What is non-oliguric (without decreased urine output) acute kidney injury?

Non-Oliguric Acute Kidney Injury

Non-oliguric acute kidney injury is AKI that occurs with preserved urine output (≥0.5 mL/kg/hour), diagnosed solely by serum creatinine criteria without meeting the oliguria thresholds defined by KDIGO guidelines.

Definition and Diagnostic Criteria

Non-oliguric AKI is defined as meeting the KDIGO serum creatinine criteria for AKI (increase ≥0.3 mg/dL within 48 hours OR ≥50% increase from baseline within 7 days) while maintaining urine output ≥0.5 mL/kg/hour for 6 hours. 1, 2

• The KDIGO criteria include both creatinine-based and urine output-based thresholds, but patients need only meet ONE criterion to be diagnosed with AKI 3
• Oliguria is specifically defined as urine output <0.5 mL/kg/hour for at least 6 consecutive hours 4
• When urine output remains above this threshold despite rising creatinine, the patient has non-oliguric AKI 5

Clinical Significance and Prognosis

Non-oliguric AKI carries significantly better prognosis than oliguric AKI, with lower morbidity and mortality rates. 5

• Most contemporary cases of acute kidney injury actually present as non-oliguric, contrary to historical teaching that oliguria was a cardinal feature 5
• Non-oliguric AKI can occur across all etiologies including prerenal azotemia, intrinsic renal disease, postrenal obstruction, and acute tubular necrosis 5
• The preserved urine output indicates less severe tubular dysfunction and better preservation of nephron function 5

Special Clinical Contexts Where Urine Output Criteria Are Unreliable

In patients with cirrhosis and ascites, urine output criteria should be completely disregarded for AKI diagnosis, relying exclusively on serum creatinine changes. 3

• Cirrhotic patients are frequently oliguric due to avid sodium retention despite maintaining relatively normal glomerular filtration rate 3
• Diuretic therapy in these patients artificially increases urine output without improving kidney function, making output measurements misleading 3
• The International Club of Ascites consensus specifically recommends abandoning urine output criteria in this population 3

Patients receiving diuretics should have AKI diagnosis based primarily on creatinine criteria rather than urine output. 4

• Diuretic administration can change oliguria classification without changing actual kidney function 4
• This creates false reassurance when output appears adequate but kidney injury is progressing 4

Diagnostic Approach

Diagnose non-oliguric AKI by monitoring serum creatinine at 48-hour intervals to detect the 0.3 mg/dL threshold, regardless of maintained urine output. 1

• Use the most recent known creatinine value from the medical record as baseline—this is superior to imputation methods 3, 1
• If no baseline exists, back-calculate using the MDRD equation assuming GFR of 75 mL/min/1.73 m² 3, 1
• Small increases in serum creatinine (≥0.3 mg/dL) are independently associated with approximately fourfold increase in hospital mortality 1

Common Pitfalls to Avoid

Do not wait for oliguria to develop before diagnosing AKI—this delays recognition and intervention in the majority of cases. 5, 6

• Historical teaching emphasized oliguria as essential for AKI diagnosis, but this is outdated 5
• Most acute kidney injury occurs with well-maintained urine output 5
• Relying solely on urine output without monitoring creatinine misses the majority of AKI cases 3

Do not use the outdated threshold of creatinine ≥1.5 mg/dL to diagnose AKI, as this often indicates GFR has already fallen to approximately 30 mL/min. 3

• The fixed threshold of 1.5 mg/dL fails to capture dynamic changes in creatinine that occur early in kidney injury 3
• Focus on temporal changes from baseline rather than absolute values 3

In obese patients, consider using adjusted body weight to calculate urine output thresholds, as the weight-based definition becomes problematic. 4

• The relationship between body weight and expected urine output is nonlinear 4
• Standard calculations may misclassify obese patients 4

Management Implications

Non-oliguric AKI requires the same fundamental management as oliguric AKI: identify and treat the underlying cause, optimize volume status, discontinue nephrotoxins, and adjust medication dosing for renal function. 6, 2, 7

• The preserved urine output does not eliminate the need for nephrology consultation when meeting criteria for stage 2 or 3 AKI 2, 7
• Uncontrolled studies suggest that early intervention with volume expansion and diuretics may convert oliguric to non-oliguric AKI, though prospective trials are needed 5
• The better prognosis of non-oliguric AKI does not justify less aggressive monitoring or management 5