CONTENTS
- Rapid Reference: Approach to AKI 🚀
- Definition & significance of AKI
- Causes of AKI
- Evaluation of the cause of AKI
- Tests to evaluate the cause of AKI
- Approach to oliguria
- Management of AKI
- Related
- Podcast
- Questions & discussion
- Pitfalls
evaluation of the cause of AKI
labs
- Basic labs:
- Electrolytes (including Ca/Phos/Mg).
- Creatinine Kinase.
- Urinalysis (table below; if urinalysis suggests glomerulonephritis or acute interstitial nephritis, consult nephrology to review the urine microscopy).
- Additional labs:
- Relevant drug levels (e.g. vancomycin, aminoglycoside, cyclosporine, tacrolimus).
- Uric acid if concern for tumor lysis syndrome. 📖
renal & bladder ultrasound
- The main role is 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 abdominal CT scan was recently done for another reason, this is adequate to exclude hydronephrosis.
management of AKI
treat any identifiable cause(s) 📖
medication management
potassium
- D/C potassium supplementation, potassium-sparing diuretics, or PRN potassium orders (hold potassium unless K<3.0 mM). 📖
- Treat hyperkalemia if present. 📖
phosphate
- Renal diet in severe AKI.
- Consider phosphate binder if phosphate >6 mg/dL. 📖
- 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. 📖
hemodynamic optimization 📖
- Defend the MAP.
- Hold antihypertensives if soft Bp (especially negative inotropes).
KDIGO criteria for acute kidney injury (assign based on most worrisome feature)
- Stage I AKI
- Cr 1.5-1.9 times baseline.
- Cr increase >0.3 mg/dL.
- Urine output <0.5 ml/kg/hr for 6-12 hours.
- Stage II AKI
- Cr 2-2.9 times baseline.
- Urine output <0.5 ml/kg/hr for 12-24 hours.
- Stage III 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 (figure above).(25568178) Some specific types bear mention:
- Isolated oliguria (low urine output with stable creatinine).
- These patients rarely required 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 creatinine from a dilutional effect, due to receiving lots of intravenous fluid. 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 renal failure (elevated creatinine with normal urine output)
- The vast majority of these patients (99.7% overall) won't require dialysis.
pre-renal: disorders of perfusion
- Shock of any etiology (e.g., hypovolemic shock, cardiogenic shock).
- Hepatorenal syndrome.
- Congestive nephropathy (systemic congestion impairs venous outflow).
- 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
- Prostate obstruction.
- Occluded or malpositioned Foley catheter.
- Nephrolithiasis.
- Antibiotics:(31665764)
- Vancomycin.
- Aminoglycosides, Colistimethate (Colistin).
- Amphotericin.
- Sulfonamides.
- Pentamidine.
- Antivirals:
- Acyclovir, ganciclovir, valacyclovir, valganciclovir, foscarnet.
- Indinavir, cidofovir, tenofovir.
- Beta-lactams esp. nafcillin (can rarely cause interstitial nephritis).
- ACE-inhibitors, Angiotensin receptor blockers (ARBs).
- NSAIDs.
- Cardiac medications:
- 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.
- Calcineurin inhibitors (cyclosporine, tacrolimus, sirolimus).
- Chemotherapeutics (carboplatin, cisplatin, ifosfamide, methotrexate, mitomycin).
- Mannitol.
- Intravenous immunoglobulin (IVIG).
- Inflammatory bowel disease medications (mesalamine, sulfasalazine).
- Bisphosphonates (pamidronate, zoledronic acid).
- Antiepileptics (topiramate, zonisamide).
- Sodium chloride (0.9% or 3% in large quantity).
- Urine electrolytes & fractional excretion of sodium (FENa).
- Urine eosinophils has poor performance for diagnosing acute tubulointerstitial nephritis.(24052222)
significance of oliguria
- Oliguria is a subset of acute kidney injury defined by low urine output (<0.3-0.5 ml/kg/hr for several hours, or roughly <500 ml/day).(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 sufficiently severe).
This is intended merely as a rough conceptual schema to oliguria, not a rigid protocol. For example, if evaluation reveals the presence of a specific 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 reflexively administering fluids.
#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 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 flushing) is reasonable, but not infallible.
#2: hemodynamic evaluation
- Perform a brief chart review focusing on vital sign trends, new medications added (e.g. antihypertensives), cardiac history.
- The focus of this evaluation is generally on volume status, but other factors should be considered as well (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 fluid 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 combined with echocardiogram showing hypovolemia.
- (3) POCUS suggesting volume depletion.
- If the patient is hypertensive this argues against hypovolemia, making fluid 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 hours with an infusion of norepinephrine or phenylephrine (e.g. to MAP >75 mm). If this stimulates urine output, then maintain 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 confirms a diagnosis of cardiogenic shock. In this case, continue to treat the cardiogenic shock as discussed here: 📖.
#3d: furosemide stress test
- This is a validated test of renal function, which predicts the likelihood of persistent renal failure and dialysis.(24053972, 25655065, 29344743, 29673370)
- If the patient fails the furosemide stress test, this suggests significant intrinsic renal failure. In this situation, further hemodynamic manipulation is unlikely to help. This can be helpful to support a decision to stop giving the patient fluids.
- (More about the furosemide stress test in the next section)
definition of a furosemide stress test
- Administration of a defined 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). 🌊
- 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 towards dialysis. Thus, a fluid-conservative strategy might be more beneficial.
- 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 in a more rigorous fashion.
Renal failure in the ICU is generally multifactorial. Treatment involves identifying and addressing all contributory factors (e.g., nephrotoxins as listed above). In addition, a variety of supportive therapies are important.
- Note that calculations of the glomerular filtration rate (GFR) based on creatinine level will be misleading in the context of acute kidney injury.
- Formulas for the GFR only work in steady state (equilibrium) conditions. This usually isn't the case in acute kidney injury.
- 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).
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)
- When in doubt, consider a vasopressor challenge: give the patient pressor to increase the MAP, and determine whether this improves urine output.
- In terms of renal outcomes, vasopressin might have a small advantage over other vasopressors, particularly among patients with tachycardia and systemic vasodilation.(27483065)
maintain euvolemia
- Generally avoid fluids.
- Non-oliguric AKI generally isn't due to hypoperfusion and shouldn't be an indication for extra fluids.
- Fluid should be given only if, after thoughtful assessment, there is evidence of hypovolemia (more on this above).
- If fluids are used, choose the best one.
- For patients with hypovolemia and uremic acidosis, the fluid of choice is isotonic bicarbonate (D5W with 150 mEq/L sodium bicarbonate). More on this below.
- For patients with hypovolemia and normal serum bicarbonate, the fluid of choice is a balanced crystalloid (e.g. lactated Ringers or plasmalyte). Avoid normal saline.(27230984, 29485926, 29485925) Contrary to popular dogma, lactated Ringers or plasmalyte are entirely safe in hyperkalemia (whereas normal saline is unsafe).
- Avoid volume 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 flow out of 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 fluid or repeated fluid boluses.
- Follow fluid 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 net 1-2 liters positive per day this will rapidly become a major 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.
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 for treatment of anion-gap metabolic acidosis does indeed avoid dialysis.(29910040) It's not entirely clear whether bicarbonate actually improves renal function, or whether it merely improves the acidosis. Regardless, avoidance of dialysis is a meaningful patient-centered outcome.
- Sodium bicarbonate is generally the first-line therapy for uremic acidosis. The exact target level isn't clear, but shooting for a pH >7.2 may be reasonable (this is often equivalent to a bicarbonate level over ~17 mEq/L).(29910040)
- Dialysis is the second-line therapy for acidosis, in situations where bicarbonate is ineffective or contraindicated.
formulations & route of bicarbonate:
- Isotonic 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 bicarbonate ampules (50 ml ampules of 1 mEq/ml bicarbonate) are great for patients with hyponatremia. For example, two ampules (100 mEq/L) will 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 a baseline sodium over ~140 mEq/L, it may cause hypernatremia.
- Oral bicarbonate tablets can be used for patients with mild acidosis, to 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.
- 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 who is progressively accumulating fluid 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.
- Initiate phosphate binder if phosphate is >6 mg/dL.
- Calcium acetate (PHOSLO)
- 667 mg tablets, start with two tablets TID with meals
- Useful in patients with hypocalcemia. Avoid in hypercalcemia or vitamin D intoxication.
- Sevelamer (RENAGEL)
- Start at 800 mg PO TID with meals, double dose if needed.
- Nonabsorbable resin avoids problems with Mg, Ca (may be preferable for patients on dialysis).
- May impair absorption of some drugs from the gut.
clinical findings:
- Clinical context:
- GFR is usually <10-15 ml/min.
- Acute renal failure carries a higher risk than chronic renal failure.
- Movement disorders:
- Myoclonus and asterixis (“negative myoclonus”). Myoclonus has an extensive differential diagnosis 📖. In the absence of alternative 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
- 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 📖 (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)
- (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 (figure below).
- (2) Posterior Reversible Encephalopathy Syndrome (PRES): Uremia may promote the development of PRES, especially in combination with hypertension.📖
- (3) Acute toxic leukoencephalopathy.
differential diagnosis
- The differential diagnosis is broad, including other causes of delirium as discussed here: 📖
- 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 may be delayed for some days (e.g., the first dialysis run may cause transient worsening). (Louis 2021)
- 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)
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- Failing to fully evaluate AKI in the ICU. Most cases of AKI will resolve without specific intervention (e.g. with treatment of underlying sepsis). However, occasionally a specific issue is identified which requires specific therapy (e.g. Foley catheter obstruction, glomerulonephritis). Finding these patients is a bit like hunting for a needle in a haystack.
- Measurement of urine electrolytes and calculation of fractional excretion of sodium (FENa) isn't helpful.(27236480, 26689284, 27670788)
- Blind assumption that any patient with oliguria requires a fluid bolus.
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