Acute kidney injury (formally known as acute renal failure) is a common problem in the ICU. AKI is a syndrome characterized by the rapid loss of the kidney’s excretory function and is typically diagnosed by the accumulation of the end products of nitrogen metabolism (urea and creatinine) or decreased urine output or both [1, 2]. Although serum creatinine (Scr) is not a perfect marker of GFR, it is frequently used as a surrogate to estimate GFR. Currently, additional biomarkers are undergoing investigation as more sensitive indicators of AKI (cystatin C, IL-18, neutrophil gelatinase-associated lipocalin, kidney injury molecule 1, etc.) [2, 3]. AKI is defined as a twofold or greater increase in Scr, a GFR decrease of >50 % or urine output of 0.5 ml/kg/h for 12 h [2]. AKI represents a spectrum from risk to kidney injury to kidney failure to complete loss of kidney function. The RIFLE criteria have been used to define and classify AKI (see Table 41.1) [4]. In critically ill patients AKI is usually the result of extrarenal insults, most commonly sepsis, trauma, hypovolemic “shock”, and rhabdomyolysis. The pathophysiology of AKI in patients with sepsis is complex and poorly understood; however decreased renal blood flow does not appear to play a role [2]. AKI occurs in up to two-thirds of ICU patients and increasing severity of AKI is associated with increasing mortality [5]. Even modest degrees of AKI not resulting in dialysis treatment increase the risk of death approximately fivefold [6]. Coca and colleagues demonstrated that elevations of the Scr less than used in the RIFLE classification are associated with a twofold risk of short-term death [7]. In this study patients with a 10–24 % increase in Scr had a relative risk of death of 1.8 (95 % CI, 1.3–2.5). The mortality of patients who require dialysis has remained in excess of 50 % despite improvements in renal-replacement therapy and aggressive supportive care [8]. It is therefore essential that all efforts be made to avoid this complication; i.e. appropriate fluid resuscitation and avoidance of potentially nephrotoxic drugs. The therapeutic intervention of choice in patients with intravascular volume depletion and oliguria is fluid resuscitation and not furosemide/Lasix™. However, as discussed in Chap. 9, excessive volume resuscitation with a high central venous pressure will “paradoxically” impair renal function (see Chap. 8). A rational evidence-based approach to fluid resuscitation is therefore essential to reduce the risk of renal dysfunction in critically ill patients.

While low-dose dopamine increases renal blood flow and urine output in patients with normal renal function, dopamine does not improve renal function, reduce the need for dialysis or alter the course of AKI in critically ill patients [9]. In addition, studies have demonstrated that furosemide is of no value in modifying azotemia, reducing the need for dialysis, altering the time to recovery of renal function, reducing hospital stay or impacting survival in established AKI [10–12]. Indeed, diuretics have been reported to be associated with a significant increase in the risk of death and non-recovery of renal function [13]. A meta-analysis concluded that furosemide was not associated with any significant clinical benefit and perhaps an increased risk of harm [14]. Diuretics in any form (bolus, continuous infusion, topical) have no role in the management/prevention of acute renal failure (the only exceptions are patients with hypercalcemia/tumor lysis as part of a forced diuresis protocol). Optimization of intravascular volume, cardiac output and mean arterial pressure remains the cornerstone of both the prevention and treatment of AKI. No pharmacologic intervention has yet to be demonstrated to (positively) alter the clinical course of patients with renal dysfunction. In patients who remain oliguric/anuric after adequate fluid resuscitation it is important to exclude urinary tract obstruction (and urinary catheter obstruction), as this as an immediately reversible cause of acute renal failure. In patients with compromised renal function nephrotoxic drugs (particularly aminoglycosides and contract agents) should be avoided.