Version July 2025
INTRODUCTION —
The glomerular filtration rate (GFR) may fall to very low levels in patients with intrinsic acute kidney injury (AKI). However, a low GFR is not necessarily associated with a parallel reduction in urine output [1,2]. This topic addresses urine output in AKI and associations between lower urine volume, AKI severity, and increased mortality.
The evaluation and management of AKI, as well as kidney and patient outcomes after AKI, are discussed separately:
●(See "Evaluation of acute kidney injury among hospitalized adult patients".)
●(See "Overview of the management of acute kidney injury (AKI) in adults".)
●(See "Possible prevention and therapy of ischemic acute tubular necrosis".)
●(See "Kidney and patient outcomes after acute kidney injury in adults".)
PRINCIPLES AND DEFINITIONS
Determinants of urine output in AKI — The difference in urine output between oliguric and nonoliguric acute kidney injury (AKI) is due to variations in either the glomerular filtration rate (GFR), the rate of tubular reabsorption, or both. Nonoliguric patients may have a higher GFR than those with oliguria, and/or they may reabsorb less filtrate in the renal tubules. Healthy kidneys typically reabsorb more than 98 to 99 percent of filtered fluid, but kidneys with tubular injury may reabsorb substantially less. For example, if the GFR falls to 7 L/day (equal to 5 mL/min), the urine output will be relatively normal at 1 to 2 L/day if only 5 to 6 L (or approximately 70 to 85 percent) of filtered fluid is reabsorbed.
Definition of oliguria — Oliguria is a volume of urine that is insufficient to excrete the daily solute load. Commonly used values of urine output to define oliguria vary, ranging from <0.3 to 0.5 mL/kg per hour to <400 to 500 mL/day. The lack of a universally accepted value is due to between-person and within-person differences in the daily renal solute load, which is determined by solute intake (predominantly sodium and protein) and the catabolic state.
URINE OUTPUT AND CAUSE OF AKI
Oliguric versus non-oliguric AKI — AKI is often, but not always, characterized by oliguria. Normal urine output can be maintained even with an abnormally low glomerular filtration rate (GFR), especially in patients with less severe ATN or in patients with ATN characterized by a pronounced concentrating defect, as in cisplatin nephrotoxicity. (See 'Determinants of urine output in AKI' above.)
Causes of anuric AKI — In contrast to oliguria, which is common in patients with AKI, anuria (<50 to 100 mL/day) is rare. Anuria reflects severe AKI, which will likely require dialytic therapy unless there is prompt recovery. Anuria generally occurs as a result of the following conditions:
●Severe ATN due to prolonged shock
●Bilateral urinary tract obstruction, or unilateral obstruction with an absent or nonfunctional contralateral kidney
●Bilateral renal artery obstruction, as seen in abdominal aortic dissection
●Pregnancy-related cortical necrosis
Oliguria may progress to genuine anuria in other cases of severe AKI, such as untreated thrombotic microangiopathy and rapidly progressive (crescentic) glomerulonephritis.
OLIGURIA AND AKI SEVERITY —
The prognosis of nonoliguric AKI is generally better than oliguric or anuric disease [1,3-5].
●Oliguria as a risk factor for severe AKI – Oliguria may predict the development of severe AKI. This was suggested in a retrospective analysis of 390 critically ill patients with septic shock [6]. Oliguria, defined as urine output <0.5 mL/kg per hour and observed within the first three to five hours following recognition of septic shock, was positively associated with the development of stage 2 or 3 AKI (defined by Kidney Disease: Improving Global Outcomes [KDIGO] criteria (table 1)) and the need for kidney replacement therapy (KRT). In this study, ≥5 hours of consecutive oliguria predicted subsequent stage 2 or 3 AKI with an accuracy of 82 percent [6].
●Oliguria as a marker of severe AKI – Studies in animal models have shown that there is less morphologic and functional damage in nonoliguric compared with oliguric AKI [7]. There is also evidence in humans suggesting that the absence of oliguria in AKI generally reflects less severe disease [1,8-10]. The following observations from different studies are illustrative:
•One report noted a direct correlation between the urine flow rate and the residual GFR in patients with three to six days of AKI [8]. Oliguric patients generally had a GFR (measured by creatinine and inulin clearance) of <5 mL/min compared with 10 to 15 mL/min in patients with a urine volume of 50 to 100 mL/hour.
•In other studies, nonoliguric patients had a lower peak serum creatinine concentration (6 versus 9 mg/dL [528 versus 792 micromol/L]) than oliguric patients [1] and a lower incidence of requiring dialysis during the acute phase of the illness (28 versus 84 percent and 46 versus 82 percent in different studies) [1,9].
•In an analysis of an electronic database derived from patients admitted to the intensive care unit in one medical center, the relationship of absolute and relative serum creatinine increments and urine output decrements over a continuous spectrum of observation time intervals was evaluated [11]. Among 14,526 patients included in the analysis, oliguria <0.5 mL/kg per hour was associated with a sharp increase in the requirement for KRT.
•More recent analyses underscore the prognostic importance of oliguria in addition to serum creatinine-based criteria for AKI in the clinical setting [12,13]. One such study included data from 32,045 patients treated at a single center, 74.5 percent of whom developed AKI according to the KDIGO staging criteria [12]. While oliguria criteria alone and serum creatinine increment criteria alone were associated with only a 2.1 percent and 4.9 percent need for KRT, respectively, the combination of oliguria and serum creatinine increment criteria was associated with a 25 percent need for KRT.
●Conversion of oliguric to non-oliguric AKI – Although the administration of diuretics in AKI has not been shown to improve kidney function or creatinine trajectory (see 'Limited role of diuretics' below), an increase in urine output (ie, the conversion of anuric or oliguric AKI to nonoliguric AKI) spontaneously or with the use of diuretics often reflects less severe kidney injury or kidney function recovery [14]. This phenomenon is illustrated by studies examining the use of furosemide “stress tests” to predict the severity of AKI [15,16]. In one such study, 77 critically ill patients with early AKI (defined as stage 1 or 2 AKI using Acute Kidney Injury Network [AKIN] criteria) received a standardized dose of intravenous furosemide [15]. In the six hours following furosemide, the mean hourly urine output of the 52 patients who did not progress to stage 3 AKI was significantly greater than that of the 25 patients who did progress to stage 3 AKI. For patients with a urine volume <200 ml in the two hours after furosemide administration, the sensitivity and specificity for the development of stage 3 AKI were 87 percent and 84 percent, respectively. A subsequent study reported that a furosemide stress test outperformed the use of urinary biomarkers for the prediction of AKI severity [16].
OLIGURIA, POSITIVE FLUID BALANCE, AND INCREASED MORTALITY —
Both oliguria and a positive fluid balance are independently associated with increased mortality in patients with acute kidney injury (AKI) in multiple prospective observational studies [3,6,11,13,17-25].
The following findings are illustrative:
●In a study of critically ill patients that included 1120 patients with AKI, oliguric patients had a greater mean positive fluid balance than nonoliguric patients (620 versus 270 mL) and a significantly higher 60-day mortality rate (41 versus 33 percent) [18].
●In a cohort of 1453 patients enrolled in the Randomized Evaluation of Normal versus Augmented Level renal replacement therapy trial, the mean daily fluid balance was +560 mL/day among nonsurvivors compared with -234 mL/day among survivors [20]. A negative mean daily fluid balance was independently associated with a significantly lower risk of death at 90 days (odds ratio [OR] 0.32, 95% CI 0.24-0.43).
●In the Fluids and Catheters Treatment Trial, 306 of 1000 patients developed AKI [21]. Among these patients, positive fluid balance was associated with an increased adjusted 60-day mortality (OR 1.6 per L/day, 95% CI 1.3-2.0).
●A retrospective analysis from a single center evaluated 15,395 patients who were transferred from an intensive care unit to a regular medical or surgical ward [22]. The adjusted hazard ratio for 90-day mortality was higher in the fourth (median +7.6 liters) compared with the first (-1.5 liters) quartile of fluid balance (adjusted hazard ratio 1.35, 95% CI 1.13-1.61). These results were driven by patients suffering from congestive heart failure, AKI, or kidney function impairment. [23,24]
However, nonoliguric AKI is not necessarily associated with a better prognosis in all settings. In an observational study of patients with AKI who required dialysis, a higher urine volume was independently associated with increased time from admission to start of dialysis and higher in-hospital mortality (OR 3.8, 95% CI 1.1-12.8) [26]. Delay in initiation of dialysis, prompted by response to diuretic therapy and anticipation of recovery of kidney function, may be a contributing factor to the increase in mortality in some patients with nonoliguric AKI.
The connections between oliguria, positive fluid balance, and increased mortality do not suggest that fluids should be withheld from patients with oliguric AKI. Rather, an individualized approach is appropriate that combines accurate assessment of the effective volume status and the hemodynamic and urine output response to fluid bolus administration. The immediate physiologic benefits of volume expansion in patients with circulatory failure and volume depletion should not be overlooked. This was demonstrated in a study of 49 critically ill patients with hypotension, need for vasopressors, oliguria, or reduced central or mixed venous oxygen saturation who were compared with 39 control subjects [27]. Fluid administration resulted in a small but consistent decrease in Doppler sonographically measured resistivity index (RI) in renal interlobar arteries and increases in mean arterial pressure and urine output. The increase in urine output was predicted by changes in RI, but not changes in mean arterial pressure in this analysis.
LIMITED ROLE OF DIURETICS —
The main indication for diuretic therapy in patients with acute kidney injury (AKI) is short-term treatment for volume control. However, such use should not postpone the initiation of dialysis, if required [28]. The use of diuretics to increase urine output in patients with established oliguric AKI does not shorten the duration of kidney failure, decrease the requirement for dialysis, or improve survival. Among patients with oliguria and established AKI, diuretics should not be used as a possible therapy of AKI [28,29]. (See "Overview of the management of acute kidney injury (AKI) in adults", section on 'Role of diuretics' and "Possible prevention and therapy of ischemic acute tubular necrosis", section on 'Treatment'.)
In a blinded, placebo-controlled trial of 73 adults with AKI admitted to the intensive care unit, furosemide did not impact the trajectory of AKI or reduce the need for kidney replacement therapy [30]. Furthermore, patients in the intervention group were more likely to suffer from electrolyte abnormalities. This trial is consistent with a large observational study of patients admitted to five adult intensive care units, which found that loop diuretic use in patients with AKI was not associated with the progression of AKI [31]. On the other hand, another observational study of critically ill patients with AKI reported an association between furosemide administration and improved short-term survival and recovery of kidney function [32]. However, in the latter observational study furosemide was used more frequently in surgical patients and in patients with milder AKI.
SUMMARY AND RECOMMENDATIONS
●Principles and definitions – The difference in urine output between oliguric and nonoliguric acute kidney injury (AKI) may be due to variations in the glomerular filtration rate (GFR) and/or the rate of tubular reabsorption. Oliguria is a volume of urine that is insufficient to excrete the daily solute load. Commonly used values of urine output to define oliguria vary, ranging from <0.3 to 0.5 mL/kg per hour to <400 to 500 mL/day. (See 'Principles and definitions' above.)
●Urine output and cause of AKI – In contrast to oliguria, which is common in patients with AKI, anuria (urine output <50 to 100 mL/day) is rare. Anuria reflects severe AKI, which will likely require dialytic therapy unless there is prompt recovery. Anuria generally occurs as a result of the following conditions (see 'Urine output and cause of AKI' above):
•Severe ATN due to prolonged shock
•Bilateral urinary tract obstruction, or unilateral obstruction with an absent or nonfunctional contralateral kidney
•Bilateral renal artery obstruction, as seen in abdominal aortic dissection
•Pregnancy-related cortical necrosis
Oliguria may progress to genuine anuria in other cases of severe AKI, such as untreated thrombotic microangiopathy and rapidly progressive (crescentic) glomerulonephritis.
●Oliguria and prognosis – The prognosis of nonoliguric AKI is generally better than oliguric or anuric disease. (See 'Oliguria and AKI severity' above and 'Oliguria, positive fluid balance, and increased mortality' above.)
●Limited role of diuretics – The main indication for diuretic therapy in patients with AKI is short-term treatment for volume control. The use of diuretics to increase urine output in patients with established oliguric AKI does not shorten the duration of kidney failure, decrease the requirement for dialysis, or improve survival. (See 'Limited role of diuretics' above.)
