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
A1 albuminuria
Normal to mildly increased
ACR <30
<30mg/24hr
A2 albuminuria
Moderately increased
ACR 30/300
30-300mg/24hr
A3 albuminuria
Severely increased albuminuria
ACR > 300
>300mg/24hrs
Nephrotic-range proteinuria
>3000mg/24hrs
T1D monitoring for albuminuria
5 years after diagnosis
Twice annually if ACR > 300mg/g and/or GFR 30-60
T2D monitoring for albuminuria
Immediately
Twice annually if ACR > 300mg/g or GFR 30-60
Goal BP via KDIGO
SBP 120
BP management
Start ACE/ARB with any degree of proteinuria, even if normotensive. Monitor BP, SCr, K within 2-4 weeks
(Hold if K >5.6 or SCr increases by more than 30%)
Add thiazide if Stage 1-3; Loop if stage 4-5
CCB as second line to ACE/ARB
A1c goal
<7%
SGLT2i
Use if CKD & T2DM, with GFR >20 (can consider if no diabetes)
Can continue if GFR falls below 20
If still uncontrolled, add GLP1
Finerenone
nonsteroidal MRA
Add if on max ACE/ARB, T2DM, normal potassium, GFR >25 and ACR >30
When to NOT start a statin
dialysis-dependent CKD
If already on statin when start dialysis, can continue
Indication for RRT
Acidosis (not responding to bicarb)
Electrolyte abnormality (hyperkalemia, hyperphosphatemia)
Intoxication (ethylene glycol, lithium, methanol, phenobarbital, salicylate, theophylline)
Overload (fluid)
Uremia
Preferred access for HD
arteriovenous fistula
Urea Reduction Ratio (URR)
URR = [(preBUN - postBUN)/preBUN] * 100%
Goal >65% with target of 70%
Demonstrates adequacy of dialysis
Most common organism for HD infection
S. aureus
Thrombosis of catheter
Alteplase or reteplase
Sieving coefficient
SC = concentration of drug in ultrafiltrate / concentration of drug in blood
Predicts drug removal in continuous RRT
Common pathogen for PD infection; Empiric regimen
S. epi, S. aureus, streptococci, E. coli, P. aeruginosa
Vanco OR first gen ceph
+
Third gen ceph or aminoglycoside
Cefepime monotherapy
Intraperitoneal administration preferred
When to start anemia workup
CrCl <60
or
Hgb < 12
Frequency of Hgb/Hct monitoring in CKD stages
Stage 3: annually
Stage 4: twice per year
Stage 5: every 3 months
TSAT
(Serum iron / TICB) * 100
Assesses available iron
Goal between >20 - <30% depending on source
Monitor every 3 months
Ferritin
measures stored iron
Goal varies between >100 and <500 depending on source
Monitor every 3 months
ESAs
Start if Hgb <10 (in dialysis; or along w/ other factors in non-dialysis)
AVOID if hx of stroke or cancer
CI in uncontrolled HTN
Replace iron stores FIRST. Iron deficiency is most common cause of erythropoeitin resistance
Maz increase in Hgb is ~ 1 every 2-4 weeks; do not adjust dose more than every 4 weeks. Adjust in 25% increments
Epoetin alfa
50-100 units/kg three times per week
Same molecular structure as human erythropoietin
Darbepoetin alfa (Aranesp)
Non-dialysis: 0.45mcg/kg every 4 weeks
Dialysis: 0.45 mcg/kg weekly or 0.75mcg/kg every 2 weeks
Modified to be longer acting
Mircera
methoxy polyethylene glycol-epoetin beta
0.6mcg/kg every 2 weeks
Modified for longer duration of action
Onset = 1-2 weeks
Iron therapy in dialysis
Avoid PO replacement
Generally use standard 1000mg over 10 days
Parenteral iron requiring test dose
iron dextran
Corrected calcium
Serum Ca + 0.8 (4- albumin)
Phosphate goal Stage 5 CKD
2-9x ULN
First line phosphate binders in stage 3-4 CKD
Calcium carbonate
Calcium acetate (PhosLo, Phoslyra)
Limited by hypercalcemia
Sevelamer (Renvela)
Nonabsorbable phosphate binder
Primary therapy in CKD Stage 5, especially if hypercalcemic
Lanthanum carbonate
Not widely used; indication similar to sevelamer – if patient has hypercalcemia
Ferric citrate
Iron based phosphate binder
Can be used for iron supplementation if not on dialysis
GI upset
Sucroferric oxyhydroxyide
iron based phosphate binder
chew
GI upset
Target vitamin d goal
> 30 ng/mL
Calcitriol
FDA approved to manage hypocalcemia and preventing/treating secondary hyperparathyroid
High incidence of hypercalcemia
Not routinely used in CKD 3a-5
Paricalcitol
vitamin D analog approved for treatment/prevention of secondary hyperparathyroidism
Lower incidence of hypercalcemia than calcitriol
Doxercalciferol
vitamin D analog for treatment/prevention of secondary hyperparathyroidism
Lower risk of hypercalcemia than calcitriol
Cinacalcet (sensipar)
Calcimimetic - indicated for secondary hyperparathyroidism
Increases sensitivity of receptors to serum calcium, thus reducing PTH
30mg daily
Caution in seizure disorder
CYP2D6 inhibitor, 3A4 substrate