ASN QBank Pearls - AKI, ICU Nephrology, HTN, and Pharmacology Flashcards
what filtration fraction is associated with increased clotting on CVVH?
> 25-30%
how do you calculate filtration fraction for POSTfilter CVVH?
(QR + UF)/(QB x (1-Hct)) x 60 min/hr
?Units??
how do you calculate filtration fraction for PREfilter CVVH?
(QR + UF)/((QB x (1-Hct)) x 60 min/hr) + QR
total body water (TBW)
weight x % body water
- male 0.6, elderly male 0.5
- female 0.5, elderly female 0.45
Na+ requirement formula
TBW x (desired Na+ - serum Na+)
infusion rate formula for hyponatremia
(Na+ requirement x 1000)/(infusate Na+ x time)
- Na+ requirement = TBW x (desired Na+ - serum Na+)
Na+ concentration in 3% saline
513 meq/l
total water deficit formula
TBW x (1 - desired Na+/serum Na+)
electrolyte-free water clearance (EFWC) formula
urine volume × (1 − ((UNa+ + UK+)/SNa+))
free water clearance (FWC) formula
urine volume × (1 − (Uosm/Sosm)
indications for HD in lithium toxicity
- > 5 withOUT CKD
- > 4 WITH CKD
- > 2 with neurologic or cardiac effects and AKI
clearance rate formula
- equal to effluent rate
- (QR + UF) x 1 hr/60 min
fluid overload at time of dialysis initiation has been a/w increased risk of
mortality
have any RRT modalities shown that removal of myoglobin can shorten or prevent the course of AKI from rhabdomyolysis?
no
- in a patient with acute brain injury, what dialysis modality should be avoided?
- why?
- how?
- iHD
- may worsen neurological status
- compromises cerebral perfusion pressure d/t hypotension and disequilibrium
- in a patient with acute brain injury, what dialysis modality should be used?
- why?
- CRRT
- slow removal of fluids and solutes decreases risk of worsening acute brain injury
what is the MC acid-base disturbance in the immediate postoperative period and is most prominent during the first 24-48 hours after surgery?
metabolic alkalosis
why is metabolic alkalosis the MC acid-base disturbance immediately post-op?
large citrate load from stored PRBC and FFP that’s metabolized to bicarbonate
what are the benefits of using bicarbonate as a buffer in the dialysate or replacement fluid of AKI patients with circulatory problems or liver dysfunction?
- better correction of acidosis
- lower lactate levels
- improved hemodynamic tolerance
expected effect on systolic and diastolic BP after using CPAP
-3/-2 mmHg
what is the likelihood of identifying adrenal cancer or a hyperfunctioning lesion (pheochromocytoma, primary aldosteronism, Cushing’s) in the setting of discovering an adrenal “incidentaloma” mass?
10-20%
what is the BEST way to dose antibiotics for a patient on CRRT at 25 ml/kg/hr?
measure effluent UF and dialysate and calculate a CrCl
what is an independent risk factor for AKI in a patient undergoing surgery?
obesity
what is the most important risk factor for AKI in a patient undergoing surgery?
CKD
what is the “gold standard” test to diagnose white coat HTN?
ambulatory BP monitoring
ARB exposure during the second and third trimesters has been a/w
neonatal renal failure and death
can diuretics be continued during pregnancy?
yes, especially in women with sodium-sensitive HTN or edema and when they were already on them
treatment of resistant HTN
- lifestyle modifications
- w/d of interfering meds
- correction of secondary HTN causes
- MR antagonists (spironolactone, amiloride, eplerenone)
a trial published in 2008 demonstrated that antihypertensive therapy in patients > 80 yoa is a/w
- decrease in stroke
- decrease in cardiovascular mortality
older patients with HTN are more likely to be salt-sensitive and responsive to what therapy?
diuretics
in pregnant women with DM what is associated with a high incidence of fetal malformations?
poor glycemic control in the first trimester
patients with AKI in the setting of decompensated liver disease may have HRS, but what must be ruled out first and how?
- intravascular volume depletion
- evaluating clinical response to IVF
- increased hemodynamic instability
- worsening respiratory failure with increased airway pressures and increasing difficulty with oxygenation
- tense abdomen on exam
- oliguric kidney failure
abdominal compartment syndrome
diagnosis of intra-abdominal hypertension and abdominal compartment syndrome is accomplished by
transduction of bladder pressure
intervention a/w greatest reduction in the risk for contrast-induced nephropathy
isotonic crystalloids prior to and following iv contrast
acyclovir, methotrexate, ethylene glycol toxicity and TLS can all present with
crystalluria
needle shaped crystals
acyclovir crystals
amorphous brown-colored precipitates in urine
methotrexate
dumbbell and needle-shaped calcium oxalate monohydrate crystals, and envelope-shaped calcium oxalate dihydrate crystals
ethylene glycol toxicity
what is the probability that AKI is d/t AIN when urinary eosinophils are present?
30%
single most probable cause of secondary HTN is
fibromuscular dysplasia
fibromuscular dysplasia is most likely to be identified on
CT angiography
localized kidney ischemia and/or infarction from dissection/contusion of the kidney following trauma
Page kidney
pathophysiology of Page kidney
perinephric hematoma compressing renal parenchyma, causing renal ischemia and RAAS activation
treatment of Page kidney
RAAS blockade
most patients, 52%, with longstanding atherosclerotic renovascular disease have “stabilization” of creatinine; what is the most probable outcome of renal revascularization?
GFR remains unchanged
MOST useful data regarding the salvageability of renal function with renal revascularization
LOW resistive indices
what is the MOST helpful procedure post revascularization during annual f/u renovascular disease?
renal artery duplex US
how do NSAIDs cause hyperkalemia?
- inhibit PGs –> reduces renin –> inhibits RAAS pathway –> hypoaldosterone state –> hyperkalemia
how do NSAIDs cause hyponatremia?
- reduces PGE2 –> increased ADH effect –> increased H2O reabsorption
- counteract effect of diuretics by reducing RBF –> increased proximal urine Na+ reabsorption –> and increased urine concentrating ability
drug toxicity
- protease inhibitors
nephrolithiasis
drug toxicity
- nucleoside reverse transcriptase inhibitors (eg, stavudine, didanosine)
- lactic acidosis
- hepatic steatosis
drug toxicity
- nucleotide reverse transcriptase inhibitors (eg, tenofovir)
- ATN
- Fanconi syndrome
drug toxicity
- interferon
nephrotic syndrome
best stain for calcium phosphate crystals
von Kossa stain
chronic lithium use can lead to which renal syndrome?
- nephrogenic DI
- distal, type 1, RTA
- CKD
- MCD
- FSGS
lithium nephrotoxicity may be prevented by use of
amiloride
a known, serious complication of stem cell transplantation
hepatic veno-occlusive disease (VOD), aka sinusoidal obstruction syndrome
hepatic veno-occlusive disease (VOD), aka sinusoidal obstruction syndrome clinical presentation
- similar to HRS
- AKI
- low BP
- sodium retentive state
pathophysiology of hepatic veno-occlusive disease (VOD), aka sinusoidal obstruction syndrome
sinusoidal obstruction –> portal HTN –> microvascular intrahepatic portosystemic shunting
what is the mechanism of proteinuria following bevacizumab therapy?
loss of vascular endothelial growth factor (VEGF)
- HL
- massive kidneys on CT scan
- AKI
lymphomatous infiltration of kidneys
what is the MOST effective therapy to lower methotrexate levels in a patient with AKI?
glucarbidase
- bone marrow suppression
- stomatitis (painful swelling and sores inside the mouth)
- AKI
methotrexate toxicity
can dialysis remove methotrexate?
need high flux HD for 8-12 hours (otherwise, rebound)
MOST effective oral treatment to remove sustained release lithium from GI tract
polyethylene glycol (PEG)
- AKI
- severe HTN
- GI bleeding
- following invasive vascular procedure
cholesterol embolization (AED)
- acute myelomonocytic leukemia (AMML); tissue invasive leukemia
- large kidneys on US
- AKI
leukemic infiltration of renal interstitium
- HTN
- AKI
- proteinuria
- MAB against VEGF
- decreased NO
- increased endothelin
bevacizumab
enters proximal tubular cells via APICAL membrane megalin receptor pathway
genatmicin
enters cells via BASOlateral organic ANion transporter pathway
tenofovir
enter proximal tubular cells via BASOlateral organic CATion transporter pathway
- cimetidine
- ifosfamide
- trimethoprim
- “CIT CAT”
tenofovir causes proximal tubular injury, AKI and Fanconi syndrome, through what mechanism?
mitochondrial dysfunction
drug that can cause AKI, Fanconi syndrome, and nephrogenic DI?
tenofovir
what medication is most likely to cause nephrolithiasis?
atazanavir
what urine pH is atazanavir most soluble in?
< 4.5
MCC of AKI in ecstasy (MDMA) ingestion
nontraumatic rhabdomyolysis
AKI in setting of;
- overdosing of abx
- alkaline urine
- underlying kidney injury
- old age
ciprofloxacin-associated crystalline nephropathy
fluid management strategy a/w increased risk of AKI in critically ill septic patient
hydroxyethyl starch (HES)
MOST common adverse effect of rasburicase therapy
hemolytic reaction in patients who have underlying G6PD deficiency
ethylene glycol metabolites
glycolic acid, glyoxalate, and oxalic acid
dose adjustment for rasburicase in renal and/or liver failure
none needed
rasburicase metabolism
peptide hydrolysis
which IV vasopressor can raise serum K+ concentration and potentially worsen hyperkalemia?
phenylephrine
how can phenylephrine cause hyperkalemia?
nonselective α-agonist that blocks cellular uptake of K+
which vasopressors can cause hypokalemia?
epinephrine and norepinephrine
how can epinephrine and norepinephrine cause hypokalemia?
β2 agonism increases cellular uptake of K+
why is CRRT the best option for a patient awaiting liver transplant?
slow removal of solutes –> decreased risk of osmotic disequilibrium and increase in ICP
MOST likely mechanism of HTN and proteinuria in preeclampsia
decreased VEGF (vascular endothelial growth factor)
what effect does tight glucose control with insulin therapy in critically ill patients with sepsis in the ICU have?
increased risk of hypoglycemia
- LOW PRA
- high renin level
- low AG2
- low PAC
aliskiren (renin inhibitor)
- HIGH PRA
- high renin level
- LOW AG2
- low PAC
ACEI
- HIGH PRA
- high renin level
- HIGH AG2
- low PAC
ARB
- HIGH PRA
- HIGH renin level
- HIGH AG2
- HIGH PAC
- antagonize MR
spironolactone (aldosterone antagonist)
what type of replacement fluid for CVVH is a/w higher solute clearance?
POSTfilter
what is the most effective way to increase urea clearance in a patient on CVVH with a QB of 150 ml/min?
increase QB
first step in evaluation and management in a patient with a differential diagnosis of prerenal azotemia secondary to volume depletion, HRS, or ATN
adequate volume repletion with IV isotonic crystalloid
- AKI
- anemia
- hypercalcemia
- low AG
- discrepancy between urine dipstick (trace protein) and UPC
MM with light chain cast nephropathy
amyloidosis can also be associated with presence of paraprotein, like MM, but on urine studies what is different?
significant albuminuria and NO discrepancy between protein by urine dipstick and UPC
- decompensated cirrhosis
- progressively worsening renal function
- low BP
- low urine Na+
HRS
pathophysiology of AKI in setting of heart failure
- venous congestion –> activates sympathetic and RAA systems –> intrarenal vasoconstriction
- increased intraabdominal pressure
best initial treatment to reduce risk of intratubular cast formation and AKI in rhabdomyolysis
rapid infusion of IV 0.9% saline
antibiotics, plasmapheresis, antimotility agents, and antiplatelet agents are not recommended in what condition?
diarrhea-associated HUS
home BP measurements have been established to lead to
improved medication adherence
patients with renovascular disease treated with what have reduced morbidity and mortality as compared with treatment with other agents?
RAAS blockade
treatment in a patient with renovascular HTN with a solitary functioning kidney
endovascular stent placement of renal artery for functioning kidney
elevated renin levels represent a loss of perfusion pressure to the juxtaglomerular apparatus, not a
decrease in oxygen levels
best treatment for a pregnant patient with increase in BP 2/2 FMD
renal angiography and percutaneous transluminal renal angioplasty (PTRA)
What are the major trials about AKI and timing of RRT
AKIKI
IDEAL-ICU
STARRT-AKI
10-15% pts admitted to icu will need RRT
-early initiation didnt improve outcomes
-BUT studies excluded pts w/ obvious needs for RRT: hyperK, sev met acid, vol overload
complications of hypophos in ICU pts (importance of monitoring while on CRRT)
difficulty weaning from vent, greater need for trach, alter oxygen carrying capacity by affecting levels of 2,3 bisphosphoglycerate -> lower levels increase hob oxygen binding = decreased release to peripheral tissues
-> AVOID low phos enteral formulas
-> caution with IV phos d/t risk hypocalcemia + arrythmias
Post-obstructive diuresis management
TX: 0.45% saline at 0.75ml/ml of UOP over the first 24hrs
urine is relatively hypotonic -> replace with hypotonic IVF
how long does it take for hydronephrosis to resolve after appropriate treatment
varies; minutes to several months (typically weeks to months); normal for residual hydro at 2wks.
US: fluid is black (hypoechoic); blood, stent = hyper echoic
adrenal vein sampling calculations
selectivity index (adrenal vein to IVC cortisol ratio)
=> tells if AVS Cath is in adrenal vein
=> at least 5
Lateralization index
=> aldosterone measured in both veins -> cal if unilateral or b/l
=> R:L if one side. >4 -> unilateral dz; <3 bilateral dz
what happens with black licorice ingestion
Syndrome of Apparent Mineralocorticoid Excess [SAME]
-> glycyrrhetinic acid inhibits enzyme beta hydroxysteroid dehydrogenase type 2 -> cortisol is not detoxified to cortisone
->nml = intracellular cortisol higher than Aldo and can activate MR
=> inhibit eznzyme = hyperaldo phenotype but ALDO ISNT ELEVATED
What is Glucocorticoid remediable aldosteronism (GRA)?
AD
- translocation of ACTH-sensitive promoter w/ gene for aldosterone synthase
=> leads to ACTG-mediated aldosterone secretion
=>dexamethasone suppress test = glucocorticoids would suppress aldosterone release
What is normal renin and aldosterone level?
PRA: 0.2-3.6, upright
PA: <= 10, seated
OSA is associated with what other issues?
Resistant HTN
Primary aldosteronism
Diabetes
Afib
Fatigue
Nocturnal non-dipping of BP (decrease <10%) on ABPM
-> nml nocturnal BP decr by 10-20%
What did the TIME trial show?
What are the indications for SGLT2i
DM albuminuria reduced eGFR CHF
example of IRAEs (immune related adverse events) associated with ICI use
Hypothyroidism (or hyper)
10% - unknown mechanism
?AI thyroids caused by T cells
-mental status change, fatigue, narrow PP, Brady
-hypophysitis -> 2ndary hypoadrenalism -> hyperkalemia/hypotension
how does hypothyroidism lead to HTN
bradycardia -> reduced cardiac output -> incr SVR and slowed ventricular relaxation -> high SBP and narrow PP
beta blockers ** the PRA by ** the secretion of renin
beta blockers reduce the PRA by reducing the secretion of renin
how do ACE inhibitors reduce the PAC and can increase the PRA
by reducing the availability of angiotensin II
