For updates on diagnosis and management of coexisting conditions during the pandemic, see our topic "Management of coexisting conditions in the context of COVID-19".

Treatment approaches for AKI vary according to the type of insult. The underlying illness requires treatment.

General therapy includes intervention in electrolyte and acid/base abnormalities and optimization of volume status, either by replacing volume in the volume-contracted patient or by fluid removal (either diuresis or renal replacement therapy) in patients with volume overload.

Sodium and volume restriction are generally required along with limiting potassium and phosphorus intake.

Dose adjustment of medications is likely required in all cases and should not be overlooked. Patients with AKI should not be given potentially nephrotoxic drugs unless there is no alternative. Electrolyte and acid-base balance should be monitored and optimized. Early involvement by a nephrologist may be valuable;[90] however, automated electronic alerts to identify AKI have not improved outcomes.[91]

Prerenal renal failure

Prerenal azotemia is managed with techniques to improve the hemodynamic status of the patient.

The volume-contracted patient requires volume expansion with crystalloid or colloid (but not hydroxyethyl starch [HES]) to restore euvolemia.

Crystalloid (normal saline or lactated Ringers) or colloid (considered in cases of significant hypoalbuminemia) fluids are infused, along with packed red blood cells if there is significant anemia.[5] The use of semisynthetic HES is not advised, as mortality appears to be increased.[92]

All fluid resuscitation should be performed by a clinician with expertise in this area, with close patient monitoring.

Vasopressors are recommended if hypotension is severe, to augment blood pressure while optimizing the patient's volume status.[5] A common goal of vasopressors in this setting is to keep the 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.)

Management is often difficult if renal hypoperfusion results from impaired cardiac function due to poor left ventricular systolic function. It requires optimization of cardiac output and volume status by use of inotropes, diuretics, or renal replacement therapy as indicated by the clinical scenario, along with close monitoring of renal function and urine production during therapy.[5]

Vasopressors and inotropic agents should be used only with appropriate hemodynamic monitoring in place.

Renal replacement therapy may be needed if severe acid/base, electrolyte, or uremic complications are present while the underlying cardiac or volume issues are treated. The use of diuretics may be helpful to manage volume in patients with ineffective circulating volume and prerenal AKI. Diuretic-unresponsive volume overload, increased potassium, severe metabolic acidosis, or uremic symptoms are indications to proceed to renal replacement therapy by means of dialysis or filtration.[5]

Intrinsic renal failure

Management of intrinsic renal failure varies according to etiology.

Volume expansion is required when coexisting prerenal azotemia exists. It is unclear whether a chloride-sparing intravenous fluid strategy improves outcomes in critically ill patients.[69][70] Larger randomized studies remain necessary to alter practice.[70]

Generally, patients with volume overload require sodium restriction. The amount of sodium restriction depends on the clinical setting. Volume overload may be managed with diuretics when effective.

Removal of offending drugs, when possible, is necessary in cases of interstitial nephritis or drug-induced AKI.

Acute glomerulonephritis and vasculitis management may also require corticosteroids, cytotoxic agents, or other immune-modifying drugs depending on the specific diagnosis, often determined by renal biopsy and serology studies.

The management of acute glomerulonephritis requires a nephrologist consultation, particularly regarding the use of cytotoxic and immune-modifying agents. Doses and protocols for many of the drugs used vary by center. The Kidney Disease: Improving Global Outcomes (KDIGO) clinical practice guideline for glomerulonephritis can be consulted. KDIGO clinical practice guideline for glomerulonephritis external link opens in a new window

There is no specific therapy for acute tubular necrosis aside from maintaining volume status and controlling electrolyte and acid/base abnormalities. Nephrotoxins should be removed or minimized. Renal replacement therapy is generally required if there is severe acidosis, volume expansion refractory to diuretics, hyperkalemia, or uremia.

Obstructive renal failure

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

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

Renal replacement therapy is generally required if there is severe acidosis, volume overload unresponsive to diuretics, or electrolyte or uremic complications while the underlying obstructive issue is being addressed.

Renal replacement therapy

Renal replacement therapy is indicated for refractory severe hyperkalemia, acidosis, volume overload, or uremia.

Conventional hemodialysis is often used when the indications for dialysis arise. Other modes of renal replacement include sustained low-efficiency dialysis (SLED), extended daily dialysis (EDD), or continuous renal replacement therapy (CRRT).[93] Arteriovenous and venovenous techniques may be used, although the most frequent approach is continuous venovenous treatment through a large double lumen catheter placed into the central venous system, such as the internal jugular or femoral vein. Major commonly used modalities include continuous venovenous hemofiltration (CVVH), continuous venovenous hemodialysis (CVVHD), and continuous venovenous hemodiafiltration (CVVHDF).[93][94][95][96]

CRRT is mostly used in hemodynamically unstable patients or those in whom aggressive ultrafiltration within the conventional 4- to 6-hour treatment of hemodialysis would not be tolerated. Such patients include septic patients requiring vasopressors, or patients with severe heart failure with volume overload and a blood pressure that would not support conventional hemodialysis. Despite improved hemodynamic stability, studies have shown that CRRT or more intensive/frequent dialysis in critically ill patients with AKI confers no increased benefit with respect to other complications or mortality.[94][95][96]

Early dialysis appeared to reduce mortality compared with a delayed strategy in one small single-center randomized trial of critically ill patients with AKI,[97] but a larger study and meta-analysis found no benefit associated with early initiation of renal replacement therapy.[98][99]

Peritoneal dialysis has generally been thought ineffective in AKI and hypercatabolic states, although some studies suggest comparable effectiveness in appropriate subjects. In developing countries, high-volume peritoneal dialysis (HVPD) provides an alternative form of therapy in selected cases.[100][101][102]

Peripheral venous cannulation: animated demonstrationPeripheral venous cannulation: animated demonstration

Female urethral catheterisation: animated demonstrationFemale urethral catheterisation: animated demonstration

Male urethral catheterisation: animated demonstrationMale urethral catheterisation: animated demonstration

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