Understanding urine output in critically ill patients

Abstract

Urine output often is used as a marker of acute kidney injury but also to guide fluid resuscitation in critically ill patients. Although decrease of urine output may be associated to a decrease of glomerular filtration rate due to decrease of renal blood flow or renal perfusion pressure, neurohormonal factors and functional changes may influence diuresis and natriuresis in critically ill patients. The purpose of this review is to discuss the mechanisms of diuresis regulation, which may help to interpret the urine output in critically ill patients and the appropriate treatment to be initiated in case of changes in urine output.

Figure 1

Schematic representation of the glomerular capillary hydraulic and oncotic pressure in normal kidneys (A and B) and pathologic kidneys with decrease of the total ultrafiltration surface (C and D). The difference between the hydraulic pressure difference [P_GC, glomerular capillary hydraulic pressure-P_T hydraulic pressure in Bowman's space) and the intracapillary oncotic pressure (∏_GC) represents the effective filtration pressure gradient. In normal condition (A), the P_GC-_PT slightly decreases along the glomerular capillary axe and the ∏_GC increases leading to equilibrium between the opposing forces to filtration. If renal perfusion pressure and P_GC increase (B), the point of equilibrium is reached earlier along the axe due to increase of filtration fraction. GFR does not change and only increase of renal plasma flow and decrease of filtration fraction causes the GFR to increase (B). GFR is likely to increase with rise of renal perfusion pressure if the filtration surface is impaired, the point of equilibrium not being reached (C and D). Note the role of plasma oncotic pressure. Infusion of crystalloid decreases plasma oncotic pressure due to hemodilution favoring the net filtration pressure while infusion of colloids increases plasma oncotic pressure therefore reducing GFR. GFR, glomerular filtration rate.

Figure 2

Schematic view of regulating factors of diuresis and natriuresis. Renal blood flow, renal perfusion pressure, and plasma oncotic pressure influence the effective filtration pressure gradient. Afferent and efferent glomerular arteriole tone can further influence the glomerular capillary hydraulic pressure while tubular cast accumulation increases the Bowman's hydrostatic pressure decreasing the effective filtration pressure gradient. Finally intrarenal blood flow distribution, conformational changes of tubule Na+/H+ exchanger, urea, and chloride channels and aquaporin-2 expression regulate water and sodium (Na⁺) handling of the ultrafiltrate (see text for further details). GFR, glomerular filtration rate.