KDIGO Clinical Practice Guideline for Acute Kidney Injury
Oliguria and anuria

Oliguria and anuria

Although urine output is both a reasonably sensitive functional index for the kidney as well as a biomarker of tubular injury, the relationship between urine output and GFR, and tubular injury is complex. For example, oliguria may be more profound when tubular function is intact. Volume depletion and hypotension are profound stimuli for vasopressin secretion. As a consequence the distal tubules and collecting ducts become fully permeable to water. Concentrating mechanisms in the inner medulla are also aided by low flow through the loops of Henle and thus, urine volume is minimized and urine concentration maximized ( > 500 m Osmol/kg). Conversely, when the tubules are injured, maximal concentrating ability is impaired and urine volume may even be normal (i.e., nonoliguric renal failure). Analysis of the urine to determine tubular function has a long history in clinical medicine. Indeed, a high urine osmolality coupled with a low urine sodium in the face of oliguria and azotemia is strong evidence of intact tubular function. However, this should not be interpreted as ‘‘benign’’ or even prerenal azotemia. Intact tubular function, particularly early on, may be seen with various forms of renal disease (e.g., glomerulonephritis). Sepsis, the most common condition associated with ARF in the intensive-care unit (ICU)⁷ may alter renal function without any characteristic changes in urine indices.^8,9 Automatically classifying these abnormalities as ‘‘prerenal’’ will undoubtedly lead to incorrect management decisions. Classification as ‘‘benign azotemia’’ or ‘‘acute renal success’’ is not consistent with available evidence. Finally, although severe oliguria and even anuria may result from renal tubular damage, it can also be caused by urinary tract obstruction and by total arterial or venous occlusion. These conditions will result in rapid and irreversible damage to the kidney and require prompt recognition and management.