Acute Kidney Injury Search the site ...

March 16, 2023 by Josh

Josh Farkas
Farkas

TOC ABOUT THE IBCC TWEET US RSS IBCC PODCAST

CONTENTS
Rapid Reference: Approach to AKI (#rapid_reference:_approach_to_AKI)

De<nition & signi<cance of AKI (#de<nition_&_signi<cance_of_AKI)

Causes of AKI (#causes_of_AKI)
Nephrotoxins (#nephrotoxins)
Evaluation of the cause of AKI (#evalaki)
Tests not to order (#tests_not_to_order)
Tests to evaluate the cause of AKI (#tests_to_evaluate_the_cause_of_AKI)
Approach to oliguria (#approach_to_oliguria)
Furosemide stress test (#furosemide_stress_test)
Management of AKI (#management_of_AKI)
Dose-adjust renally cleared medications (#dose-
adjust_renally_cleared_medications)

Hemodynamic optimization (#hemodynamic_optimization)

Treatment of acidosis (#treatment_of_acidosis)
Dialysis (#dialysis)
Phosphate binder (#phosphate_binder)
Related/miscellaneous
Uremic encephalopathy (#uremic_encephalopathy)
Dialysis disequilibrium syndrome (#dialysis_disequilibrium_syndrome)
Dialysis modalities (#dialysis_modalities)

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 Estimating GFR from vancomycin clearance
(#estimating_GFR_based_on_vancomycin_clearance)

rapid reference: approach to AKI

(back to contents) (#top)

evaluation of the cause of AKI

labs

Basic
Basic labs:
labs:
Electrolytes
Electrolytes (including Ca/Phos/Mg).
Creatinine
Creatinine Kinase.
Kinase.
Urinalysis
Urinalysis (table below; if urinalysis suggests glomerulonephritis or
acute interstitial nephritis, consult nephrology to review the urine
microscopy).
Additional
Additional labs
labs:
Relevant drug levels (e.g., vancomycin, aminoglycoside, cyclosporine,
tacrolimus).
Uric acid if concern for tumor lysis syndrome.
(https://emcrit.org/ibcc/tls/#diagnosis)

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 (https://emcrit.org/ibcc/aki/attachment/urinalysisjp/)

renal & bladder ultrasound

The primary role is the exclusion of hydronephrosis. However, this may

provide additional information (e.g., scarred or polycystic kidneys).
Immediate bedside ultrasonography may expedite diagnosis (don't forget to
look at the bladder).
If an abdominal CT scan was recently done for another reason, this is
adequate to exclude hydronephrosis.

management of AKI

treat any identifiable cause(s) (#causes_of_AKI)

medication management

Discontinue nephrotoxins. (#nephrotoxins)

Dose-adjust renally cleared medications. (#dose-

adjust_renally_cleared_medications)

potassium

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 D/C potassium supplementation, potassium-sparing diuretics, or PRN
potassium orders (hold potassium unless K<3.0 mM).
(https://emcrit.org/ibcc/hypokalemia/#target_potassium_level?)

Treat hyperkalemia if present.

(https://emcrit.org/ibcc/hyperkalemia/#rapid_reference:_treatment_severe_hyperkalemia)

phosphate

Renal diet in severe AKI.

Consider phosphate binder if phosphate >6 mg/dL. (#phosphate_binder)

In hypocalcemia: calcium carbonate or calcium acetate (~600 or ~667

mg TID with meals).
Otherwise: sevelamer 800 mg TID with meals.

acidosis management

Consider bicarbonate for uremic metabolic acidosis. (#treatment_of_acidosis)

hemodynamic optimization (#hemodynamic_optimization)

Defend the MAP.

Hold antihypertensives if soft Bp (especially negative inotropes).

definition & significance of AKI

(back to contents) (#top)

KDIGO criteria for acute kidney injury (assigned based on most

worrisome feature)

Stage
Stage II AKI
AKI
Cr 1.5-1.9 times baseline.

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 Cr increase >0.3 mg/dL.
Urine output <0.5 ml/kg/hr for 6-12 hours.
Stage
Stage IIII AKI
AKI
Cr 2-2.9 times baseline.
Urine output <0.5 ml/kg/hr for 12-24 hours.
Stage
Stage III
III AKI
AKI
Cr >3 times baseline.
Cr >4 mg/dL.
Initiation of dialysis.
Urine output <0.3 ml/kg/hr for >24 hours.
Anuria >12 hours.

more detailed understanding of types of AKI

Prognosis depends on changes in urine output and creatinine (agure above).

(25568178 (https://pubmed.ncbi.nlm.nih.gov/25568178/) ) Some speciac types bear
mention:
Isolated
Isolated oliguria
oliguria (low urine output with stable creatinine).
These patients rarely require dialysis, unless oliguria is profound (Stage
3).
This may often represent “pre-renal” renal failure – the kidney is
compensating for hypoperfusion by reducing urine output, but is
continuing to function adequately.
Be careful, however, because sometimes patients maintain a stable

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 creatinine from a dilutional effect due to receiving lots of intravenous
fuid. In that situation, creatinine may overestimate the renal function.
Oliguria should be taken seriously and evaluated adequately. However,
<12 hours of oliguria isn't necessarily a disaster – especially if the
creatinine remains stable.
Non-oliguric
Non-oliguric renal
renal failure
failure (elevated creatinine with normal urine output)
The vast majority of these patients (99.7% overall) won't require dialysis.

causes of AKI
(back to contents) (#top)

pre-renal: disorders of perfusion

Shock of any etiology (e.g., hypovolemic shock, cardiogenic shock).

Hepatorenal syndrome.
Congestive nephropathy (systemic congestion impairs venous outfow).
Abdominal compartment syndrome.
Hypertensive emergency.
Thrombotic thrombocytopenic purpura & hemolytic uremic syndrome.

intrinsic renal failure

Nephrotoxic medications (listed below).

Cellular lysis (rhabdomyolysis, hemolysis, tumor lysis syndrome).
Acute glomerulonephritis.
Acute tubulointerstitial nephritis (ATIN).
Acute tubular necrosis (ATN).

post-renal: Urologic obstruction

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 Prostate obstruction.
Occluded or malpositioned Foley catheter.
Nephrolithiasis.

nephrotoxins
(back to contents) (#top)

cardiovascular medications

Direct:
ACE inhibitors and angiotensin receptor blockers (ARBs).
Triamterene.
Indirect:
For patients with borderline cardiac output, medications that reduce
cardiac output may be nephrotoxic (e.g., beta-blockers, diltiazem).
For patients with borderline hypotension, antihypertensives may be
nephrotoxic.

antibiotics

Aminoglycosides.
Beta-lactams rarely cause interstitial nephritis (especially penicillins such as
nafcillin, piperacillin, and ampicillin).
Colistimethate (Colistin).
Sulfonamides.
Vancomycin.

antifungals

Amphotericin.

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 Pentamidine. (31665764 (https://pubmed.ncbi.nlm.nih.gov/31665764/) )

antivirals (not exhaustive)

Acyclovir, ganciclovir, valacyclovir, valganciclovir (crystal deposition).

Cidofovir.
Foscarnet.
Indinavir.
Tenofovir.

chemotherapy (not exhaustive)

Many newer biologics and small-molecule inhibitors (not listed individually).

Bevacizumab.
Busulfan.
Carboplatin.
Checkpoint inhibitors.
Cisplatin.
Cyclophosphamide
Ifosfamide.
Methotrexate.
Mitomycin.
Oxaliplatin.

miscellaneous

Antiepileptics (topiramate, zonisamide).

Bisphosphonates (pamidronate, zoledronic acid).
Immunosuppressives:
Calcineurin inhibitors (cyclosporine, tacrolimus).
mTOR inhibitors (sirolimus, everolimus).
Infammatory bowel disease medications (mesalamine, sulfasalazine).

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 Intravenous immunoglobulin (IVIG).
Mannitol.
NSAIDs. (39230007 (https://pubmed.ncbi.nlm.nih.gov/39230007/) )

tests not to order

(back to contents) (#top)

Urine electrolytes & fractional excretion of sodium (FENa).

Previously, it was believed that urine sodium excretion and fractional
excretion of sodium (FENa) could help differentiate between “prerenal”
and “intrinsic renal” failure. However, more recent evidence shows that
FENa performs poorly. (27236480
(https://pubmed.ncbi.nlm.nih.gov/27236480/) , 26689284
(https://pubmed.ncbi.nlm.nih.gov/26689284/) , 27670788
(https://pubmed.ncbi.nlm.nih.gov/27670788/) )

Urine eosinophils have poor performance for diagnosing acute

tubulointerstitial nephritis. (24052222 (https://pubmed.ncbi.nlm.nih.gov/24052222/) )

approach to oliguria
(back to contents) (#top)

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 significance of oliguria

Oliguria is a subset of acute kidney injury deaned by low urine output (<0.3-
0.5 ml/kg/hr for several hours, or roughly <500 ml/day). (29156029
(https://pubmed.ncbi.nlm.nih.gov/29156029/) )

Although oliguria has traditionally often been interpreted as a surrogate for

hypovolemia, this is not accurate. Oliguria can be caused by any type of renal
failure (if sunciently severe).

This is intended merely as a rough conceptual schema to oliguria, not a rigid

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 protocol. For example, if evaluation reveals the presence of a speciac diagnosis
(e.g., septic or cardiogenic shock), then further treatment will be aimed at that
problem. The main issue is to put some thought into this rather than refexively
administering fuids.

#1: exclude obstruction

Obstruction is rare, but this is a must-not-miss diagnosis.

The gold standard is bedside ultrasonography of the bladder and kidneys.
Simply performing a bladder ultrasound is probably adequate since this
may evaluate for urethral obstruction. Unilateral ureteral obstruction
shouldn't cause oliguria due to urine production from the contralateral kidney
Trouble-shooting the Foley catheter (via fushing) is reasonable, but not
infallible.

#2: hemodynamic evaluation

Perform a brief chart review focusing on vital sign trends, new medications
added (e.g., antihypertensives), and cardiac history.
Evaluation generally focuses on volume status, but other factors should also
be considered (e.g., cardiac output).
If the patient is hypertensive, this suggests the presence of intrinsic renal
failure (rather than shock or hypovolemia).

#3a: volume challenge?

Indicated for total-body hypovolemia.

The best indications for providing fuid are one of the following:
(1) Input/output trends showing that the patient is substantially net
negative over the past day (e.g., salt-wasting nephropathy or aggressive
diuresis).
(2) Clinical history of nausea/vomiting, diarrhea, and poor oral intake

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 combined with echocardiogram showing hypovolemia.
(3) POCUS suggesting volume depletion.
If the patient is hypertensive, this argues against hypovolemia, making fuid
administration less likely to help.

#3b: vasopressor challenge?

Although a MAP >65 mm is adequate for most patients, some patients with
chronic hypertension may require a higher blood pressure to perfuse their
kidneys adequately.
If there is concern that the MAP is too low, then the blood pressure can be
raised for a couple of hours with an infusion of norepinephrine or
phenylephrine (e.g., to MAP >75 mm). If this stimulates urine output, the
higher MAP should be maintained.

#3c: inotrope challenge?

If there is evidence of poor cardiac output and concern for cardiogenic

shock, it may be reasonable to trial an inotrope.
Improved urine output following inotrope initiation conarms a diagnosis of
cardiogenic shock. In this case, continue to treat the cardiogenic shock as
discussed here: (https://emcrit.org/ibcc/chf/) .

#3d: furosemide stress test

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 This is a validated test of renal function, which predicts the likelihood of
persistent renal failure and dialysis. (24053972
(https://pubmed.ncbi.nlm.nih.gov/24053972/) , 25655065
(https://pubmed.ncbi.nlm.nih.gov/25655065/) , 29344743
(https://pubmed.ncbi.nlm.nih.gov/29344743/) , 29673370
(https://pubmed.ncbi.nlm.nih.gov/29673370/) )

If the patient fails the furosemide stress test, this suggests signiacant
intrinsic renal failure. In this situation, further hemodynamic manipulation is
unlikely to help. This can help support a decision to stop giving the patient
fuids.
(More about the furosemide stress test in the next section)

furosemide stress test

(back to contents) (#top)

definition of a furosemide stress test

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 Administration of a deaned dose of furosemide:
1 mg/kg for patients who are furosemide naive.
1.5 mg/kg for patients with prior exposure to furosemide.
Monitoring urine output
>200 ml within two hours indicates adequate response.

significance

Failure to respond to a furosemide stress test suggests renal failure (with an

increased risk of requiring hemodialysis).
(https://emcrit.org/pulmcrit/furosemide-stress-test/)

Please note that failure to respond doesn't exclude the possibility of renal
recovery – especially if other resuscitative steps are available to improve
renal function (e.g., improvement in blood pressure and/or perfusion).

clinical utility of a furosemide stress test?

(1) The oliguric patient: Will additional hemodynamic manipulation help?

A furosemide stress test may be useful to obtain a concept of whether
the patient has intractable intrinsic renal failure.
Failure to respond to furosemide implies that the kidneys are less likely
to respond to hemodynamic manipulation (e.g., volume administration)
and more likely to progress toward dialysis. Thus, a fuid-conservative
strategy might be more beneacial.
Response to a furosemide stress test reveals that the kidneys are
functional. Therefore, hemodynamic manipulations to maintain urine
output (e.g., volume administration, inotropes, vasopressors) may be
more likely to succeed.
(2) A patient who is volume overloaded and requires diuresis:
Using the dose of furosemide prescribed in the furosemide stress test
can help interpret the patient's response more rigorously.

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 management of AKI
(back to contents) (#top)

Renal failure in the ICU is generally multifactorial. Treatment involves identifying

and addressing all contributory factors (e.g., nephrotoxins (#nephrotoxins) as listed
above). In addition, a variety of supportive therapies are important.

dose-adjust renally cleared medications

(back to contents) (#top)

Note that calculations of the glomerular altration rate (GFR) based on

creatinine level will be misleading in acute kidney injury.
Formulas for the GFR only work in steady-state (equilibrium)
conditions. This usually isn't the case in acute kidney injury.

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 For example, with complete cessation of renal function, the creatinine
will often increase by roughly ~1 mg/dL daily. So, if a patient's
creatinine increases from 0.7 mg/dL to 1.7 mg/dL, their GFR may be
extremely low (much lower than the calculated GFR).

hemodynamic optimization
(back to contents) (#top)

maintain an adequate MAP

MAP >65 mm is usually the target MAP for patients in AKI. MAP >80 mm
may improve renal outcomes in some patients, especially those with chronic
hypertension. (27230984 (https://pubmed.ncbi.nlm.nih.gov/27230984/) )
When in doubt, consider a vasopressor challenge: give the patient
pressor to increase the MAP and determine whether this improves urine
output.
Regarding renal outcomes, vasopressin might have a slight advantage over
other vasopressors, particularly among patients with tachycardia and
systemic vasodilation. (27483065 (https://pubmed.ncbi.nlm.nih.gov/27483065/) )

maintain euvolemia

Generally
Generally avoid
avoid cuids.
cuids.
Non-oliguric AKI generally isn't due to hypoperfusion and shouldn't be
an indication for extra fuids.
Fluid should be given only if, after thoughtful assessment, there is
evidence of hypovolemia (more on this above).
If
If cuids
cuids are
are used,
used, choose
choose the
the best
best one.
one.
For patients with hypovolemia and uremic acidosis, the fuid of choice is

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 isotonic bicarbonate (D5W with 150 mEq/L sodium bicarbonate). More
on this below (#treatment_of_acidosis) .
For patients with hypovolemia and normal serum bicarbonate, the fuid
of choice is a balanced crystalloid (e.g., lactated Ringers or plasmalyte).
Avoid normal saline. (27230984 (https://pubmed.ncbi.nlm.nih.gov/27230984/) ,
29485926 (https://pubmed.ncbi.nlm.nih.gov/29485926/) , 29485925
(https://pubmed.ncbi.nlm.nih.gov/29485925/) ) Contrary to popular dogma,
lactated Ringers or plasmalyte are entirely safe
(https://emcrit.org/pulmcrit/myth-busting-lactated-ringers-is-safe-in-hyperkalemia-and-

is-superior-to-ns/) in hyperkalemia (whereas normal saline is unsafe).

Avoid
Avoid volume
volume overload.
overload.
Overload may cause renal intra-capsular edema (swelling within the
kidney that impairs perfusion, a bit like compartment syndrome).
Furthermore, increased central venous pressure impairs renal perfusion
by hampering venous blood fow from the kidney (a.k.a. congestive
nephropathy). Among patients with marked systemic venous
congestion, diuresis may often improve renal function!
Basic steps to avoid volume overload include avoiding maintenance
fuid or repeated fuid boluses.
Follow fuid balance (inputs vs. outputs) and avoid ongoing volume
accumulation or total net gain of more than a few liters. For example, if
the patient is running a net of 1-2 liters positive per day, this will rapidly
become a signiacant problem.
Diuresis (furosemide with or without a thiazide) should be used to
prevent or treat volume overload. Patients with renal failure may require
prodigious diuretic doses. If this isn't effective, dialysis may be needed
to control the volume status.

treatment of acidosis

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 (back to contents) (#top)

bicarbonate vs. dialysis

Nephrologists have used bicarbonate to stave off dialysis for decades. More
recently, the BICAR-ICU trial demonstrated that bicarbonate use in the ICU to
treat anion-gap metabolic acidosis does indeed avoid dialysis. (29910040
(https://pubmed.ncbi.nlm.nih.gov/29910040/) ) It's not entirely clear whether
bicarbonate actually improves renal function or whether it merely improves
acidosis. Regardless, avoidance of dialysis is a meaningful patient-centered
outcome.
Sodium bicarbonate is generally the arst-line therapy for uremic acidosis.
The exact target level isn't clear, but shooting for a pH >7.2 may be
reasonable (often equivalent to a bicarbonate level over ~17 mEq/L).
(29910040 (https://pubmed.ncbi.nlm.nih.gov/29910040/) )
Dialysis is the second-line therapy for acidosis in situations where
bicarbonate is ineffective or contraindicated.

formulations & route of bicarbonate:

Isotonic
Isotonic bicarbonate
bicarbonate is useful for patients with volume depletion (D5W
with 150 mEq/L sodium bicarbonate). The problem with isotonic bicarbonate
is that for patients who are euvolemic or hypervolemic, it provides a
substantial volume load.
Hypertonic
Hypertonic bicarbonate
bicarbonate ampules
ampules (50 ml ampules of 1 mEq/ml
bicarbonate) are great for patients with hyponatremia. For example, two
ampules (100 mEq/L) typically increase the bicarbonate and sodium by ~3
mEq/L. Ampules should be pushed slowly over ~10 minutes each to avoid
rapid swings in pH. The problem with this strategy is that for patients with
baseline sodium over ~140 mEq/L, it may cause hypernatremia.
Oral
Oral bicarbonate
bicarbonate tablets
tablets can be used for patients with mild acidosis to

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 prevent worsening over time.
Each 650 mg tablet contains 7.6 mEq of sodium bicarbonate (which
isn't much).
1300 mg BID or TID provides 30 or 45 mEq bicarb daily, respectively.

dialysis
(back to contents) (#top)

Potential indications:
Acidosis refractory to IV bicarbonate.
Electrolyte abnormalities (typically diuresis-refractory hyperkalemia).
Fluid overload refractory to diuretics.
Uremic symptoms (e.g., delirium, asterixis, pericardial effusion).
Early versus late initiation of dialysis remains controversial. The best
indication for earlier dialysis may be a patient progressively accumulating
fuid and developing severe volume overload. As discussed above, even in
the absence of frank pulmonary edema, systemic congestion may directly
harm the kidneys, perpetuating renal dysfunction.

phosphate binder
(back to contents) (#top)

Initiate phosphate binder if phosphate is >6 mg/dL.

Calcium
Calcium acetate
acetate (http://reference.medscape.com/drug/eliphos-phoslo-calcium-acetate-
344430) (PHOSLO)

667 mg tablets, start with two tablets TID with meals

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 Useful in patients with hypocalcemia. Avoid in hypercalcemia or vitamin
D intoxication.
Sevelamer
Sevelamer (http://reference.medscape.com/drug/renagel-renvela-sevelamer-343208)
(RENAGEL)
Start at 800 mg PO TID with meals, double dose if needed.
Nonabsorbable resin avoids problems with Mg and Ca (may be
preferable for patients on dialysis).
May impair absorption of some drugs from the gut.

uremic encephalopathy
(back to contents) (#top)

clinical findings:

Clinical context:
GFR is usually <10-15 ml/min.
Acute
Acute renal
renal failure
failure carries a higher risk than chronic renal failure.
Movement disorders:
Myoclonus
Myoclonus and asterixis
asterixis (“negative myoclonus”). Myoclonus has an
extensive differential diagnosis (https://emcrit.org/ibcc/move/#myoclonus) .

In the absence of an alternative explanation for myoclonus, this may be

highly suggestive of uremic encephalopathy.
Tremor.
Muscle spasms (including spontaneous carpopedal spasm). (Louis
2021)
Delirium.
Seizures.

lumbar puncture

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 Not indicated to evaluate uremic encephalopathy, but may be needed to
exclude alternative diagnoses.
Protein may be mildly elevated (>100 mg/dL), occasionally with a mild
pleocytosis. (Louis 2021)

EEG

Background slowing may occur.

GPDs
(https://emcrit.org/ibcc/eeg/#GPDs_%E2%80%93_Generalized_Periodic_Discharges)

(generalized periodic discharges) with triphasic morphology may appear.

NCSE (nonconvulsive status epilepticus) may occur – and this is important
to recognize since treatment may cause dramatic improvement. (Louis
2021)

neuroimaging findings:

Three patterns may be seen:(31589567

(https://pubmed.ncbi.nlm.nih.gov/31589567/) )

(1) Basal ganglia involvement may be the most common:

Basal ganglia hyperintensities are seen.
“Lentiform fork sign” – bright rim highlights the medial and lateral edges
of the putamen (agure below).
(2) Posterior Reversible Encephalopathy Syndrome (PRES): Uremia may
promote the development of PRES, especially in combination with
hypertension. (https://emcrit.org/ibcc/pres/#imaging)

(3) Acute toxic leukoencephalopathy.

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 (https://emcrit.org/ibcc/aki/attachment/lentiformfork/)

di"erential diagnosis

The differential diagnosis is broad, including other causes of delirium as

discussed here: (https://emcrit.org/ibcc/delirium/#top)

Accumulation of renally cleared medications should be carefully considered.

NCSE (nonconvulsive status epilepticus).
PRES (posterior reversible encephalopathy syndrome).
Metabolic disturbances (e.g., severe electrolyte abnormalities).

management

Evaluate and treat for any/all coexisting causes of delirium.

Uremic encephalopathy generally responds well to dialysis, but this response

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 may be delayed for some days (e.g., the arst dialysis run may cause transient
worsening). (Louis 2021)

dialysis disequilibrium syndrome

(back to contents) (#top)

Dialysis disequilibrium syndrome usually occurs following initiation of

dialysis among patients with severe baseline azotemia.
Symptoms vary from nausea and mild headache to delirium and seizures.
The central pathophysiology appears to be a rapid reduction in blood urea
nitrogen levels, causing osmotic shifts that result in cerebral edema.
The differential diagnosis is similar to the differential diagnosis of uremic
encephalopathy (listed above).
Management:
Use of dialysate with higher sodium concentration may avoid osmotic
shifts.
In patients with persistent and severe symptoms, hypertonic saline may
be considered to reverse cerebral edema. (Louis 2012)

dialysis modalities
(back to contents) (#top)

hemodialysis (hemodialyzer machine)

IHD (intermittent hemodialysis)

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 Diffusion promotes solute clearance.
Urea, creatinine, and potassium usually leave blood.
Bicarbonate and usually calcium enter the blood.
Sodium may enter or leave (to equilibrate with dialysate).
Convection (via ultraaltration) allows for volume removal.
High blood fow rate (~350-400 ml/min) and high dialysate fow rate (500-
800 ml/min). (Schmidt 2024)

SLED (sustained low-e#ciency dialysis)

May be used as a PIRRT (prolonged intermittent renal replacement therapy).

The blood fow rate is lower than with IHD (150-250 ml/min), as is the
dialysate fow rate (100-200 ml/min). (Schmidt 2024)
Typically, a slow hemodialysis session is performed over 8-12 hours daily.
(Vincent 2024)
The primary advantage of SLED is that it may allow for patient mobilization
during the day.
SLED is rarely used, usually in response to resource constraints. (Irwin 2023)

UF (ultrafiltration)

Isolated ultraaltration is performed, which solely removes fuid.

Used for patients with isolated volume overload.

dialysate composition

Potassium level: 1-4 mM.

1 mEq/L used for severe hyperkalemia (does carry the risk of
arrhythmias due to rapid potassium clearance). (Irwin 2023)
Bicarbonate:
Usually 33-35 mM.
40 mEq/L may be used for chronic hypercapnia, or severe acidosis.

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 Calcium:
Usually 2.5 mM.
3-3.5 mM may be used to avoid hypocalcemia (especially with acidosis
correction). (Irwin 2023)

CRRT (continuous renal replacement therapies using a hemofilter)

SCUF (slow continuous ultrafiltration)

Fluid removal with minimal solute clearance.

Similar to ultraaltration (used for volume removal).

CVVH (continuous venovenous hemofiltration)

CVVH = SCUF plus replacement fuid. Convection is used to achieve solute

clearance and fuid removal.
Ultraaltrate is generated at 1-4 liters/hour and replaced with RF (replacement
fuid). This creates high volumes of ultraaltrate (~48-96 liters/day). (Irwin
2023)
Convective clearance removes small and middle-sized molecules (<5000
Da), including cytokines. (Schmidt 2024)

CVVHD (continuous venovenous hemodialysis)

This is purely dialysis, causing solute clearance via diffusion.

The blood fow rate is slower than IHD (~100-250 ml/min), but the major
difference is that the dialysate fow rate is much slower (25-30 ml/min, or
~1-2 liters/hour). This causes complete equilibration of solutes with the
dialysate. (Irwin 2023)
Effectively clears small molecules (<100 Da).

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 CVVHDF (continuous venovenous hemodiafiltration)

This combines dialysis (diffusive clearance) and altration (convective

clearance).
Dialysate is infused at 1-2 liters/hour.
Replacement fuid is added at 1-2 liters/hour.
May be unnecessarily complex (newer CVVHD machines are adequate and
more straightforward). (Irwin 2023)

anticoagulation with CRRT

Heparin is often necessary (e.g., bolus of 1000-2000 IU, followed by 10

IU/kg/hr to target an aPTT of 1.5-2 times normal). (Irwin 2023)
Regional citrate anticoagulation limited to the CRRT circuit is recommended
for patients without contraindications by the KDIGO-AKI Clinical Practice
Guidelines. (Irwin 2023)
Advantages of regional citrate anticoagulation may include prolonged
alter life, lower transfusion requirement, and reduced incidence of
hemorrhagic complications. (Vincent 2024)
Ionized calcium must be monitored carefully, especially in patients with
hepatic dysfunction (who may accumulate citrate, leading to reduced
ionized calcium levels with elevated anion gap metabolic acidosis).
Other risks include hypernatremia and hypomagnesemia.

electrolyte monitoring and adjustments

Hypophosphatemia is common, but this may be mitigated by adding

phosphate to dialysate.

dose of CRRT

CRRT is dosed in terms of the esuent fow rate, with a range of 20-35
ml/kg/hr.

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 Esuent reaches equilibrium with the blood, so the esuent rate equals
the clearance rate.
A minimum dose of 20-25 ml/kg/hr should be delivered. (Schmidt 2024)
Risk of inadequate dosing: poor metabolic control of acidosis or uremia.
Risk of excessive dosing: micronutrient deaciency, excessive clearance of
medications.

selection of IHD vs. CRRT

advantages of CRRT

[1] CRRT promotes greater hemodynamic stability (avoiding hypotension

may promote renal recovery).
[2] CRRT is superior for volume management. (CRRT is capable of slowly and
continuously removing volume, which may achieve much higher amounts of
fuid removal when multiple across 24 hours. Alternatively, IHD leads to intra-
dialytic fuid accumulation.)
[3] CRRT is preferred for patients with ICP elevation:
Less fuctuation in cerebral perfusion pressure and intracranial
pressure.
Recommended by KDIGO guidelines for patients with cerebral edema.
[4] CRRT is preferred in ALF (acute liver failure):
IHD may cause rapid clearance of water and solutes, causing elevated
intracranial pressure.
EASL (European Association for the Study of the Liver) and KDIGO-AKI
recommend CRRT instead of IHD.
Hyperammonemia may be an indication for dialysis in the context of
acute liver failure to avoid intracranial pressure crises (discussed
further: (https://emcrit.org/ibcc/alf/#neurology) ).

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 [5] CRRT can be safely utilized in severe hyponatremia:
IHD will immediately increase the sodium to a normal level. It is often
impossible to reduce the dialysate sodium concentration to <130 mM.
CRRT may avoid rapid sodium shifts by adjusting the dialysate fuid
(table below). An alternative strategy is to run a separate infusion of
hypotonic fuid independent of the dialysate. (34218456
(https://pubmed.ncbi.nlm.nih.gov/34218456/) )

[6] Rhabdomyolysis or tumor lysis syndrome.

CRRT may be more effective than IHD for clearance of
hyperphosphatemia.

advantages of IHD

Preferred for intoxications due to more rapid toxin clearance.

Preferred for extreme hyperkalemia.
May facilitate physical therapy.
May facilitate off-unit testing or procedures.

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 criteria for discontinuation of CRRT in acute kidney injury

Criteria utilized in the ATN study:

Urine output >30 ml/hour.

Six-hour timed urine collection utilized to calculate creatinine clearance:
Creatinine Clearance = (Urine [Cr])x(Urine volume)//(Plasma [Cr])(360
minutes)
Creatinine clearance <12 ml/min: continue CRRT.
Creatinine clearance 12-20 ml/min: Individualize ongoing CRRT.
Creatinine clearance >20 ml/min: Discontinue CRRT. (18492867
(https://pubmed.ncbi.nlm.nih.gov/18492867/) )

estimating GFR based on vancomycin clearance

(back to contents) (#top)

There are two methods to estimate GFR based on vancomycin clearance.

method #1: single compartment model

Baseline assumptions:
Vancomycin clearance = 0.82(creatinine clearance). (19933799
(https://pubmed.ncbi.nlm.nih.gov/19933799/) ) Various studies have reported a
ratio between 0.75-0.9, so 0.82 seems reasonable.
Volume of distribution = 0.7 L/kg. This factor is subject to greater
variation between studies, but 0.7 L/kg seem to be a reasonable agure
that is often quoted in pharmacokinetic textbooks.
Vancomycin is modeled using single-compartment pharmacokinetics.

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 Based on these assumptions, GFR (creatinine clearance) may be estimated
based on the concentration at two time points, the time elapsed between
measurements, and the patient's weight:
GFR in ml/min = 14*ln(C2/C1)*(wt in kg)/(Δ time in hours)

method #2: Creighton equation

The elimination constant (Kel) of vancomycin is linearly related to the

creatinine equation based on the following equation: (6732213
(https://pubmed.ncbi.nlm.nih.gov/6732213/) )

Kel (/hr) = 0.00083(Creatinine clearance in ml/min) + 0.0044

Kel = ln (C2/C1)/(Δ time in hours)
This equation is widely cited in pharmacokinetic literature and has been the
basis of some studies on vancomycin pharmacokinetics. (32166646
(https://pubmed.ncbi.nlm.nih.gov/32166646/) ) However, when various authors try to
replicate this equation, the results are somewhat variable
(https://www.rxkinetics.com/vanmodel.html) .

comparison of methods

The online calculator below will estimate GFR using both methods.
For weights around 70 kg, the results are similar. For higher weights, the 1-
compartment model will produce a higher GFR (since it's calculating an
absolute creatinine clearance). Alternatively, the Creighton equation yields
the same GFR regardless of weight (effectively calculating a GFR corrected
for body surface area).

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:
 podcast
(back to contents) (#top)

(https://i0.wp.com/emcrit.org/wp-

content/uploads/2016/11/apps.40518.14127333176902609.7be7b901-15fe-4c27-

863c-7c0dbfc26c5c.5c278f58-912b-4af9-88f8-a65fff2da477.jpg)

Follow us on iTunes (https://itunes.apple.com/ca/podcast/the-internet-book-of-

critical-care-podcast/id1435679111)

The Podcast Episode

00:00 00:00

Want to Download the Episode?

Right Click Here and Choose Save-As
(http://trahc.libsyn.com/ibccpodcast/IBCC_EP_18_AKI_Final.mp3)

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Page 31 of 36
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 questions & discussion
(back to contents) (#top)

To keep this page small and fast, questions & discussion about this post can be
found on another page here
here (https://emcrit.org/pulmcrit/acute-kidney-injury/) .

Failing to evaluate AKI in the ICU fully. Most cases of AKI will resolve without
speciac intervention (e.g., with treatment of underlying sepsis). However,
occasionally, a speciac issue is identiaed which requires particular therapy
(e.g., Foley catheter obstruction, glomerulonephritis). Finding these patients
is like hunting for a needle in a haystack.
Measurement of urine electrolytes and calculating fractional excretion of
sodium (FENa) isn't helpful. (27236480
(https://pubmed.ncbi.nlm.nih.gov/27236480/) , 26689284
(https://pubmed.ncbi.nlm.nih.gov/26689284/) , 27670788
(https://pubmed.ncbi.nlm.nih.gov/27670788/) )

Blind assumption that any patient with oliguria requires a fuid bolus.

Guide to emoji hyperlinks

= Link to online calculator.

= Link to Medscape monograph about a drug.
= Link to IBCC section about a drug.

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 = Link to IBCC section covering that topic.
= Link to FOAMed site with related information.
= Link to supplemental media.

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39230007 Barreto EF, Gaggani AM, Hernandez BN, Amatullah N, Culley
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Medications That Are Renally Eliminated and Nephrotoxic in the Acutely Ill.
Ann Pharmacother. 2024 Sep 4:10600280241273191 (tel:1060028024127319
1) . doi: 10.1177/10600280241273191 [PubMed (https://pubmed.ncbi.nlm.nih.go
v/39230007/) ]

The Internet Book of Critical Care is an online textbook written

by Josh Farkas (@PulmCrit), an associate professor of Pulmonary
and Critical Care Medicine at the University of Vermont.

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