What Is the Treatment of Acute Tubular Necrosis in Critically Ill Patients?
Acute tubular necrosis (ATN) is a primary cause of acute kidney injury. In critically ill patients, management requires coordinated attention to fluid balance, haemodynamic stabilisation, and metabolic support to limit further renal injury.
Clinical Situation
This protocol addresses general supportive management of ATN, with specific considerations for critically ill patients in whom volume status, haemodynamic support, and nutritional and metabolic optimisation are central to care.
Treatment Approach
Management involves intravascular volume expansion with a specific class of fluid, haemodynamic support with vasopressors where vasomotor shock is present, and structured nutritional and metabolic care delivered via a preferred route. The complete protocol defines the priorities and the decision points for each component.
Full details — including fluid choice, vasopressor strategy, nutrition route, and metabolic targets — are in the structured protocol below.
Key Clinical Goal
In critically ill patients, the protocol specifies a defined plasma glucose target range as a measurable endpoint of metabolic management.
References
- In the absence of hemorrhagic shock, we 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.
- We recommend the use of vasopressors in conjunction with fluids in patients with vasomotor shock with, or at risk for, AKI.
- In critically ill patients, we suggest insulin therapy targeting plasma glucose 110–149 mg/dl (6.1–8.3 mmol/l).
- We suggest achieving a total energy intake of 20–30 kcal/kg/d in patients with any stage of AKI.
- We suggest providing nutrition preferentially via the enteral route in patients with AKI.
- We suggest not using diuretics to treat AKI, except in the management of volume overload.