Approach
Early consultation with a nephrologist or an intensive care specialist improves the outcome of patients with ATN. The goals of management are avoidance of further kidney damage, treatment of underlying conditions, and aggressive treatment of complications. General issues include intervention in electrolyte and acid-base abnormalities and optimisation of volume status by replacing fluids. Dose adjustment of medicines is required in all cases along with removal or minimisation of potential nephrotoxins.
General treatment
There is no specific therapy for ATN apart from supportive care (i.e., maintaining volume status and controlling electrolyte and acid-base abnormalities).[5] Adequate maintenance of haemodynamics and renal perfusion is the basis of care. The use of vasopressors in conjunction with fluids in patients with vasomotor shock with, or at risk for, acute kidney injury (AKI) is recommended by the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines.[3]
Vasopressors are used under specialist guidance. Nephrotoxins (e.g., non-steroidal anti-inflammatory drugs, aminoglycosides, amphotericin-B, chemotherapeutic agents such as cisplatin, radiocontrast media) should preferably be ceased or, if this is not possible, dose should be decreased.
Dopamine, a selective renal vasodilator, has been used to increase urine output but does not alter the course of ATN. Moreover, it may be risky in critically ill patients.[5]
Volume replacement
The underlying cause of volume contraction or blood loss needs to be treated along with restoring euvolaemia and haemodynamic stability. Crystalloid (normal saline or lactated Ringer's) is sufficient in most cases for volume expansion. In the absence of haemorrhagic shock, the KDIGO guidelines suggest using isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume in patients at risk for AKI or with AKI.[3] Nevertheless, there is controversy and contradictory information in the literature when comparing balanced crystalloids versus normal isotonic saline in the critical care patient.[40] Normal isotonic saline has been associated with an increased risk of AKI and hyperchloraemic metabolic acidosis. Some of the balanced solutions are considered hypotonic given the lower sodium concentration compared with plasma and could be associated with metabolic alkalosis, hyperlactaemia, and hypotonicity.[41] A recent meta-analysis concludes that there are no significant differences between balanced crystalloids and isotonic saline in the incidence of in-hospital mortality, AKI, intensive care unit (ICU) mortality, or renal replacement therapy (RRT) in critically ill patients.[42] However, patients with AKI are especially at risk of fluid overload and this can contribute to the persistence of AKI. Therefore, in critically ill patients, it is important to take into account strategies like goal-directed therapies (GDT) to guide fluid therapy based on haemodynamic targets, which can protect against spare unwarranted fluid therapy.[43]
Contrast-induced AKI
Volume expansion with normal saline has been demonstrated to be beneficial in reducing the risk of contrast-induced nephropathy in patients at risk for contrast-induced AKI.[44][Evidence C] Target doses of normal saline at 1 mL/kg/hour have been demonstrated to have benefit.[45] Most studies suggest starting fluid therapy at least 1 hour before contrast and maintaining for 3-6 hours after. It is important to maintain a good diuretic rate >150 mL/hour after the procedure in order to achieve a euvolaemic diuresis. Current guidelines from the American College of Radiology recommend administration of 100 mL/hour intravenous isotonic saline for 6 to 12 hours before and 4 to 12 hours after radiocontrast exposure.[23] The European Society of Cardiology guidelines on myocardial revascularisation recommend intravenous isotonic saline 1-1.5 mL/kg/hour for 12 hours before and up to 24 hours after the procedure.[24] For outpatient or urgent procedures, administration of isotonic saline 1 to 3 hours before and 6 hours after could be beneficial.
The lowest possible dose of contrast medium should be used in patients at risk for contrast-induced AKI. The KDIGO guidelines recommend using either iso-osmolar or low-osmolar iodinated contrast media, rather than high-osmolar iodinated contrast media, in patients at increased risk of contrast-induced AKI.[3] No preventive benefit of RRT has been demonstrated. No pharmacological measure has shown any clear benefit. Routine administration of N-acetylcysteine is not recommended.[21][23][25] There are insufficient data to recommend discontinuing diuretics or ACE inhibitors. It would be appropriate to suspend other nephrotoxic agents (especially anti-inflammatories), and it is reasonable to temporarily stop treatment with metformin due to concern that lactic acidosis might develop.[21]
Use of diuretics
Diuretics should be used only if extracellular fluid volume and cardiac function are first carefully assessed and found to be adequate. Diuretics present some theoretical benefits; however, the administration of diuretics such as furosemide in controlled studies increases diuresis, facilitating the management of fluid balance, hyperkalaemia, and hypercalcaemia, but does not improve the course of the disease. Furosemide has not shown efficacy in terms of the duration of renal failure, need for dialysis, or the time to recovery of renal function. In one study, furosemide did not reduce the rate of worsening AKI, nor did it improve recovery or reduce RRT in critically ill patients. It was, however, associated with greater electrolyte abnormalities.[46] It is important to monitor electrolytes to avoid and/or correct hypokalaemia and hypomagnesaemia, as well as acid-base status, because chloride losses exceed sodium losses and hypochloraemic metabolic alkalosis could develop.
The KDIGO guidelines suggest not using diuretics to treat AKI, except in the management of volume overload.[3]
Mannitol, another diuretic, although not routinely used, has been reported to be useful in ATN caused by crush injury if administered early in the course of treatment.[5]
Renal replacement therapy
RRT (i.e., haemodialysis, haemofiltration, haemodiafiltration) may be required if the patient has severe metabolic acidosis, organ dysfunction due to diuretic-resistant fluid overload, severe hyperkalaemia, or uraemia complications (e.g., pericarditis, encephalopathy). The KDIGO guidelines provide recommendations on RRT for AKI.[3] However, agreement on the thresholds is lacking. However, agreement on the thresholds is lacking. There are other factors to take into account when considering RRT, such as the tolerability to water overload (e.g., poor in acute or severe chronic cardiorespiratory pathology), potential for short-term reversibility of underlying disease, and trends in kidney function. It is also important to consider dialysis-related complications.[47]
There are several options for supporting lost renal function and selection involves evaluation of the patient's overall condition with haemodynamic and laboratory evaluation. Determining the type of support and therapy and when to start is at the recommendation of the nephrologist. In critically ill patients, a multidisciplinary care team composed of nephrologists and intensivists is required.
The timing of RRT in the critical care patient with AKI is a source of intense debate and must therefore be considered on an individual basis. One study concluded that among patients with septic shock who had severe AKI, there was no significant difference in overall mortality at 90 days between patients who were assigned to an early strategy for the initiation of RRT and those who were assigned to a delayed strategy.[48] However, there are other populations (e.g., post-operative cardiac surgery patients) where the results are conflicting.[49]
Conventional haemodialysis is often used in haemodynamically stable patients.
Other modes of renal replacement include the continuous renal replacement therapies (CRRT). Major commonly used modalities include continuous venovenous haemofiltration (CVVH), continuous venovenous haemodialysis (CVVHD), and continuous venovenous haemodiafiltration (CVVHDF).
Use of CRRT is most beneficial in haemodynamically unstable patients or those in whom aggressive ultra-filtration within the conventional 4- to 6-hour treatment of haemodialysis would not be tolerated. These patients include septic patients requiring vasopressors, or patients with severe heart failure with volume overload and a blood pressure that would not support conventional haemodialysis.[50][51][52]
In addition to continuous or intermittent modalities, combination approaches such as hybrid therapies may be used. A large double lumen catheter has to be placed into the central venous system, usually through the internal jugular or femoral vein. Prolonged intermittent renal replacement therapies (PIRRT) combine characteristics of both techniques and could be indicated in unstable patients with low doses of vasoactive drugs. The combined approaches have improved haemodynamic tolerability, greater 'down time' for diagnosis and therapeutic procedures, reduction of the duration of exposure to anticoagulation, and lower cost.
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