Oliguria in critically ill patients: a narrative review

Abstract

Oliguria is often observed in critically ill patients. However, different thresholds in urine output (UO) have raised discussion as to the clinical importance of a transiently reduced UO of less than 0.5 ml/kg/h lasting for at least 6 h. While some studies have demonstrated that isolated oliguria without a concomitant increase in serum creatinine is associated with higher mortality rates, different underlying pathophysiological mechanisms suggest varied clinical importance of reduced UO, as some episodes of oliguria may be fully reversible. We aim to explore the clinical relevance of oliguria in critically ill patients and propose a clinical pathway for the diagnostic and therapeutic management of an oliguric, critically ill patient.

Keywords: Acute kidney injury; Biomarker; Oliguria; Renal replacement therapy.

Fig. 1

Physiological and pathological stimuli leading to oliguria (RAA renin–angiotensin–aldosterone system, AKI acute kidney injury)

Fig. 2

4-step approach (step 1 - hemodynamic stabilization, step 2a - response to diuretics and FST, step 2b - biomarkers [steps 2a and 2b may be considered as alternative approaches], step 3 - AKI workup, step 4 - management and treatment of volume overload)  to the clinical management of the oliguric patient (UO urine output, MAP mean arterial pressure, FST furosemide stress test, AKI acute kidney injury, CysC cystatin C, NGAL neutrophil gelatinase-associated lipocalin, TIMP-2 x IGFBP-7 tissue inhibitor of metalloproteinase 2 × insulin-like growth factor binding protein 7, BUN blood urea nitrogen, RRT renal replacement therapy)