 days after test
6. Aminoglycosides (10-26%)
ATN—What to do
Remove any offending agent
Try Lasix if euvolemic pt is not peeing
Most pts return to baseline Cr in 7-21 days
>20:1 10-15:1 BUN/Cr Cr improves with IVF Cr won’t improve much Response to volume Normal epi cells, granular casts UA UNa<20 FeNa<1% UNa>40 FeNa >2% U Na, FeNa increases slower than 0.3 /day increases at 0.3-0.5 /day Cr Prerenal ATN
Which UA is most compatible w/contrast-induced ATN?
Spec grav 1.012, 20-30 RBC, 15-20 WBC, +Eos
Spec grav 1.010, 1-3 WBC, 5-10 renal tubular cells, many granular casts, occasional renal tubular cell casts, no eos
Spec grav 1.012, 5-10 RBC, 25-50 WBC, many bact, occasional fine granular casts, no eos
Spec grav 1.020, 10-20 RBC, 2-4 WBC, 1-3 RBC casts, no eos
B. Spec grav 1.010, 1-3 WBC, 5-10 renal tubular cells, many granular casts, occasional renal tubular cell casts, no eos
Dilute urine: failure to concentrate urine
No RBC casts or WBC casts in ATN
Eos classically in AIN or renal atheroemboli, but nonspecific
56yo woman with previously normal renal function now has BUN=24, Cr 1.8. Which drug is responsible?
Kidney bx : Extensive cellular crescents with or w/o immune complexes
Can develop ESRD in days to weeks.
Treat w/glucocorticoids & cyclophosphamide.
Rapidly Progressive Glomerulonephritis
Usually after strep infxn of upper respiratory tract or skin – 8-14 day latent period
Can also occur in subacute bacterial endocarditis, visceral abscesses, osteomyelitis, bacterial sepsis
Hematuria, HTN, edema, proteinuria
Positive antistreptolysin O titer (90% upper respiratory and 50% skin)
Treatment is supportive
Screen family members with throat culture and treat with antibiotics if necessary
Postinfectious Proliferative Glomerulonephritis
A 19yo woman with Breast Cancer s/p chemo in the ER has weakness, fever, rash. WBC=15.4, Hct 24, Cr 2.9, LDH 600, CK=600. UA=3+ prot, 3+blood, 20 RBC. What next test do you order? What’s her likely dx?
Order blood smear to r/o TTP
TTP associated with malignancy, chemo
TTP may mimic Glomerulonephritis on UA (RBCs, WBCs)
Thrombocytopenia, anemia not consistent with nephrotic or nephritic syndrome
Need CK in the thousands to cause ARF
Platelets form thrombi and deposit in kidneys Glomerular capillary occlusion or thrombosis