Nephrology Flashcards
anuric
UOP less than 50 mL/24 hours
oliguric
UOP less than 0.5 mL/mkg/hr for 12 hours or more
nonoliguric
UOP more than 500 mL/24 hours
Stage I AKI
SCr >= 0.3 increase or 1.5-2x baseline
UOP < 0.5 ml/kg/hr for 6-12 hrs
Stage II AKI
SCr 2-3x baseline
UOP < 0.5 mL/kg/hr for >= 12 hrs
Stage III AKI
SCr >3x baseline or SCr >=4 or on RRT
UOP <0.3 mL/mkg/hr for >= 24 hours or anuria for >=12 hours
prerenal AKI
hypoperfusion
BUN/SCr > 20:1
Urinary Na <20
FENa <1% ( hold onto water, sodium)
functional AKI
AKA prerenal azotemia
Undamaged kidneys
BUN/SCr > 20:1
Urinary Na <20
FENa <1% (hold onto water, sodium)
intrinsic AKI
kidney damage
May have rash, fever, persistent hypotension
Positive urinary WBC, RBC, proteinuria
Muddy brown granular casts; tubular epithelial casts; hyaline casts
postrenal AKI
kidney stones, BPH
Normal UA
FENa calculation
(Urinary Na/Serum Na) / (Urinary Cr/SCr) * 100
Meds causing pseudo-nephrotoxicity
Alter serum creatinine without affecting GFR
trimethoprim, cimetidine, steroids, tetracycline, cefoxitin
Aminoglycosides
Cause ATN (intrinsic AKI)
Starts ~6-10 days after therapy
Nonoliguric (500ml/24hrs)
Hypokalemia, hypomagnesemia
Risk if trough >2
Contrast
Cause ATN (intrinsic AKI)
SCr rises within 24 hours and peaks 2-5 days after procedure
Risk of oliguria, dialysis
Give NS or NaBicarb 6-12 hrs prior to procedure, avoid diuretics, and hold metformin for 48 hours after
Contrast treated as drug by Joint Commission
Gadolinium-based agents at risk for nephrogenic systemic fibrosis
Cisplatin
Causes ATN (intrinsitc AKI) - potentially irreversible
SCr peaks 10-12 days after therapy
May have hypokalemia and hypocalcemia (due to renal magnesium wasting)
Aggressively hydrate prior to treatment
Amifostine: cisplatin-chelating agent
Amphotericin B
Causes ATN (intrinsic AKI) - vasoconstriction decreases blood flow to kidney
Damage occurs after 2-3 g (2-5 days post initiation)
Electrolyte wasting
Hydrate with 1L NS prior to each dose
Use liposomal product
ACE/ARB
Causes functional AKI
Expect to rise 30% within 2-5 days, stabilize in 2-3 weeks
Inc >30% harmful
Avoid with diuretics (during drug initiation), NSAIDs
NSAIDs
Cause functional AKI (low urinary volume, Na; Inc in BUN, SCr, K, edema, weight)
Occurs within days of starting therapy
Avoid with concomitant meds of RAAS
Rapid recovery
Cyclosporine, tacrolimus
Cause functional AKI
Occurs days after starting therapy, along w/ HTN, Hyperkalemia, hypomagnesemia
Dose related
Monitor levels, use with other non-nephrotoxic immunosuppressants (steroids, mycophenolate)
Acute allergic interstitial nephritis
Allergic hypersensitivity reaction affecting interstitium of kidney
Caused by penicillins, nsaids (prolonged use)
DC offending agent, start steroid
Chronic interstitial nephritis
Progressive, irreversible
Caused by lithium, tacrolimus, cyclosporine after longterm use
Stage 1/G1 CKD
Kidney damage, normal GFR
Stage 2/ G2 CKD
Kidney damage with mildly decreased GFR 60-89)
Stage 3 / G3a,b CKD
Moderate decrease in GFR (30-59)
G3a: 45-59
G3b: 30-44
Stage 4/ G4 CKD
Severe decrease in GFR 15-29
Stage 5/G5 CKD
Kidney failure <15