What urine output is considered low (oliguria)?
<400 mL/day
What urine output is considered anuric?
<50 mL/day
RIFLE
RISK of kidney dysfunction, INJURY to the kidney, FAILURE or LOSS of kidney function, and END-STAGE renal disease (ESRD)
RISK
1.5x increase in SCr or 25% decrease in GFR or UOP <0.5 ml/kg/hr for 6 hrs
Injury
2x increase in SCr or 50% decrease in GFR or UOP <0.5 ml/kg/hr for 12 hrs
Failure
3x increase in SCr or 75% decrease in GFR or UOP <0.3 ml/kg/hr for 24 hrs or anuria for 12 hrs
Loss
complete loss (need for RRT) for more than 4 weeks
ESRD
complete loss (need for RRT) for more than 3 months
Difference between RIFLE and AKIN staging criteria
AKIN removed loss of kidney function (stage 1,2,3) so stage 3 would include these patients
KDIGO definitition of AKI
increase in SCr by >0.3 mg/dL within 48 hrs, increase in SCr by 1.5x baseline within prior 7 days, or a urine volume <0.5 ml/kg/h for 6 hrs
KDIGO AKI stage 1
increase in SCr by at least 0.3 mg/dL or 1.5-1.9x baseline, UOP <0.5 ml/kg/hr x6-12 hrs
KDIGO AKI stage 2
increase in SCr >2-2.9x baseline or UOP <0.5 ml/kg/h for over 12 hrs
KDIGO AKI stage 3
increase in SCr >3x baseline, increase of SCr >4 mg/dL, need for RRT, UOP <0.3 ml/kg/hr for >24 hrs or anuria for >12 hrs, or in children a decrease of GFR to <35
symptoms of uremia
weakness, SOB, fatigue, mental status changes, N/V, bleeding, loss of appetite, edema
causative agents of prerenal AKI
ACEi, ARB, COX-2 inh, cyclosporine, tacrolimus, diuretics, NSAIDs, radiocontrast, renin inhibitors
causative agents of intrinsic AKI
Vasculitis/thrombosis: bevacizumab, cisplatin, cyclosporine, hydralazine, methamphetamines, mitimycin C, PTU, tacrolimus
Cholesterol emboli: warfarin, thrombolytic agents
Glomerular: COX-2, NSAIDs, gold, heroin, lithium, pamidronate, phenytoin
Allergic in
caustive agents of postrenal AKI
acyclovir, foscarnet, indinavir, methotraxate, oxalate, sulfonamides, allopurinol, indinavir, triamterenes, oral sodium phopsphate solutions
most common cause of intrinsic AKI
tubular (90%)which includes intrarenal vasoconstriction, direct tubular toxicity, and intratubular obstruction, prolonged ischemia from prerenal causes, and toxins
laboratory findings to differentiate prrenal and intrinsic AKI
BUN:SCr ratio >20:1 in prerenal and <15:1 in intrinsic, granular casts and cells seen in intrinsic, urine osmolality higher in prerenal (>500 mOsm/kg), urinary Cr:SCr higher in prerenal (>40:1 vs <20:1 in intrinsic), specific gravity higher in prerenal (>
FENA
fractional excretion of sodium, low suggests retention of sodium and water (prerenal)
Why do contrast agents increase risk for AKI
contrast agents are hyperosmolar compared to plasma osmolality, can cause osmotic diuresis, dehydration, and renal ischemia
Risk factors for CIN
diabetes, heart failure, age >75, hypotension, eGFR<60
which thiazide is effective at GFR<30
metolazone
Treatment of AKI
loop diuretics if fluid overloaded, fluids, consider restricting electrolytes, RRT
What drug characteristics would make a drug more likely to be removed from dialysis
small molecular weight, low protein binding, low Vd
Indications for RRT
A: acidosis
E: electrolyte abnormalities
I: intoxication
O: volume overload
U: uremia (BUN>100 mg/dL) or uremic symptoms
How does KDIGO classify CKD?
CGA (cause, GFR, and albuminuria)
GFR categories
G1 normal >90
G2 mildly decreased 60-89
G3a mildly to moderately decreased 45-59
G3b moderately to severely decreased 30-44
G4 severely decreased 15-29
G5 kidney failure <15
cause of anemia in CKD
mainly due to decrease in production of erythropoietin by kidney, also RBC lifespan decreased from 120 to 60 days, also iron deficiency and blood loss (from uremic bleeding or dialysis)
Get normochromic, normocytic anemia
at what Hgb level should further evaluation for anemia occur
females <12, males <13.5
normal PTH levels
10-60 pg/mL
corrected calcium equation
measured calcium + 0.8 x (4-albumin)
KDIGO BP goal for CKD
<140/90 mmHg if albumin excretion rate (AER) <30 mg/24 h or <130/80 if AER>30 mg/24h
When should patients be on a protein restriction (<0.8 g/kg/day)?
Adults with GFR <25 ONLY because of risk of malnutrition, also consider for patients with >1 g/day proteinuria despite bp control with ACEi/ARB
target Hgb in anemia
max target 11 g/dL
ESA BBW
do not exceed target Hgb 11 based on studies showing greater risk of death, serious adverse CV reactions, and stroke when ESA were used to target higher Hgb
when should ESA be initiated?
Patients on dialysis when Hgb <10 AND (1) rate of Hgb decline indicates likelihood of requiring RBC tranfusion and (2) goal is to reduce risk of alloimmunization and risks of RBC tranfusion
When should the ESA dose be reduced or interrupted?
if Hgb >11 in patients with CKD on dialysis or >10 if not on dialysis
When is iron supplementation recommended?
When TSat <30% and ferritin <500 ng/mL
Why can ferritin sometimes not reflect iron status accurately?
acute phase reactant and may be elevated during infection or inflammation
Routes of admin for ESAs
SC and IV - SC generally preferred for patients not on HD (without IV access)
Starting dose of epoetin alfa (Epogen/Procrit)
50-100 units/kg 1-3x per week
Starting dose of darbepoetin alfa (Aranesp)
Not on dialysis - 0.45 mcg/kg q4weeks
On dialysis - 0.45 mcg/kg weekly or 0.75 mcg/kg q2weeks
Starting dose of methoxy PEG-epoetin beta (Mircera)
0.6 mcg/kg q2weeks
How to switch dosing from epoetin to darbepoetin
If receiving epoetin 2-3x/week, give darbepoetin weekly; if receiving epoetin weekly, give darbepoetin q2weeks. conversion table given in PI
How to adjust the ESA dose
Allow at least 2-4 weeks before making a change!
If Hgb change <1 g/dL in 4 week period and iron stores are adequate, increase dose by 25%
If Hgb change >1 g/dL in 2 week period, reduce dose 25%
Recommended dose of oral iron
200 mg elemental iron per day
Iron sucrose (Venofer) dose
100 mg diluted in 100 mL NS given over at least 15 minutes or undiluted over 2-5 minutes
Nondialysis - 200 mg x5 doses within 14 days
PD - 300 mg in NS over 1.5 hrs, then 300 mg 14 days later and 400 mg over 2.5 hrs 14 days later
Iron dextran (INFeD/Dexferrum) dose
100 mg given over 2 minutes IV push (Give 25 mg test dose)
Sodium ferric gluconate (Ferrlecit) dose
125 mg in 100 mL NS given over 1 hr or undiluted up to 12.5 mg/min
Ferrumoxytol (Faraheme) dose
510 mg single dose, followed by 510 mg 3-8 days later, administer over minimum 15 min
Ferric carboxymaltose (Injactafer) dose
Up to 1500 mg total (750 mg x2 separated by at least 7 days)
Phosphorus daily restriction in CKD
800-1000 mg/day
Dosing of cinacalcet
Initial 30 mg daily, adjust no more frequently than every 2-4 weeks through 30, 60, 90, 120, then 180 mg daily
Adverse effects of ESAs
hypertension, RBC aplasia, seizures, polycythemia, thrombocytosis
Causes of resistance to ESAs
iron deficiency, secondary hyperparathyroidism, inflammatory conditions, aluminum accumulation, other disease states causing anemia (cancer, HIV, etc.)
PhosLo
Calcium acetate (capsule)
Phoslyra
Calcium acetate (liquid)
Calphron
Calcium acetate (OTC tablet)
Fosrenol
Lanthanum carbonate (chewable)
Renvela versus Renagel
sevelamer carbonate vs hydrochloride (same dosing, carbonate has less risk of metabolic acidosis)
Auryxia
Ferric citrate (tablet)
Velphoro
Sucroferric oxyhydroxide (chewable)
Which vitamin D forms are preferred in advanced CKD
calcitriol, doxercalciferol, paricalcitol
signs of hypercalcemia
weakness, headache, decreased appetite, lethargy
A pt with nephrotoxicity caused by tobramycin would likely present with an increase in SCr
a) immediately after starting therapy and with nonoliguria
b) immediately after starting therapy and with oliguria
c) 5-7 days after starting therapy and with oligu
D. Aminoglycoside-induced nephrotoxicity is characterized by a delay in changes in SCr (5-7 days) and relatively normal urine output
When administered intravenously, darbepoetin has a terminal half-life approximately ____________ that of epoetin alfa
three times longer than
In the GI tract, calcitriol promotes
a) absorption of calcium and inhibits absorption of phosphorus
b) absorption of both calcium and phosphorus
c) decreased binding of calcium and phosphorus
d) increased elimination of calcium and phosphorus
B
Primary treatment of elevated PTH
vitamin D
What is Veltassa
patiromer - Used for treatment of hyperkalemia, binds K in the GI tract (slow onset, 7 hrs so not for acute or emergency use), also binds many drugs so must be separated by other drugs by at least 3 hrs
Is metabolic acidosis or alkalosis a complication of kidney failure any why
metabolic acidosis - ability of kidney to generate bicarbonate decreases
Sovaldi
sofosbuvir
Harvoni
sofosbuvir + ledipasvir
Epclusa
Sofosbuvir + velpatasvir
Viekira pak
Paritaprevir/ ritonavir/ ombitasvir + dasabuvir
Zepatier
Elbasvir/ grazoprevir
Hep C direct acting antivirals DDI
All are CI with strong CYP3A4 inducers!
sofosbuvir and declatasvir can increase bradycardic effect of amio and can increase risk of myopathy with statins
Harvoni & Epclusa - sep from antacids by 4 hrs, take H2RAs at same time or 12 hrs, take PPI at same t
How long must a patient avoid pregnancy after taking ribavirin
6 months
Why is interferon alfa not used much
Side effects - CNS (fatigue, depression, anxiety), GI upset, inc LFTs, myelosuppression, flu-like syndrome
Which NRTIs can be used to treat Hep B
tenofovir, entecavir, adefovir, lamivudine, telbivudine
Key drugs that have warnings for liver damage
APAP, isoniazid, nevirapine, NRTIs, tipranavir, valproic acid
Treatment of alcoholic liver disease
Withdrawal: BDZ or anticonvulsants; Preventing relapse: naltrexone, acamprosate, disulfiram; vitamins; Thiamine for Wernicke
Treatment of variceal bleed
octreotide or vasopressin, antibiotic prophylaxis (ceftriaxone or quinolone), and non-selective beta-blocker for secondary prevention
Ratio of furosemide to spironolactone used for ascites
40:100
treatment of hepatorenal syndrome
albumin, octreotide, midodrine