Treatment algorithm

Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer

ACUTE

prerenal azotemia

1st line – volume expansion and/or red blood cell transfusion

Back
ACUTE
|
prerenal azotemia
1st line – 

volume expansion and/or red blood cell transfusion

The underlying cause of volume contraction or blood loss must be treated, along with restoring euvolemia and hemodynamic stability.

Crystalloid (normal saline or balanced solutions, such as Ringer’s lactate [Hartmann's solution]) is sufficient in most cases for volume expansion.[5][114]​​ Colloid might be used if there is significant hypoalbuminemia. 

In the US, the Food and Drug Administration (FDA) issued safety labeling changes in July 2021 for solutions containing hydroxyethyl starch (HES) stating that HES products should not be used unless adequate alternative treatment is unavailable.[115] Solutions containing HES are associated with adverse outcomes including kidney injury and death, particularly in critically ill patients and those with sepsis.[116][117] In view of the serious risks posed to these patient populations, the Pharmacovigilance Risk Assessment Committee of the European Medicines Agency in February 2022 recommended suspending HES solutions for infusion in Europe.[118]

The US National Kidney Foundation states that crystalloids are preferred over colloids for most patients with acute kidney injury, and recommends that hydroxyethyl starches are avoided.[111]

Evidence regarding the prevention of contrast-induced AKI is weak and often conflicting. Administration of normal saline at a dose of 1 mL/kg/hour for several hours before and after the contrast is believed to be beneficial in the prevention of contrast nephropathy.[60] However, a large study did not show benefit in patients at risk of contrast-induced nephropathy according to current guidelines.[63]

As prerenal azotemia predisposes the kidney to injury from other means, such as contrast or nephrotoxins, care should be given to minimize exposures and dose-adjust drugs to maximize recovery potential.

Hemorrhage requires blood product replacement.

Plus – vasopressor

Back
ACUTE
|
prerenal azotemia
|
with severe hypotension
Plus – 

vasopressor

Treatment recommended for ALL patients in selected patient group

Vasopressors are recommended for severe hypotension, often with the goal of keeping mean arterial pressure (MAP) >60 mmHg. (MAP is the diastolic pressure plus one third of the pulse pressure, where the pulse pressure is the systolic pressure minus the diastolic pressure.) All vasopressors should be used only with appropriate hemodynamic monitoring in place.

The underlying cause of hypotension needs to be treated along with restoring euvolemia and hemodynamic stability.

The septic patient requires hemodynamic support with vasopressors as needed to support MAP and organ perfusion.

Management is often difficult if renal hypoperfusion results from impaired cardiac function.[5][114]​​ It requires optimizing cardiac output and volume status. Inotropes, diuretics, or renal replacement therapy may be required.

Consult a specialist for guidance on suitable vasopressor regimen.

Consider – diuretic

Back
ACUTE
|
prerenal azotemia
|
with volume overload
Consider – 

diuretic

Treatment recommended for SOME patients in selected patient group

The use of diuretics may be helpful to manage volume in patients with ineffective circulating volume and prerenal AKI. Diuretic-unresponsive volume overload is an indication to proceed to renal replacement therapy by means of dialysis or filtration.

Impaired urine production and volume expansion are commonly seen in cases of AKI.

Loop diuretics (e.g., furosemide) and metolazone may be effective in promoting diuresis, although diuretic resistance is often seen.

Patients also require sodium restriction.

It is important to remove or minimize any nephrotoxins.

Primary options

furosemide: 40-80 mg intravenously initially, increase by 20 mg/dose increments every 2 hours as necessary until clinical response

Secondary options

torsemide: 20 mg intravenously once daily initially, increase gradually according to response, maximum 200 mg/day

OR

bumetanide: 1-2 mg intravenously initially, may repeat in 2-3 hours for up to 2 doses if necessary, maximum 10 mg/day

OR

metolazone: 5-20 mg orally once daily

Consider – renal replacement therapy

Back
ACUTE
|
prerenal azotemia
|
with uremia, severe metabolic acidosis, hyperkalemia refractory to medical management, or volume overload unresponsive to diuretics
Consider – 

renal replacement therapy

Treatment recommended for SOME patients in selected patient group

Nephrologist consultation is required.

Conventional hemodialysis for 4 to 6 hours is used in hemodynamically stable patients.

Other modes of renal replacement include sustained low-efficiency dialysis (SLED), extended daily dialysis (EDD), or continuous renal replacement therapy (CRRT).[122] Major commonly used modalities include continuous venovenous hemofiltration (CVVH), continuous venovenous hemodialysis (CVVHD), and continuous venovenous hemodiafiltration (CVVHDF).

CRRT is mostly used in hemodynamically unstable patients (e.g., patients with sepsis, or with severe congestive heart failure) or those in whom aggressive ultrafiltration within the conventional 4- to 6-hour treatment of hemodialysis would not be tolerated.

Studies have shown that intensive dialysis in critically ill patients with AKI confers no increased benefit.[122][123][124][125][137]

Early dialysis appeared to reduce mortality compared with a delayed strategy in one small single-center randomized trial of critically ill patients with AKI.[126] However, a larger study and meta-analysis found no benefit associated with early initiation of renal replacement therapy.[127][138]

intrinsic renal failure

1st line – treatment of underlying condition

Back
ACUTE
|
intrinsic renal failure
1st line – 

treatment of underlying condition

Management of intrinsic renal failure varies according to etiology. Nephrotoxic agents should be stopped and the patient referred to a nephrologist if specific treatment is required. This might include dialysis, management of fluids/acid-base status, treatment for severe hyperkalemia, or consideration for corticosteroids, immunosuppressants, or other immune-modifying drugs.

Consider – diuretic

Back
ACUTE
|
intrinsic renal failure
|
with volume overload
Consider – 

diuretic

Treatment recommended for SOME patients in selected patient group

The use of diuretics in the management of AKI is primarily for volume control. Diuretic-unresponsive volume overload is an indication to proceed to renal replacement therapy by means of dialysis or filtration.

Impaired urine production and volume expansion are commonly seen in cases of AKI.

Loop diuretics (e.g., furosemide) and metolazone may be effective in promoting diuresis, although diuretic resistance is often seen.

Patients also require sodium restriction.

It is important to remove or minimize any nephrotoxins.

Primary options

furosemide: 40-80 mg intravenously initially, increase by 20 mg/dose increments every 2 hours as necessary until clinical response

Secondary options

torsemide: 20 mg intravenously once daily initially, increase gradually according to response, maximum 200 mg/day

OR

bumetanide: 1-2 mg intravenously initially, may repeat in 2-3 hours for up to 2 doses if necessary, maximum 10 mg/day

OR

metolazone: 5-20 mg orally once daily

Consider – volume expansion

Back
ACUTE
|
intrinsic renal failure
|
with pre-existing prerenal azotemia
Consider – 

volume expansion

Treatment recommended for SOME patients in selected patient group

Crystalloid (normal saline or balanced solutions, such as Ringer’s lactate [Hartmann's solution]) is sufficient in most cases for volume expansion.[5][114]​​ Colloid might be used if there is significant hypoalbuminemia.

In the US, the Food and Drug Administration (FDA) issued safety labeling changes in July 2021 for solutions containing hydroxyethyl starch (HES) stating that HES products should not be used unless adequate alternative treatment is unavailable.[115] Solutions containing HES are associated with adverse outcomes including kidney injury and death, particularly in critically ill patients and those with sepsis.[116][117]​ In view of the serious risks posed to these patient populations, the Pharmacovigilance Risk Assessment Committee of the European Medicines Agency in February 2022 recommended suspending HES solutions for infusion in Europe.[118]

The US National Kidney Foundation states that crystalloids are preferred over colloids for most patients with acute kidney injury, and recommends that hydroxyethyl starches are avoided.[111]

As prerenal azotemia predisposes the kidney to injury from other means, such as contrast or nephrotoxins, care should be given to minimize exposures and dose-adjust drugs to maximize recovery potential.

Consider – renal replacement therapy

Back
ACUTE
|
intrinsic renal failure
|
with uremia, severe metabolic acidosis, hyperkalemia refractory to medical management, or volume overload unresponsive to diuretics
Consider – 

renal replacement therapy

Treatment recommended for SOME patients in selected patient group

Nephrologist consultation recommended.

Conventional hemodialysis is used in hemodynamically stable patients.

Other modes of renal replacement include sustained low-efficiency dialysis (SLED), extended daily dialysis (EDD), rapid-start peritoneal dialysis, or continuous renal replacement therapy (CRRT).[120][121]​ Major commonly used modalities include continuous venovenous hemofiltration (CVVH), continuous venovenous hemodialysis (CVVHD), and continuous venovenous hemodiafiltration (CVVHDF).

CRRT is mostly used in hemodynamically unstable patients (e.g., patients with sepsis or severe congestive heart failure) or those in whom aggressive ultrafiltration within the conventional 4-to 6-hour treatment of hemodialysis would not be tolerated.

Studies have shown that intensive dialysis in critically ill patients with AKI confers no increased benefit.[122][123][124][125][137]

Early dialysis appeared to reduce mortality compared with a delayed strategy in one small single-center randomized trial of critically ill patients with AKI, but subsequent meta-analyses found no clear benefit associated with early initiation of renal replacement therapy.[72][126][127][128][129]​​

obstructive renal failure

1st line – bladder catheterization

Back
ACUTE
|
obstructive renal failure
1st line – 

bladder catheterization

Treatment of obstructive renal failure requires mechanical decompression at the level of obstruction.

Bladder catheter placement should be done in all cases of AKI if bladder outlet obstruction cannot be quickly ruled out by ultrasound.

2nd line – relief of obstruction above bladder neck

Back
ACUTE
|
obstructive renal failure
2nd line – 

relief of obstruction above bladder neck

Further decompression more proximal in the genitourinary tract may be required if bladder neck obstruction is not the cause of the obstruction.

Urologic, radiologic, or surgical assistance for ureteral stenting, urinary diversion, debulking procedures, or other case-specific requirements may become necessary.

Surgical consultation may be needed if the cause is tumor with mass effect.

Primary options

ureteral stenting: if there is a ureteral stricture, stone or extrinsically obstructing mass

OR

lithotripsy: stones present at the ureteropelvic junction causing obstruction may require lithotripsy or surgical removal

OR

exploratory laparotomy: compressing tumors may require surgical removal; may be done following ureteral stenting

OR

percutaneous nephrostomy: placement of a catheter into the renal pelvis percutaneously for drainage of urine from a distal obstruction may be done by a urologist, surgeon or interventional radiologist

Consider – diuretic

Back
ACUTE
|
obstructive renal failure
|
with volume overload
Consider – 

diuretic

Treatment recommended for SOME patients in selected patient group

Diuretics should not be used in suspected complete obstruction.

The use of diuretics in the management of AKI is primarily for volume control.

Diuretic-unresponsive volume overload is an indication to proceed to renal replacement therapy by means of dialysis or filtration.

Impaired urine production and volume expansion are commonly seen in cases of AKI.

Loop diuretics (e.g., furosemide) and metolazone may be effective in promoting diuresis, although diuretic resistance is often seen.

Patients also require sodium restriction.

It is important to remove or minimize any nephrotoxins.

Primary options

furosemide: 40-80 mg intravenously initially, increase by 20 mg/dose increments every 2 hours as necessary until clinical response

Secondary options

torsemide: 20 mg intravenously once daily initially, increase gradually according to response, maximum 200 mg/day

OR

bumetanide: 1-2 mg intravenously initially, may repeat in 2-3 hours for up to 2 doses if necessary, maximum 10 mg/day

OR

metolazone: 5-20 mg orally once daily

Consider – renal replacement therapy

Back
ACUTE
|
obstructive renal failure
|
with uremia, severe metabolic acidosis, or hyperkalemia refractory to medical management, or volume overload unresponsive to diuretics
Consider – 

renal replacement therapy

Treatment recommended for SOME patients in selected patient group

Nephrologist consultation is recommended.

Conventional hemodialysis is used in hemodynamically stable patients. Other modes of renal replacement include sustained low-efficiency dialysis (SLED), extended daily dialysis (EDD), or rapid-start peritoneal dialysis; continuous renal replacement therapy (CRRT) is used if the patient is hemodynamically unstable despite full support.[120][121]​ 

Renal replacement therapy may be required to manage complications of obstruction while surgical interventions are planned and implemented.

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Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups. See disclaimer

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